Viruses which lack a complete genome so that they cannot completely replicate or cannot form a protein coat. Some are host-dependent defectives, meaning they can replicate only in cell systems which provide the particular genetic function which they lack. Others, called SATELLITE VIRUSES, are able to replicate only when their genetic defect is complemented by a helper virus.
Acquired defect of cellular immunity that occurs in mice infected with mouse leukemia viruses (MuLV). The syndrome shows striking similarities with human AIDS and is characterized by lymphadenopathy, profound immunosuppression, enhanced susceptibility to opportunistic infections, and B-cell lymphomas.
Viruses which enable defective viruses to replicate or to form a protein coat by complementing the missing gene function of the defective (satellite) virus. Helper and satellite may be of the same or different genus.
The process of intracellular viral multiplication, consisting of the synthesis of PROTEINS; NUCLEIC ACIDS; and sometimes LIPIDS, and their assembly into a new infectious particle.
A phenomenon in which infection by a first virus results in resistance of cells or tissues to infection by a second, unrelated virus.
Species of GAMMARETROVIRUS, containing many well-defined strains, producing leukemia in mice. Disease is commonly induced by injecting filtrates of propagable tumors into newborn mice.
The functional hereditary units of VIRUSES.
Deoxyribonucleic acid that makes up the genetic material of viruses.
Ribonucleic acid that makes up the genetic material of viruses.
Proteins found in any species of virus.
Established cell cultures that have the potential to propagate indefinitely.
The complete genetic complement contained in a DNA or RNA molecule in a virus.
Viruses whose genetic material is RNA.
A test used to determine whether or not complementation (compensation in the form of dominance) will occur in a cell with a given mutant phenotype when another mutant genome, encoding the same mutant phenotype, is introduced into that cell.
The type species of ORTHOPOXVIRUS, related to COWPOX VIRUS, but whose true origin is unknown. It has been used as a live vaccine against SMALLPOX. It is also used as a vector for inserting foreign DNA into animals. Rabbitpox virus is a subspecies of VACCINIA VIRUS.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Specific molecular components of the cell capable of recognizing and interacting with a virus, and which, after binding it, are capable of generating some signal that initiates the chain of events leading to the biological response.
Process of growing viruses in live animals, plants, or cultured cells.
The expelling of virus particles from the body. Important routes include the respiratory tract, genital tract, and intestinal tract. Virus shedding is an important means of vertical transmission (INFECTIOUS DISEASE TRANSMISSION, VERTICAL).
A general term for diseases produced by viruses.
A species of POLYOMAVIRUS originally isolated from Rhesus monkey kidney tissue. It produces malignancy in human and newborn hamster kidney cell cultures.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
The assembly of VIRAL STRUCTURAL PROTEINS and nucleic acid (VIRAL DNA or VIRAL RNA) to form a VIRUS PARTICLE.
Viruses parasitic on plants higher than bacteria.
Viruses whose nucleic acid is DNA.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
The type species of ALPHAVIRUS normally transmitted to birds by CULEX mosquitoes in Egypt, South Africa, India, Malaya, the Philippines, and Australia. It may be associated with fever in humans. Serotypes (differing by less than 17% in nucleotide sequence) include Babanki, Kyzylagach, and Ockelbo viruses.
The type species of MORBILLIVIRUS and the cause of the highly infectious human disease MEASLES, which affects mostly children.
A subtype of INFLUENZA A VIRUS with the surface proteins hemagglutinin 1 and neuraminidase 1. The H1N1 subtype was responsible for the Spanish flu pandemic of 1918.
The type species of LYSSAVIRUS causing rabies in humans and other animals. Transmission is mostly by animal bites through saliva. The virus is neurotropic multiplying in neurons and myotubes of vertebrates.
A subtype of INFLUENZA A VIRUS comprised of the surface proteins hemagglutinin 5 and neuraminidase 1. The H5N1 subtype, frequently referred to as the bird flu virus, is endemic in wild birds and very contagious among both domestic (POULTRY) and wild birds. It does not usually infect humans, but some cases have been reported.
A subtype of INFLUENZA A VIRUS comprised of the surface proteins hemagglutinin 3 and neuraminidase 2. The H3N2 subtype was responsible for the Hong Kong flu pandemic of 1968.
The type species of the genus ORTHOHEPADNAVIRUS which causes human HEPATITIS B and is also apparently a causal agent in human HEPATOCELLULAR CARCINOMA. The Dane particle is an intact hepatitis virion, named after its discoverer. Non-infectious spherical and tubular particles are also seen in the serum.
A species of FLAVIVIRUS, one of the Japanese encephalitis virus group (ENCEPHALITIS VIRUSES, JAPANESE). It can infect birds and mammals. In humans, it is seen most frequently in Africa, Asia, and Europe presenting as a silent infection or undifferentiated fever (WEST NILE FEVER). The virus appeared in North America for the first time in 1999. It is transmitted mainly by CULEX spp mosquitoes which feed primarily on birds, but it can also be carried by the Asian Tiger mosquito, AEDES albopictus, which feeds mainly on mammals.
A group of viruses in the PNEUMOVIRUS genus causing respiratory infections in various mammals. Humans and cattle are most affected but infections in goats and sheep have also been reported.
The mechanism by which latent viruses, such as genetically transmitted tumor viruses (PROVIRUSES) or PROPHAGES of lysogenic bacteria, are induced to replicate and then released as infectious viruses. It may be effected by various endogenous and exogenous stimuli, including B-cell LIPOPOLYSACCHARIDES, glucocorticoid hormones, halogenated pyrimidines, IONIZING RADIATION, ultraviolet light, and superinfecting viruses.
Substances elaborated by viruses that have antigenic activity.
The type species of VESICULOVIRUS causing a disease symptomatically similar to FOOT-AND-MOUTH DISEASE in cattle, horses, and pigs. It may be transmitted to other species including humans, where it causes influenza-like symptoms.
The ability of a pathogenic virus to lie dormant within a cell (latent infection). In eukaryotes, subsequent activation and viral replication is thought to be caused by extracellular stimulation of cellular transcription factors. Latency in bacteriophage is maintained by the expression of virally encoded repressors.
Membrane glycoproteins from influenza viruses which are involved in hemagglutination, virus attachment, and envelope fusion. Fourteen distinct subtypes of HA glycoproteins and nine of NA glycoproteins have been identified from INFLUENZA A VIRUS; no subtypes have been identified for Influenza B or Influenza C viruses.
Viruses that produce tumors.
A CELL LINE derived from the kidney of the African green (vervet) monkey, (CERCOPITHECUS AETHIOPS) used primarily in virus replication studies and plaque assays.
Species of the genus LENTIVIRUS, subgenus primate immunodeficiency viruses (IMMUNODEFICIENCY VIRUSES, PRIMATE), that induces acquired immunodeficiency syndrome in monkeys and apes (SAIDS). The genetic organization of SIV is virtually identical to HIV.
A species of CERCOPITHECUS containing three subspecies: C. tantalus, C. pygerythrus, and C. sabeus. They are found in the forests and savannah of Africa. The African green monkey (C. pygerythrus) is the natural host of SIMIAN IMMUNODEFICIENCY VIRUS and is used in AIDS research.
The type species of RUBULAVIRUS that causes an acute infectious disease in humans, affecting mainly children. Transmission occurs by droplet infection.
A species of RESPIROVIRUS also called hemadsorption virus 2 (HA2), which causes laryngotracheitis in humans, especially children.
Viruses which produce a mottled appearance of the leaves of plants.
The infective system of a virus, composed of the viral genome, a protein core, and a protein coat called a capsid, which may be naked or enclosed in a lipoprotein envelope called the peplos.
A species in the genus HEPATOVIRUS containing one serotype and two strains: HUMAN HEPATITIS A VIRUS and Simian hepatitis A virus causing hepatitis in humans (HEPATITIS A) and primates, respectively.
A species of ALPHAVIRUS isolated in central, eastern, and southern Africa.
Group of alpharetroviruses (ALPHARETROVIRUS) producing sarcomata and other tumors in chickens and other fowl and also in pigeons, ducks, and RATS.
Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly.
The measurement of infection-blocking titer of ANTISERA by testing a series of dilutions for a given virus-antiserum interaction end-point, which is generally the dilution at which tissue cultures inoculated with the serum-virus mixtures demonstrate cytopathology (CPE) or the dilution at which 50% of test animals injected with serum-virus mixtures show infectivity (ID50) or die (LD50).
Method for measuring viral infectivity and multiplication in CULTURED CELLS. Clear lysed areas or plaques develop as the VIRAL PARTICLES are released from the infected cells during incubation. With some VIRUSES, the cells are killed by a cytopathic effect; with others, the infected cells are not killed but can be detected by their hemadsorptive ability. Sometimes the plaque cells contain VIRAL ANTIGENS which can be measured by IMMUNOFLUORESCENCE.
The binding of virus particles to receptors on the host cell surface. For enveloped viruses, the virion ligand is usually a surface glycoprotein as is the cellular receptor. For non-enveloped viruses, the virus CAPSID serves as the ligand.
A species of POLYOMAVIRUS apparently infecting over 90% of children but not clearly associated with any clinical illness in childhood. The virus remains latent in the body throughout life and can be reactivated under certain circumstances.
Infections produced by oncogenic viruses. The infections caused by DNA viruses are less numerous but more diverse than those caused by the RNA oncogenic viruses.
Viruses whose taxonomic relationships have not been established.
A species of POLYOMAVIRUS, originally isolated from the brain of a patient with progressive multifocal leukoencephalopathy. The patient's initials J.C. gave the virus its name. Infection is not accompanied by any apparent illness but serious demyelinating disease can appear later, probably following reactivation of latent virus.
The type species of ALPHARETROVIRUS producing latent or manifest lymphoid leukosis in fowl.
The relationships of groups of organisms as reflected by their genetic makeup.
A family of RNA viruses causing INFLUENZA and other diseases. There are five recognized genera: INFLUENZAVIRUS A; INFLUENZAVIRUS B; INFLUENZAVIRUS C; ISAVIRUS; and THOGOTOVIRUS.
The type species of ORBIVIRUS causing a serious disease in sheep, especially lambs. It may also infect wild ruminants and other domestic animals.
Virus diseases caused by the ORTHOMYXOVIRIDAE.
Any of the processes by which cytoplasmic factors influence the differential control of gene action in viruses.
The type species of RESPIROVIRUS in the subfamily PARAMYXOVIRINAE. It is the murine version of HUMAN PARAINFLUENZA VIRUS 1, distinguished by host range.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) arising during the propagation of S37 mouse sarcoma, and causing lymphoid leukemia in mice. It also infects rats and newborn hamsters. It is apparently transmitted to embryos in utero and to newborns through mother's milk.
Insertion of viral DNA into host-cell DNA. This includes integration of phage DNA into bacterial DNA; (LYSOGENY); to form a PROPHAGE or integration of retroviral DNA into cellular DNA to form a PROVIRUS.
The outer protein protective shell of a virus, which protects the viral nucleic acid.
The type species of the FLAVIVIRUS genus. Principal vector transmission to humans is by AEDES spp. mosquitoes.
A genus of the family HERPESVIRIDAE, subfamily ALPHAHERPESVIRINAE, consisting of herpes simplex-like viruses. The type species is HERPESVIRUS 1, HUMAN.
The type species of TOBAMOVIRUS which causes mosaic disease of tobacco. Transmission occurs by mechanical inoculation.
Pneumovirus infections caused by the RESPIRATORY SYNCYTIAL VIRUSES. Humans and cattle are most affected but infections in goats and sheep have been reported.
The type species of LEPORIPOXVIRUS causing infectious myxomatosis, a severe generalized disease, in rabbits. Tumors are not always present.
Inactivation of viruses by non-immune related techniques. They include extremes of pH, HEAT treatment, ultraviolet radiation, IONIZING RADIATION; DESICCATION; ANTISEPTICS; DISINFECTANTS; organic solvents, and DETERGENTS.

A novel Vpr peptide interactor fused to integrase (IN) restores integration activity to IN-defective HIV-1 virions. (1/1328)

A novel approach to complement human immunodeficiency virus type I (HIV-1) integrase (IN)-defective virions has been identified. The approach involves fusion of a 23-amino-acid stretch to the N-terminus of wild-type IN and coexpression of this chimera with the IN-defective proviral template in virus producing cells. The 23-amino-acid peptide represents a Vpr "interactor," referred to as the the WxxF or WF domain, which apparently leads to docking of the domain along with the fusion partner onto HIV-1 Vpr, thus permitting virion incorporation of the chimeric protein when expressed, in trans, with other viral products. Transfection of the WF-IN expression plasmid along with HIV-1 viral clones that produce Vpr, but bear an IN mutation, results in the release of a proportion of viral particles that are competent for integration. The extent of complementation was assessed using the MAGI cell assay, where integration of viral DNA results in the eventual appearance of easily visible multinucleated blue syncytia. The efficiency of dWF-IN (double copy of WF domain) complementation is not improved markedly by incorporation of a HIV-1 protease cleavage site (PR) between the dWF domain and IN (dWF-PR-IN), unlike that observed with Vpr fusions to IN. Furthermore, the ability of Vpr-PR-IN and dWF-PR-IN to complement IN-defective proviral clones, both of which bear an intervening protease cleavage site, appear comparable. Western blotting analyses using virions isolated through sucrose cushions demonstrate clearly the incorporation of the dWF-IN fusion protein into Vpr containing HIV-1 particles but not in Vpr-deficient virions. Additional Western blotting analyses indicate that all Vpr-IN and dWF-IN chimeras, with or without a PR site, are packaged into virions. The efficiency of virion incorporation of Vpr-IN and dWF-IN chimeras appears approximately comparable by Western blotting analysis. The ability of dWF-IN to complement IN-defective proviruses with efficiency similar to that of Vpr-PR-IN and dWF-PR-IN indicates that dWF-IN retains the full complement of functions necessary for integration of proviral DNA and is likely due to the benign nature of this small domain at the amino-terminus of IN.  (+info)

Enhancer-like properties of an RNA element that modulates Tombusvirus RNA accumulation. (2/1328)

Prototypical defective interfering (DI) RNAs of the plus-strand RNA virus tomato bushy stunt virus contain four noncontiguous segments (regions I-IV) derived from the viral genome. Region I corresponds to 5'-noncoding sequence, regions II and III are derived from internal positions, and region IV represents a 3'-terminal segment. We analyzed the internally located region III in a prototypical DI RNA to understand better its role in DI RNA accumulation. Our results indicate that (1) region III is not essential for DI RNA accumulation, but molecules that lack it accumulate at significantly reduced levels ( approximately 10-fold lower), (2) region III is able to function at different positions and in opposite orientations, (3) a single copy of region III is favored over multiple copies, (4) the stimulatory effect observed on DI RNA accumulation is not due to region III-mediated RNA stabilization, (5) DI RNAs lacking region III permit the efficient accumulation of head-to-tail dimers and are less effective at suppressing helper RNA accumulation, and (6) negative-strand accumulation is also significantly depressed for DI RNAs lacking region III. Collectively, these results support a role for region III as an enhancer-like element that facilitates DI RNA replication. A scanning-type mutagenesis strategy was used to define portions of region III important for its stimulatory effect on DI RNA accumulation. Interestingly, the results revealed several differences in the requirements for activity when region III was in the forward versus the reverse orientation. In the context of the viral genome, region III was found to be essential for biological activity. This latter finding defines a critical role for this element in the reproductive cycle of the virus.  (+info)

New defective RNAs from citrus tristeza virus: evidence for a replicase-driven template switching mechanism in their generation. (3/1328)

Defective RNAs (D-RNAs) ranging in size from 1968 to 2759 nt were detected in four citrus tristeza virus (CTV) isolates by hybridization of electroblotted dsRNAs with two probes specific for the 5'- and 3'-terminal genomic regions. The RNAs that hybridized with both probes were eluted, cloned and sequenced. Comparison with the sequences of the corresponding genomic regions of the helper virus showed, in all cases, over 99% nucleotide identity and direct repeats of 4-5 nt flanking or in the vicinity of the junction sites. The presence of the repeats from two separate genome locations suggests a replicase-driven template switching mechanism for the generation of these CTV D-RNAs. Two of the CTV isolates that differed greatly in their pathogenicity contained an identical D-RNA, suggesting that it is unlikely that this D-RNA is involved in symptom modulation, which may be caused by another factor.  (+info)

The quaternary structure of the sheaths of defective phages similar to PBS X. (4/1328)

The contractile sheaths of five defective, PBS X-like bacteriophages from Bacillus subtilis and B. licheniformis were investigated by electron microscopy, dodecylsulphate gel electrophoresis and immunodiffusion. Electron microscope images of the extended and contracted sheaths were of similar appearance, although their lengths were different. The surface lattices of both the extended and the contracted sheaths were determined by optical diffraction. This showed that the quaternary structure of the sheaths of all five defective phages originated from identical surface lattices, which could be approximately expressed by the selection rules L = -2n' + 3m and L = 9N' + 17M for the extended and contracted sheaths respectively, in which 6n' = n with n = 0 or an integer multiple of 6. These results indicated that the packing of the protein subunits in these sheaths differed from those of other bacteriophages, for example T4 and millimicron [Amos and Klug, J. Mol. Biol. 99, 51--73 (1975); Admiraal and Mellema, J. Ultrastruct. Res. 56, 48--64 (1976)]. The molecular weight of the main sheath protein of the defective phages, as determined by dodecylsulphate gel electrophoresis, was approximately 50000. This value differed from that for T4, but was similar to that of millimicron [Admiraal and Mellema, J. Ultrastruct. Res. 56, 48--64 (1976); King and Laemmli, J. Mol. Biol, 75, 315--337 (1973)]. The results of immunodiffusion experiments, however, pointed to a chemical difference between the sheath proteins of the defective phages and millimicron, in addition to T4.  (+info)

Experimental gene therapy against subcutaneously implanted glioma with a herpes simplex virus-defective vector expressing interferon-gamma. (5/1328)

We investigated the feasibility of local treatment or tumor vaccination with a herpes simplex virus (HSV) type 1-defective vector. The vector was engineered to express murine interferon-gamma (IFN-gamma) for experimental gene therapy against mouse glioma Rous sarcoma virus (RSV). The murine IFN-gamma gene was driven by the cytomegalovirus promoter. The helper virus (tsk) was thermosensitive; consequently, this vector could only proliferate at 31 degrees C. A high level of murine IFN-gamma expression was confirmed in vitro and in vivo by immunohistochemistry using anti-mouse IFN-gamma monoclonal antibody. This engineered vector (dvHSV/MulFN-gamma) inhibited the proliferation of mouse glioma RSV cells in vitro, and an intratumoral (i.t.) local injection of the vector caused i.t. necrosis in vivo. The immunological effect of dvHSV/MulFN-gamma was also examined in a mouse glioma RSV cell implantation model. A subcutaneous (s.c.) implant of 1 x 10(6) mouse glioma RSV cells after treatment with dvHSV/MulFN-gamma was rejected. However, the implant after treatment with an engineered HSV-defective vector containing an antisense nucleotide sequence of the murine IFN-gamma gene was not rejected. In addition, in another group of mice in which RSV cells treated with dvHSV/MulFN-gamma were implanted into a femoral (s.c.) region and nontreated RSV cells were implanted into a contralateral femoral (s.c.) region, the implanted RSV cells were rejected. The rejection of the implanted mouse glioma RSV was blocked by anti-asialo GM1, which was known to inhibit natural killer cell activity. These results revealed that the HSV-defective vector could realize a high efficiency of transfection to glioma cells through short-time treatment, and that the IFN-gamma gene transferred to the cells had the effect of tumor vaccination, which was suggested be related to natural killer cells. In conclusion, dvHSV/MulFN-gamma may be useful for the gene therapy of malignant glioma through either i.t. local injection or a practical tumor vaccination with ex vivo gene transfer.  (+info)

Virus promoters determine interference by defective RNAs: selective amplification of mini-RNA vectors and rescue from cDNA by a 3' copy-back ambisense rabies virus. (6/1328)

Typical defective interfering (DI) RNAs are more successful in the competition for viral polymerase than the parental (helper) virus, which is mostly due to an altered DI promoter composition. Rabies virus (RV) internal deletion RNAs which possess the authentic RV terminal promoters, and which therefore are transcriptionally active and can be used as vectors for foreign gene expression, are poorly propagated in RV-infected cells and do not interfere with RV replication. To allow DI-like amplification and high-level gene expression from such mini-RNA vectors, we have used an engineered 3' copy-back (ambisense) helper RV in which the strong replication promoter of the antigenome was replaced with the 50-fold-weaker genome promoter. In cells coinfected with ambisense helper virus and mini-RNAs encoding chloramphenicol acetyltransferase (CAT) and luciferase, mini-RNAs were amplified to high levels. This was correlated with interference with helper virus replication, finally resulting in a clear predominance of mini-RNAs over helper virus. However, efficient successive passaging of mini-RNAs and high-level reporter gene activity could be achieved without adding exogenous helper virus, revealing a rather moderate degree of interference not precluding substantial HV propagation. Compared to infections with recombinant RV vectors expressing CAT, the availability of abundant mini-RNA templates led to increased levels of CAT mRNA such that CAT activities were augmented up to 250-fold, while virus gene transcription was kept to a minimum. We have also exploited the finding that internal deletion model RNAs behave like DI RNAs and are selectively amplified in the presence of ambisense helper virus to demonstrate for the first time RV-supported rescue of cDNA after transfection of mini-RNA cDNAs in ambisense RV-infected cells expressing T7 RNA polymerase.  (+info)

Genetic and fitness changes accompanying adaptation of an arbovirus to vertebrate and invertebrate cells. (7/1328)

The alternating host cycle and persistent vector infection may constrain the evolution of arboviruses. To test this hypothesis, eastern equine encephalitis virus was passaged in BHK or mosquito cells, as well as in alternating (both) host cell passages. High and low multiplicities were used to examine the effect of defective interfering particles. Clonal BHK and persistent mosquito cell infections were also evaluated. Fitness was measured with one-step growth curves and competition assays, and mutations were evaluated by nucleotide sequencing and RNA fingerprinting. All passages and assays were done at 32 degrees C to eliminate temperature as a selection factor. Viruses passaged in either cell type alone exhibited fitness declines in the bypassed cells, while high-multiplicity and clonal passages caused fitness declines in both types of cells. Bypassed cell fitness losses were mosquito and vertebrate specific and were not restricted to individual cell lines. Fitness increases occurred in the cell line used for single-host-adaptation passages and in both cells for alternately passaged viruses. Surprisingly, single-host-cell passage increased fitness in that cell type no more than alternating passages. However, single-host-cell adaptation resulted in more mutations than alternating cell passages. Mosquito cell adaptation invariably resulted in replacement of the stop codon in nsP3 with arginine or cysteine. In one case, BHK cell adaptation resulted in a 238-nucleotide deletion in the 3' untranslated region. Many nonsynonymous substitutions were shared among more than one BHK or mosquito cell passage series, suggesting positive Darwinian selection. Our results suggest that alternating host transmission cycles constrain the evolutionary rates of arboviruses but not their fitness for either host alone.  (+info)

Different doses of adenoviral vector expressing IL-12 enhance or depress the immune response to a coadministered antigen: the role of nitric oxide. (8/1328)

Joint immunization with two recombinant adenoviruses, one expressing hepatitis C virus (HCV) core and E1 proteins and another expressing IL-12 (RAdIL-12), strongly potentiates cellular immune response against HCV Ags in BALB/c mice when RAdIL-12 was used at doses of 1 x 105-1 x 107 plaque-forming units. However, cellular immunity against HCV Ags was abolished when higher doses (1 x 108 plaque-forming units) of RAdIL-12 were used. This immunosuppressive effect was associated with marked elevation of IFN-gamma and nitric oxide in the serum and increased cell apoptosis in the spleen. Administration of N-nitro-L -arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, to mice that received high doses of RAdIL-12 was lethal, whereas no apparent systemic toxicity by L -NAME was observed in those immunized with lower doses of the adenovirus. Interestingly, in mice immunized with recombinant adenovirus expressing core and E1 proteins of HCV in combination with RAdIL-12 at low doses (1 x 107 plaque-forming units), L -NAME inhibited T cell proliferation and CTL activity in response to HCV Ags and also production of Abs against adenoviral proteins. In conclusion, gene transfer of IL-12 can increase or abolish cell immunity against an Ag depending of the dose of the vector expressing the cytokine. IL-12 stimulates the synthesis of NO which is needed for the immunostimulating effects of IL-12, but apoptosis of T cells and immunosuppression ensues when IFN-gamma and NO are generated at very high concentrations.  (+info)

Defective viruses are viruses that have lost the ability to complete a full replication cycle and produce progeny virions independently. These viruses require the assistance of a helper virus, which provides the necessary functions for replication. Defective viruses can arise due to mutations, deletions, or other genetic changes that result in the loss of essential genes. They are often non-infectious and cannot cause disease on their own, but they may interfere with the replication of the helper virus and modulate the course of infection. Defective viruses can be found in various types of viruses, including retroviruses, bacteriophages, and DNA viruses.

I'm sorry for any confusion, but there seems to be a misunderstanding. Murine Acquired Immunodeficiency Syndrome (MAIDS) is not related to human medicine. It is a disease that affects mice and is caused by a retrovirus similar to the Human Immunodeficiency Virus (HIV). MAIDS is used as an animal model to study certain aspects of HIV infection and AIDS. The disease is characterized by immune system dysfunction, leading to susceptibility to various opportunistic infections and cancers, much like human AIDS. However, it's essential to clarify that MAIDS is not a human health concern.

Helper viruses, also known as "auxiliary" or "satellite" viruses, are defective viruses that depend on the assistance of a second virus, called a helper virus, to complete their replication cycle. They lack certain genes that are essential for replication, and therefore require the helper virus to provide these functions.

Helper viruses are often found in cases of dual infection, where both the helper virus and the dependent virus infect the same cell. The helper virus provides the necessary enzymes and proteins for the helper virus to replicate, package its genome into new virions, and bud off from the host cell.

One example of a helper virus is the hepatitis B virus (HBV), which can serve as a helper virus for hepatitis D virus (HDV) infection. HDV is a defective RNA virus that requires the HBV surface antigen to form an envelope around its nucleocapsid and be transmitted to other cells. In the absence of HBV, HDV cannot replicate or cause disease.

Understanding the role of helper viruses in viral infections is important for developing effective treatments and vaccines against viral diseases.

Virus replication is the process by which a virus produces copies or reproduces itself inside a host cell. This involves several steps:

1. Attachment: The virus attaches to a specific receptor on the surface of the host cell.
2. Penetration: The viral genetic material enters the host cell, either by invagination of the cell membrane or endocytosis.
3. Uncoating: The viral genetic material is released from its protective coat (capsid) inside the host cell.
4. Replication: The viral genetic material uses the host cell's machinery to produce new viral components, such as proteins and nucleic acids.
5. Assembly: The newly synthesized viral components are assembled into new virus particles.
6. Release: The newly formed viruses are released from the host cell, often through lysis (breaking) of the cell membrane or by budding off the cell membrane.

The specific mechanisms and details of virus replication can vary depending on the type of virus. Some viruses, such as DNA viruses, use the host cell's DNA polymerase to replicate their genetic material, while others, such as RNA viruses, use their own RNA-dependent RNA polymerase or reverse transcriptase enzymes. Understanding the process of virus replication is important for developing antiviral therapies and vaccines.

Viral interference is a phenomenon where the replication of one virus is inhibited or blocked by the presence of another virus. This can occur when two different viruses infect the same cell and compete for the cell's resources, such as nucleotides, energy, and replication machinery. As a result, the replication of one virus may be suppressed, allowing the other virus to predominate.

This phenomenon has been observed in both in vitro (laboratory) studies and in vivo (in the body) studies. It has been suggested that viral interference may play a role in the outcome of viral coinfections, where an individual is infected with more than one virus at the same time. Viral interference can also be exploited as a potential strategy for antiviral therapy, where one virus is used to inhibit the replication of another virus.

It's important to note that not all viruses interfere with each other, and the outcome of viral coinfections can depend on various factors such as the specific viruses involved, the timing and sequence of infection, and the host's immune response.

Medical Definition:

Murine leukemia virus (MLV) is a type of retrovirus that primarily infects and causes various types of malignancies such as leukemias and lymphomas in mice. It is a complex genus of viruses, with many strains showing different pathogenic properties.

MLV contains two identical single-stranded RNA genomes and has the ability to reverse transcribe its RNA into DNA upon infection, integrating this proviral DNA into the host cell's genome. This is facilitated by an enzyme called reverse transcriptase, which MLV carries within its viral particle.

The virus can be horizontally transmitted between mice through close contact with infected saliva, urine, or milk. Vertical transmission from mother to offspring can also occur either in-utero or through the ingestion of infected breast milk.

MLV has been extensively studied as a model system for retroviral pathogenesis and tumorigenesis, contributing significantly to our understanding of oncogenes and their role in cancer development. It's important to note that Murine Leukemia Virus does not infect humans.

Viral genes refer to the genetic material present in viruses that contains the information necessary for their replication and the production of viral proteins. In DNA viruses, the genetic material is composed of double-stranded or single-stranded DNA, while in RNA viruses, it is composed of single-stranded or double-stranded RNA.

Viral genes can be classified into three categories: early, late, and structural. Early genes encode proteins involved in the replication of the viral genome, modulation of host cell processes, and regulation of viral gene expression. Late genes encode structural proteins that make up the viral capsid or envelope. Some viruses also have structural genes that are expressed throughout their replication cycle.

Understanding the genetic makeup of viruses is crucial for developing antiviral therapies and vaccines. By targeting specific viral genes, researchers can develop drugs that inhibit viral replication and reduce the severity of viral infections. Additionally, knowledge of viral gene sequences can inform the development of vaccines that stimulate an immune response to specific viral proteins.

Viral DNA refers to the genetic material present in viruses that consist of DNA as their core component. Deoxyribonucleic acid (DNA) is one of the two types of nucleic acids that are responsible for storing and transmitting genetic information in living organisms. Viruses are infectious agents much smaller than bacteria that can only replicate inside the cells of other organisms, called hosts.

Viral DNA can be double-stranded (dsDNA) or single-stranded (ssDNA), depending on the type of virus. Double-stranded DNA viruses have a genome made up of two complementary strands of DNA, while single-stranded DNA viruses contain only one strand of DNA.

Examples of dsDNA viruses include Adenoviruses, Herpesviruses, and Poxviruses, while ssDNA viruses include Parvoviruses and Circoviruses. Viral DNA plays a crucial role in the replication cycle of the virus, encoding for various proteins necessary for its multiplication and survival within the host cell.

A viral RNA (ribonucleic acid) is the genetic material found in certain types of viruses, as opposed to viruses that contain DNA (deoxyribonucleic acid). These viruses are known as RNA viruses. The RNA can be single-stranded or double-stranded and can exist as several different forms, such as positive-sense, negative-sense, or ambisense RNA. Upon infecting a host cell, the viral RNA uses the host's cellular machinery to translate the genetic information into proteins, leading to the production of new virus particles and the continuation of the viral life cycle. Examples of human diseases caused by RNA viruses include influenza, COVID-19 (SARS-CoV-2), hepatitis C, and polio.

Viral proteins are the proteins that are encoded by the viral genome and are essential for the viral life cycle. These proteins can be structural or non-structural and play various roles in the virus's replication, infection, and assembly process. Structural proteins make up the physical structure of the virus, including the capsid (the protein shell that surrounds the viral genome) and any envelope proteins (that may be present on enveloped viruses). Non-structural proteins are involved in the replication of the viral genome and modulation of the host cell environment to favor viral replication. Overall, a thorough understanding of viral proteins is crucial for developing antiviral therapies and vaccines.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

A viral genome is the genetic material (DNA or RNA) that is present in a virus. It contains all the genetic information that a virus needs to replicate itself and infect its host. The size and complexity of viral genomes can vary greatly, ranging from a few thousand bases to hundreds of thousands of bases. Some viruses have linear genomes, while others have circular genomes. The genome of a virus also contains the information necessary for the virus to hijack the host cell's machinery and use it to produce new copies of the virus. Understanding the genetic makeup of viruses is important for developing vaccines and antiviral treatments.

RNA viruses are a type of virus that contain ribonucleic acid (RNA) as their genetic material, as opposed to deoxyribonucleic acid (DNA). RNA viruses replicate by using an enzyme called RNA-dependent RNA polymerase to transcribe and replicate their RNA genome.

There are several different groups of RNA viruses, including:

1. Negative-sense single-stranded RNA viruses: These viruses have a genome that is complementary to the mRNA and must undergo transcription to produce mRNA before translation can occur. Examples include influenza virus, measles virus, and rabies virus.
2. Positive-sense single-stranded RNA viruses: These viruses have a genome that can serve as mRNA and can be directly translated into protein after entry into the host cell. Examples include poliovirus, rhinoviruses, and coronaviruses.
3. Double-stranded RNA viruses: These viruses have a genome consisting of double-stranded RNA and use a complex replication strategy involving both transcription and reverse transcription. Examples include rotaviruses and reoviruses.

RNA viruses are known to cause a wide range of human diseases, ranging from the common cold to more severe illnesses such as hepatitis C, polio, and COVID-19. Due to their high mutation rates and ability to adapt quickly to new environments, RNA viruses can be difficult to control and treat with antiviral drugs or vaccines.

A genetic complementation test is a laboratory procedure used in molecular genetics to determine whether two mutated genes can complement each other's function, indicating that they are located at different loci and represent separate alleles. This test involves introducing a normal or wild-type copy of one gene into a cell containing a mutant version of the same gene, and then observing whether the presence of the normal gene restores the normal function of the mutated gene. If the introduction of the normal gene results in the restoration of the normal phenotype, it suggests that the two genes are located at different loci and can complement each other's function. However, if the introduction of the normal gene does not restore the normal phenotype, it suggests that the two genes are located at the same locus and represent different alleles of the same gene. This test is commonly used to map genes and identify genetic interactions in a variety of organisms, including bacteria, yeast, and animals.

Vaccinia virus is a large, complex DNA virus that belongs to the Poxviridae family. It is the virus used in the production of the smallpox vaccine. The vaccinia virus is not identical to the variola virus, which causes smallpox, but it is closely related and provides cross-protection against smallpox infection.

The vaccinia virus has a unique replication cycle that occurs entirely in the cytoplasm of infected cells, rather than in the nucleus like many other DNA viruses. This allows the virus to evade host cell defenses and efficiently produce new virions. The virus causes the formation of pocks or lesions on the skin, which contain large numbers of virus particles that can be transmitted to others through close contact.

Vaccinia virus has also been used as a vector for the delivery of genes encoding therapeutic proteins, vaccines against other infectious diseases, and cancer therapies. However, the use of vaccinia virus as a vector is limited by its potential to cause adverse reactions in some individuals, particularly those with weakened immune systems or certain skin conditions.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

Virus receptors are specific molecules (commonly proteins) on the surface of host cells that viruses bind to in order to enter and infect those cells. This interaction between the virus and its receptor is a critical step in the infection process. Different types of viruses have different receptor requirements, and identifying these receptors can provide important insights into the biology of the virus and potential targets for antiviral therapies.

Virus cultivation, also known as virus isolation or viral culture, is a laboratory method used to propagate and detect viruses by introducing them to host cells and allowing them to replicate. This process helps in identifying the specific virus causing an infection and studying its characteristics, such as morphology, growth pattern, and sensitivity to antiviral agents.

The steps involved in virus cultivation typically include:

1. Collection of a clinical sample (e.g., throat swab, blood, sputum) from the patient.
2. Preparation of the sample by centrifugation or filtration to remove cellular debris and other contaminants.
3. Inoculation of the prepared sample into susceptible host cells, which can be primary cell cultures, continuous cell lines, or embryonated eggs, depending on the type of virus.
4. Incubation of the inoculated cells under appropriate conditions to allow viral replication.
5. Observation for cytopathic effects (CPE), which are changes in the host cells caused by viral replication, such as cell rounding, shrinkage, or lysis.
6. Confirmation of viral presence through additional tests, like immunofluorescence assays, polymerase chain reaction (PCR), or electron microscopy.

Virus cultivation is a valuable tool in diagnostic virology, vaccine development, and research on viral pathogenesis and host-virus interactions. However, it requires specialized equipment, trained personnel, and biosafety measures due to the potential infectivity of the viruses being cultured.

Virus shedding refers to the release of virus particles by an infected individual, who can then transmit the virus to others through various means such as respiratory droplets, fecal matter, or bodily fluids. This occurs when the virus replicates inside the host's cells and is released into the surrounding environment, where it can infect other individuals. The duration of virus shedding varies depending on the specific virus and the individual's immune response. It's important to note that some individuals may shed viruses even before they show symptoms, making infection control measures such as hand hygiene, mask-wearing, and social distancing crucial in preventing the spread of infectious diseases.

Viral diseases are illnesses caused by the infection and replication of viruses in host organisms. These infectious agents are obligate parasites, meaning they rely on the cells of other living organisms to survive and reproduce. Viruses can infect various types of hosts, including animals, plants, and microorganisms, causing a wide range of diseases with varying symptoms and severity.

Once a virus enters a host cell, it takes over the cell's machinery to produce new viral particles, often leading to cell damage or death. The immune system recognizes the viral components as foreign and mounts an immune response to eliminate the infection. This response can result in inflammation, fever, and other symptoms associated with viral diseases.

Examples of well-known viral diseases include:

1. Influenza (flu) - caused by influenza A, B, or C viruses
2. Common cold - usually caused by rhinoviruses or coronaviruses
3. HIV/AIDS - caused by human immunodeficiency virus (HIV)
4. Measles - caused by measles morbillivirus
5. Hepatitis B and C - caused by hepatitis B virus (HBV) and hepatitis C virus (HCV), respectively
6. Herpes simplex - caused by herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2)
7. Chickenpox and shingles - both caused by varicella-zoster virus (VZV)
8. Rabies - caused by rabies lyssavirus
9. Ebola - caused by ebolaviruses
10. COVID-19 - caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)

Prevention and treatment strategies for viral diseases may include vaccination, antiviral medications, and supportive care to manage symptoms while the immune system fights off the infection.

Simian Virus 40 (SV40) is a polyomavirus that is found in both monkeys and humans. It is a DNA virus that has been extensively studied in laboratory settings due to its ability to transform cells and cause tumors in animals. In fact, SV40 was discovered as a contaminant of poliovirus vaccines that were prepared using rhesus monkey kidney cells in the 1950s and 1960s.

SV40 is not typically associated with human disease, but there has been some concern that exposure to the virus through contaminated vaccines or other means could increase the risk of certain types of cancer, such as mesothelioma and brain tumors. However, most studies have failed to find a consistent link between SV40 infection and cancer in humans.

The medical community generally agrees that SV40 is not a significant public health threat, but researchers continue to study the virus to better understand its biology and potential impact on human health.

A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.

Virus assembly, also known as virion assembly, is the final stage in the virus life cycle where individual viral components come together to form a complete viral particle or virion. This process typically involves the self-assembly of viral capsid proteins around the viral genome (DNA or RNA) and, in enveloped viruses, the acquisition of a lipid bilayer membrane containing viral glycoproteins. The specific mechanisms and regulation of virus assembly vary among different viral families, but it is often directed by interactions between viral structural proteins and genomic nucleic acid.

A plant virus is not defined in medical terms, as viruses are typically considered within the context of living organisms and plants are not classified as such. However, I can provide a general virology definition for you:

Plant viruses are small infectious agents that consist of nucleic acid (DNA or RNA) enclosed in a protein coat. They infect various plant species, causing a wide range of symptoms and diseases, which can result in significant economic losses in agriculture and horticulture. Plant viruses lack the ability to replicate outside a host cell, and they rely on the host's metabolic machinery for their reproduction. They can be transmitted through various means, such as insect vectors, seeds, or mechanical contact.

DNA viruses are a type of virus that contain DNA (deoxyribonucleic acid) as their genetic material. These viruses replicate by using the host cell's machinery to synthesize new viral components, which are then assembled into new viruses and released from the host cell.

DNA viruses can be further classified based on the structure of their genomes and the way they replicate. For example, double-stranded DNA (dsDNA) viruses have a genome made up of two strands of DNA, while single-stranded DNA (ssDNA) viruses have a genome made up of a single strand of DNA.

Examples of DNA viruses include herpes simplex virus, varicella-zoster virus, human papillomavirus, and adenoviruses. Some DNA viruses are associated with specific diseases, such as cancer (e.g., human papillomavirus) or neurological disorders (e.g., herpes simplex virus).

It's important to note that while DNA viruses contain DNA as their genetic material, RNA viruses contain RNA (ribonucleic acid) as their genetic material. Both DNA and RNA viruses can cause a wide range of diseases in humans, animals, and plants.

A mutation is a permanent change in the DNA sequence of an organism's genome. Mutations can occur spontaneously or be caused by environmental factors such as exposure to radiation, chemicals, or viruses. They may have various effects on the organism, ranging from benign to harmful, depending on where they occur and whether they alter the function of essential proteins. In some cases, mutations can increase an individual's susceptibility to certain diseases or disorders, while in others, they may confer a survival advantage. Mutations are the driving force behind evolution, as they introduce new genetic variability into populations, which can then be acted upon by natural selection.

Sindbis virus is an alphavirus that belongs to the Togaviridae family. It's named after the location where it was first isolated, in Sindbis, Egypt, in 1952. This virus is primarily transmitted by mosquitoes and can infect a wide range of animals, including birds and humans. In humans, Sindbis virus infection often causes a mild flu-like illness characterized by fever, rash, and joint pain. However, some people may develop more severe symptoms, such as neurological disorders, although this is relatively rare. There is no specific treatment for Sindbis virus infection, and management typically involves supportive care to alleviate symptoms.

Measles virus is a single-stranded, negative-sense RNA virus belonging to the genus Morbillivirus in the family Paramyxoviridae. It is the causative agent of measles, a highly contagious infectious disease characterized by fever, cough, runny nose, and a red, blotchy rash. The virus primarily infects the respiratory tract and then spreads throughout the body via the bloodstream.

The genome of the measles virus is approximately 16 kilobases in length and encodes for eight proteins: nucleocapsid (N), phosphoprotein (P), matrix protein (M), fusion protein (F), hemagglutinin (H), large protein (L), and two non-structural proteins, V and C. The H protein is responsible for binding to the host cell receptor CD150 (SLAM) and mediating viral entry, while the F protein facilitates fusion of the viral and host cell membranes.

Measles virus is transmitted through respiratory droplets and direct contact with infected individuals. The virus can remain airborne for up to two hours in a closed space, making it highly contagious. Measles is preventable through vaccination, which has led to significant reductions in the incidence of the disease worldwide.

'Influenza A Virus, H1N1 Subtype' is a specific subtype of the influenza A virus that causes flu in humans and animals. It contains certain proteins called hemagglutinin (H) and neuraminidase (N) on its surface, with this subtype specifically having H1 and N1 antigens. The H1N1 strain is well-known for causing the 2009 swine flu pandemic, which was a global outbreak of flu that resulted in significant morbidity and mortality. This subtype can also cause seasonal flu, although the severity and symptoms may vary. It is important to note that influenza viruses are constantly changing, and new strains or subtypes can emerge over time, requiring regular updates to vaccines to protect against them.

Rabies is a viral disease that affects the nervous system of mammals, including humans. It's caused by the rabies virus (RV), which belongs to the family Rhabdoviridae and genus Lyssavirus. The virus has a bullet-shaped appearance under an electron microscope and is encased in a lipid envelope.

The rabies virus primarily spreads through the saliva of infected animals, usually via bites. Once inside the body, it travels along nerve fibers to the brain, where it multiplies rapidly and causes inflammation (encephalitis). The infection can lead to symptoms such as anxiety, confusion, hallucinations, seizures, paralysis, coma, and ultimately death if left untreated.

Rabies is almost always fatal once symptoms appear, but prompt post-exposure prophylaxis (PEP), which includes vaccination and sometimes rabies immunoglobulin, can prevent the disease from developing when administered after an exposure to a potentially rabid animal. Pre-exposure vaccination is also recommended for individuals at high risk of exposure, such as veterinarians and travelers visiting rabies-endemic areas.

"Influenza A Virus, H5N1 Subtype" is a specific subtype of the Influenza A virus that is often found in avian species (birds) and can occasionally infect humans. The "H5N1" refers to the specific proteins (hemagglutinin and neuraminidase) found on the surface of the virus. This subtype has caused serious infections in humans, with high mortality rates, especially in cases where people have had close contact with infected birds. It does not commonly spread from person to person, but there is concern that it could mutate and adapt to efficiently transmit between humans, which would potentially cause a pandemic.

"Influenza A Virus, H3N2 Subtype" is a specific subtype of the influenza A virus that causes respiratory illness and is known to circulate in humans and animals, including birds and pigs. The "H3N2" refers to the two proteins on the surface of the virus: hemagglutinin (H) and neuraminidase (N). In this subtype, the H protein is of the H3 variety and the N protein is of the N2 variety. This subtype has been responsible for several influenza epidemics and pandemics in humans, including the 1968 Hong Kong flu pandemic. It is one of the influenza viruses that are monitored closely by public health authorities due to its potential to cause significant illness and death, particularly in high-risk populations such as older adults, young children, and people with certain underlying medical conditions.

Hepatitis B virus (HBV) is a DNA virus that belongs to the Hepadnaviridae family and causes the infectious disease known as hepatitis B. This virus primarily targets the liver, where it can lead to inflammation and damage of the liver tissue. The infection can range from acute to chronic, with chronic hepatitis B increasing the risk of developing serious liver complications such as cirrhosis and liver cancer.

The Hepatitis B virus has a complex life cycle, involving both nuclear and cytoplasmic phases. It enters hepatocytes (liver cells) via binding to specific receptors and is taken up by endocytosis. The viral DNA is released into the nucleus, where it is converted into a covalently closed circular DNA (cccDNA) form, which serves as the template for viral transcription.

HBV transcribes several RNAs, including pregenomic RNA (pgRNA), which is used as a template for reverse transcription during virion assembly. The pgRNA is encapsidated into core particles along with the viral polymerase and undergoes reverse transcription to generate new viral DNA. This process occurs within the cytoplasm of the hepatocyte, resulting in the formation of immature virions containing partially double-stranded DNA.

These immature virions are then enveloped by host cell membranes containing HBV envelope proteins (known as surface antigens) to form mature virions that can be secreted from the hepatocyte and infect other cells. The virus can also integrate into the host genome, which may contribute to the development of hepatocellular carcinoma in chronic cases.

Hepatitis B is primarily transmitted through exposure to infected blood or bodily fluids containing the virus, such as through sexual contact, sharing needles, or from mother to child during childbirth. Prevention strategies include vaccination, safe sex practices, and avoiding needle-sharing behaviors. Treatment for hepatitis B typically involves antiviral medications that can help suppress viral replication and reduce the risk of liver damage.

West Nile Virus (WNV) is an Flavivirus, which is a type of virus that is spread by mosquitoes. It was first discovered in the West Nile district of Uganda in 1937 and has since been found in many countries throughout the world. WNV can cause a mild to severe illness known as West Nile fever.

Most people who become infected with WNV do not develop any symptoms, but some may experience fever, headache, body aches, joint pain, vomiting, diarrhea, or a rash. In rare cases, the virus can cause serious neurological illnesses such as encephalitis (inflammation of the brain) or meningitis (inflammation of the membranes surrounding the brain and spinal cord). These severe forms of the disease can be fatal, especially in older adults and people with weakened immune systems.

WNV is primarily transmitted to humans through the bite of infected mosquitoes, but it can also be spread through blood transfusions, organ transplants, or from mother to baby during pregnancy, delivery, or breastfeeding. There is no specific treatment for WNV, and most people recover on their own with rest and supportive care. However, hospitalization may be necessary in severe cases. Prevention measures include avoiding mosquito bites by using insect repellent, wearing long sleeves and pants, and staying indoors during peak mosquito activity hours.

Respiratory Syncytial Viruses (RSV) are a common type of virus that cause respiratory infections, particularly in young children and older adults. They are responsible for inflammation and narrowing of the small airways in the lungs, leading to breathing difficulties and other symptoms associated with bronchiolitis and pneumonia.

The term "syncytial" refers to the ability of these viruses to cause infected cells to merge and form large multinucleated cells called syncytia, which is a characteristic feature of RSV infections. The virus spreads through respiratory droplets when an infected person coughs or sneezes, and it can also survive on surfaces for several hours, making transmission easy.

RSV infections are most common during the winter months and can cause mild to severe symptoms depending on factors such as age, overall health, and underlying medical conditions. While RSV is typically associated with respiratory illnesses in children, it can also cause significant disease in older adults and immunocompromised individuals. Currently, there is no vaccine available for RSV, but antiviral medications and supportive care are used to manage severe infections.

Viral activation, also known as viral reactivation or virus reactivation, refers to the process in which a latent or dormant virus becomes active and starts to replicate within a host cell. This can occur when the immune system is weakened or compromised, allowing the virus to evade the body's natural defenses and cause disease.

In some cases, viral activation can be triggered by certain environmental factors, such as stress, exposure to UV light, or infection with another virus. Once activated, the virus can cause symptoms similar to those seen during the initial infection, or it may lead to new symptoms depending on the specific virus and the host's immune response.

Examples of viruses that can remain dormant in the body and be reactivated include herpes simplex virus (HSV), varicella-zoster virus (VZV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV). It is important to note that not all viruses can be reactivated, and some may remain dormant in the body indefinitely without causing any harm.

An antigen is any substance that can stimulate an immune response, particularly the production of antibodies. Viral antigens are antigens that are found on or produced by viruses. They can be proteins, glycoproteins, or carbohydrates present on the surface or inside the viral particle.

Viral antigens play a crucial role in the immune system's recognition and response to viral infections. When a virus infects a host cell, it may display its antigens on the surface of the infected cell. This allows the immune system to recognize and target the infected cells for destruction, thereby limiting the spread of the virus.

Viral antigens are also important targets for vaccines. Vaccines typically work by introducing a harmless form of a viral antigen to the body, which then stimulates the production of antibodies and memory T-cells that can recognize and respond quickly and effectively to future infections with the actual virus.

It's worth noting that different types of viruses have different antigens, and these antigens can vary between strains of the same virus. This is why there are often different vaccines available for different viral diseases, and why flu vaccines need to be updated every year to account for changes in the circulating influenza virus strains.

Vesicular stomatitis Indiana virus (VSIV) is a single-stranded, negative-sense RNA virus that belongs to the family Rhabdoviridae and genus Vesiculovirus. It is the causative agent of vesicular stomatitis (VS), a viral disease that primarily affects horses and cattle, but can also infect other species including swine, sheep, goats, and humans.

The virus is transmitted through direct contact with infected animals or their saliva, as well as through insect vectors such as black flies and sandflies. The incubation period for VS ranges from 2 to 8 days, after which infected animals develop fever, lethargy, and vesicular lesions in the mouth, nose, and feet. These lesions can be painful and may cause difficulty eating or walking.

In humans, VSIV infection is typically asymptomatic or causes mild flu-like symptoms such as fever, muscle aches, and headache. Occasionally, individuals may develop vesicular lesions on their skin or mucous membranes, particularly if they have had contact with infected animals.

Diagnosis of VSIV infection is typically made through virus isolation from lesion exudates or blood, as well as through serological testing. Treatment is generally supportive and aimed at relieving symptoms, as there are no specific antiviral therapies available for VS. Prevention measures include vaccination of susceptible animals, vector control, and biosecurity measures to prevent the spread of infection between animals.

Virus latency, also known as viral latency, refers to a state of infection in which a virus remains dormant or inactive within a host cell for a period of time. During this phase, the virus does not replicate or cause any noticeable symptoms. However, under certain conditions such as stress, illness, or a weakened immune system, the virus can become reactivated and begin to produce new viruses, potentially leading to disease.

One well-known example of a virus that exhibits latency is the varicella-zoster virus (VZV), which causes chickenpox in children. After a person recovers from chickenpox, the virus remains dormant in the nervous system for years or even decades. In some cases, the virus can reactivate later in life, causing shingles, a painful rash that typically occurs on one side of the body.

Virus latency is an important concept in virology and infectious disease research, as it has implications for understanding the persistence of viral infections, developing treatments and vaccines, and predicting the risk of disease recurrence.

Hemagglutinin (HA) glycoproteins are surface proteins found on influenza viruses. They play a crucial role in the virus's ability to infect and spread within host organisms.

The HAs are responsible for binding to sialic acid receptors on the host cell's surface, allowing the virus to attach and enter the cell. After endocytosis, the viral and endosomal membranes fuse, releasing the viral genome into the host cell's cytoplasm.

There are several subtypes of hemagglutinin (H1-H18) identified so far, with H1, H2, and H3 being common in human infections. The significant antigenic differences among these subtypes make them important targets for the development of influenza vaccines. However, due to their high mutation rate, new vaccine formulations are often required to match the circulating virus strains.

In summary, hemagglutinin glycoproteins on influenza viruses are essential for host cell recognition and entry, making them important targets for diagnosis, prevention, and treatment of influenza infections.

Oncogenic viruses are a type of viruses that have the ability to cause cancer in host cells. They do this by integrating their genetic material into the DNA of the infected host cell, which can lead to the disruption of normal cellular functions and the activation of oncogenes (genes that have the potential to cause cancer). This can result in uncontrolled cell growth and division, ultimately leading to the formation of tumors. Examples of oncogenic viruses include human papillomavirus (HPV), hepatitis B virus (HBV), and human T-cell leukemia virus type 1 (HTLV-1). It is important to note that only a small proportion of viral infections lead to cancer, and the majority of cancers are not caused by viruses.

Vero cells are a line of cultured kidney epithelial cells that were isolated from an African green monkey (Cercopithecus aethiops) in the 1960s. They are named after the location where they were initially developed, the Vervet Research Institute in Japan.

Vero cells have the ability to divide indefinitely under certain laboratory conditions and are often used in scientific research, including virology, as a host cell for viruses to replicate. This allows researchers to study the characteristics of various viruses, such as their growth patterns and interactions with host cells. Vero cells are also used in the production of some vaccines, including those for rabies, polio, and Japanese encephalitis.

It is important to note that while Vero cells have been widely used in research and vaccine production, they can still have variations between different cell lines due to factors like passage number or culture conditions. Therefore, it's essential to specify the exact source and condition of Vero cells when reporting experimental results.

Simian Immunodeficiency Virus (SIV) is a retrovirus that primarily infects African non-human primates and is the direct ancestor of Human Immunodeficiency Virus type 2 (HIV-2). It is similar to HIV in its structure, replication strategy, and ability to cause an immunodeficiency disease in its host. SIV infection in its natural hosts is typically asymptomatic and non-lethal, but it can cause AIDS-like symptoms in other primate species. Research on SIV in its natural hosts has provided valuable insights into the mechanisms of HIV pathogenesis and potential strategies for prevention and treatment of AIDS.

'Cercopithecus aethiops' is the scientific name for the monkey species more commonly known as the green monkey. It belongs to the family Cercopithecidae and is native to western Africa. The green monkey is omnivorous, with a diet that includes fruits, nuts, seeds, insects, and small vertebrates. They are known for their distinctive greenish-brown fur and long tail. Green monkeys are also important animal models in biomedical research due to their susceptibility to certain diseases, such as SIV (simian immunodeficiency virus), which is closely related to HIV.

The Mumps virus is a single-stranded, negative-sense RNA virus that belongs to the Paramyxoviridae family and Rubulavirus genus. It is the causative agent of mumps, an acute infectious disease characterized by painful swelling of the salivary glands, particularly the parotid glands.

The Mumps virus has a spherical or pleomorphic shape with a diameter of approximately 150-250 nanometers. It is surrounded by a lipid bilayer membrane derived from the host cell, which contains viral glycoproteins that facilitate attachment and entry into host cells.

The M protein, located beneath the envelope, plays a crucial role in virus assembly and budding. The genome of the Mumps virus consists of eight genes encoding nine proteins, including two major structural proteins (nucleocapsid protein and matrix protein) and several non-structural proteins involved in viral replication and pathogenesis.

Transmission of the Mumps virus occurs through respiratory droplets or direct contact with infected saliva. After infection, the incubation period ranges from 12 to 25 days, followed by a prodromal phase characterized by fever, headache, malaise, and muscle pain. The characteristic swelling of the parotid glands usually appears 1-3 days after the onset of symptoms.

Complications of mumps can include meningitis, encephalitis, orchitis, oophoritis, pancreatitis, and deafness. Prevention relies on vaccination with the measles-mumps-rubella (MMR) vaccine, which is highly effective in preventing mumps and its complications.

Parainfluenza Virus 1, Human (HPIV-1) is a type of respiratory virus that belongs to the family Paramyxoviridae and genus Respirovirus. It is one of the four serotypes of human parainfluenza viruses (HPIVs), which are important causes of acute respiratory infections in children, immunocompromised individuals, and the elderly.

HPIV-1 primarily infects the upper respiratory tract, causing symptoms such as cough, runny nose, sore throat, and fever. However, it can also cause lower respiratory tract infections, including bronchitis, bronchiolitis, and pneumonia, particularly in young children and infants.

HPIV-1 is transmitted through respiratory droplets or direct contact with infected individuals. The incubation period for HPIV-1 infection ranges from 2 to 7 days, after which symptoms can last for up to 10 days. There is no specific antiviral treatment available for HPIV-1 infections, and management typically involves supportive care such as hydration, fever reduction, and respiratory support if necessary.

Prevention measures include good hand hygiene, avoiding close contact with infected individuals, and practicing cough etiquette. Vaccines are not currently available for HPIV-1 infections, but research is ongoing to develop effective vaccines against these viruses.

Mosaic viruses are a group of plant viruses that can cause mottled or mosaic patterns of discoloration on leaves, which is why they're named as such. These viruses infect a wide range of plants, including important crops like tobacco, tomatoes, and cucumbers. The infection can lead to various symptoms such as stunted growth, leaf deformation, reduced yield, or even plant death.

Mosaic viruses are typically spread by insects, such as aphids, that feed on the sap of infected plants and then transmit the virus to healthy plants. They can also be spread through contaminated seeds, tools, or contact with infected plant material. Once inside a plant, these viruses hijack the plant's cellular machinery to replicate themselves, causing damage to the host plant in the process.

It is important to note that mosaic viruses are not related to human or animal health; they only affect plants.

A virion is the complete, infectious form of a virus outside its host cell. It consists of the viral genome (DNA or RNA) enclosed within a protein coat called the capsid, which is often surrounded by a lipid membrane called the envelope. The envelope may contain viral proteins and glycoproteins that aid in attachment to and entry into host cells during infection. The term "virion" emphasizes the infectious nature of the virus particle, as opposed to non-infectious components like individual capsid proteins or naked viral genome.

Hepatitis A virus (HAV) is the causative agent of hepatitis A, a viral infection that causes inflammation of the liver. It is a small, non-enveloped, single-stranded RNA virus belonging to the Picornaviridae family and Hepatovirus genus. The virus primarily spreads through the fecal-oral route, often through contaminated food or water, or close contact with an infected person. After entering the body, HAV infects hepatocytes in the liver, leading to liver damage and associated symptoms such as jaundice, fatigue, abdominal pain, and nausea. The immune system eventually clears the infection, providing lifelong immunity against future HAV infections. Preventive measures include vaccination and practicing good hygiene to prevent transmission.

Semliki Forest Virus (SFV) is an alphavirus in the Togaviridae family, which is primarily transmitted to vertebrates through mosquito vectors. The virus was initially isolated from mosquitoes in the Semliki Forest of Uganda and has since been found in various parts of Africa and Asia. SFV infection in humans can cause a mild febrile illness characterized by fever, headache, muscle pain, and rash. However, it is more commonly known for causing severe disease in animals, particularly non-human primates and cattle, where it can lead to encephalitis or hemorrhagic fever. SFV has also been used as a model organism in laboratory studies of virus replication and pathogenesis.

Avian sarcoma viruses (ASVs) are a group of retroviruses that primarily infect birds and cause various types of tumors, particularly sarcomas. These viruses contain an oncogene, which is a gene that has the ability to transform normal cells into cancerous ones. The oncogene in ASVs is often derived from cellular genes called proto-oncogenes, which are normally involved in regulating cell growth and division.

ASVs can be divided into two main types: non-defective and defective. Non-defective ASVs contain a complete set of viral genes that allow them to replicate independently, while defective ASVs lack some of the necessary viral genes and require assistance from other viruses to replicate.

One well-known example of an avian sarcoma virus is the Rous sarcoma virus (RSV), which was first discovered in chickens by Peyton Rous in 1910. RSV causes a highly malignant form of sarcoma in chickens and has been extensively studied as a model system for cancer research. The oncogene in RSV is called v-src, which is derived from the normal cellular gene c-src.

Avian sarcoma viruses have contributed significantly to our understanding of the molecular mechanisms underlying cancer development and have provided valuable insights into the role of oncogenes in tumorigenesis.

Antiviral agents are a class of medications that are designed to treat infections caused by viruses. Unlike antibiotics, which target bacteria, antiviral agents interfere with the replication and infection mechanisms of viruses, either by inhibiting their ability to replicate or by modulating the host's immune response to the virus.

Antiviral agents are used to treat a variety of viral infections, including influenza, herpes simplex virus (HSV) infections, human immunodeficiency virus (HIV) infection, hepatitis B and C, and respiratory syncytial virus (RSV) infections.

These medications can be administered orally, intravenously, or topically, depending on the type of viral infection being treated. Some antiviral agents are also used for prophylaxis, or prevention, of certain viral infections.

It is important to note that antiviral agents are not effective against all types of viruses and may have significant side effects. Therefore, it is essential to consult with a healthcare professional before starting any antiviral therapy.

Neutralization tests are a type of laboratory assay used in microbiology and immunology to measure the ability of a substance, such as an antibody or antitoxin, to neutralize the activity of a toxin or infectious agent. In these tests, the substance to be tested is mixed with a known quantity of the toxin or infectious agent, and the mixture is then incubated under controlled conditions. After incubation, the mixture is tested for residual toxicity or infectivity using a variety of methods, such as cell culture assays, animal models, or biochemical assays.

The neutralization titer is then calculated based on the highest dilution of the test substance that completely neutralizes the toxin or infectious agent. Neutralization tests are commonly used in the diagnosis and evaluation of immune responses to vaccines, as well as in the detection and quantification of toxins and other harmful substances.

Examples of neutralization tests include the serum neutralization test for measles antibodies, the plaque reduction neutralization test (PRNT) for dengue virus antibodies, and the cytotoxicity neutralization assay for botulinum neurotoxins.

A viral plaque assay is a laboratory technique used to measure the infectivity and concentration of viruses in a sample. This method involves infecting a monolayer of cells (usually in a petri dish or multi-well plate) with a known volume of a virus-containing sample, followed by overlaying the cells with a nutrient-agar medium to restrict viral spread and enable individual plaques to form.

After an incubation period that allows for viral replication and cell death, the cells are stained, and clear areas or "plaques" become visible in the monolayer. Each plaque represents a localized region of infected and lysed cells, caused by the progeny of a single infectious virus particle. The number of plaques is then counted, and the viral titer (infectious units per milliliter or PFU/mL) is calculated based on the dilution factor and volume of the original inoculum.

Viral plaque assays are essential for determining viral titers, assessing virus-host interactions, evaluating antiviral agents, and studying viral pathogenesis.

A viral attachment, in the context of virology, refers to the initial step in the infection process of a host cell by a virus. This involves the binding or adsorption of the viral particle to specific receptors on the surface of the host cell. The viral attachment proteins, often located on the viral envelope or capsid, recognize and interact with these receptors, leading to a close association between the virus and the host cell. This interaction is highly specific, as different viruses may target various cell types based on their unique receptor-binding preferences. Following attachment, the virus can enter the host cell and initiate the replication cycle, ultimately leading to the production of new viral particles and potential disease manifestations.

BK virus, also known as BK polyomavirus, is a type of virus that belongs to the Polyomaviridae family. It is named after the initials of a patient in whom the virus was first isolated. The BK virus is a common infection in humans and is typically acquired during childhood. After the initial infection, the virus remains dormant in the body, often found in the urinary tract and kidneys.

In immunocompetent individuals, the virus usually does not cause any significant problems. However, in people with weakened immune systems, such as those who have undergone organ transplantation or have HIV/AIDS, BK virus can lead to severe complications. One of the most common manifestations of BK virus infection in immunocompromised individuals is hemorrhagic cystitis, a condition characterized by inflammation and bleeding in the bladder. In transplant recipients, BK virus can also cause nephropathy, leading to kidney damage or even failure.

There is no specific treatment for BK virus infection, but antiviral medications may be used to help control the virus's replication in some cases. Maintaining a strong immune system and monitoring viral load through regular testing are essential strategies for managing BK virus infections in immunocompromised individuals.

A tumor virus infection is a condition in which a person's cells become cancerous or transformed due to the integration and disruption of normal cellular functions by a viral pathogen. These viruses are also known as oncoviruses, and they can cause tumors or cancer by altering the host cell's genetic material, promoting uncontrolled cell growth and division, evading immune surveillance, and inhibiting apoptosis (programmed cell death).

Examples of tumor viruses include:

1. DNA tumor viruses: These are double-stranded DNA viruses that can cause cancer in humans. Examples include human papillomavirus (HPV), hepatitis B virus (HBV), and Merkel cell polyomavirus (MCV).
2. RNA tumor viruses: Also known as retroviruses, these single-stranded RNA viruses can cause cancer in humans. Examples include human T-cell leukemia virus type 1 (HTLV-1) and human immunodeficiency virus (HIV).

Tumor virus infections are responsible for approximately 15-20% of all cancer cases worldwide, making them a significant public health concern. Prevention strategies, such as vaccination against HPV and HBV, have been shown to reduce the incidence of associated cancers.

I'm sorry for any confusion, but "Viruses, Unclassified" is not a recognized medical or scientific category. Generally, viruses are classified based on various characteristics such as genome structure, mode of replication, host range, and symptoms they cause. The International Committee on Taxonomy of Viruses (ICTV) is the organization responsible for the formal classification of viruses.

If you have any specific questions about certain unclassified viral entities or phenomena, I'd be happy to help if I can! Please provide more context so I can give a more accurate and helpful response.

The JC (John Cunningham) virus, also known as human polyomavirus 2 (HPyV-2), is a type of double-stranded DNA virus that belongs to the Polyomaviridae family. It is named after the initials of the patient in whom it was first identified.

JC virus is a ubiquitous virus, meaning that it is commonly found in the general population worldwide. Most people get infected with JC virus during childhood and do not experience any symptoms. After the initial infection, the virus remains dormant in the kidneys and other organs of the body.

However, in individuals with weakened immune systems, such as those with HIV/AIDS or who have undergone organ transplantation, JC virus can reactivate and cause a serious brain infection called progressive multifocal leukoencephalopathy (PML). PML is a rare but often fatal disease that affects the white matter of the brain, causing cognitive decline, weakness, and paralysis.

There is currently no cure for PML, and treatment is focused on managing the underlying immune deficiency and controlling the symptoms of the disease.

Avian leukosis virus (ALV) is a type of retrovirus that primarily affects chickens and other birds. It is responsible for a group of diseases known as avian leukosis, which includes various types of tumors and immunosuppressive conditions. The virus is transmitted horizontally through the shedder's dander, feathers, and vertical transmission through infected eggs.

There are several subgroups of ALV (A, B, C, D, E, and J), each with different host ranges and pathogenicity. Some strains can cause rapid death in young chickens, while others may take years to develop clinical signs. The most common form of the disease is neoplastic, characterized by the development of various types of tumors such as lymphomas, myelomas, and sarcomas.

Avian leukosis virus infection can have significant economic impacts on the poultry industry due to decreased growth rates, increased mortality, and condemnation of infected birds at processing. Control measures include eradication programs, biosecurity practices, vaccination, and breeding for genetic resistance.

Phylogeny is the evolutionary history and relationship among biological entities, such as species or genes, based on their shared characteristics. In other words, it refers to the branching pattern of evolution that shows how various organisms have descended from a common ancestor over time. Phylogenetic analysis involves constructing a tree-like diagram called a phylogenetic tree, which depicts the inferred evolutionary relationships among organisms or genes based on molecular sequence data or other types of characters. This information is crucial for understanding the diversity and distribution of life on Earth, as well as for studying the emergence and spread of diseases.

Orthomyxoviridae is a family of viruses that includes influenza A, B, and C viruses, which are the causative agents of flu in humans and animals. These viruses are enveloped, meaning they have a lipid membrane derived from the host cell, and have a single-stranded, negative-sense RNA genome. The genome is segmented, meaning it consists of several separate pieces of RNA, which allows for genetic reassortment or "shuffling" when two different strains infect the same cell, leading to the emergence of new strains.

The viral envelope contains two major glycoproteins: hemagglutinin (HA) and neuraminidase (NA). The HA protein is responsible for binding to host cells and facilitating entry into the cell, while NA helps release newly formed virus particles from infected cells by cleaving sialic acid residues on the host cell surface.

Orthomyxoviruses are known to cause respiratory infections in humans and animals, with influenza A viruses being the most virulent and capable of causing pandemics. Influenza B viruses typically cause less severe illness and are primarily found in humans, while influenza C viruses generally cause mild upper respiratory symptoms and are also mainly restricted to humans.

Bluetongue virus (BTV) is an infectious agent that causes Bluetongue disease, a non-contagious viral disease affecting sheep and other ruminants. It is a member of the Orbivirus genus within the Reoviridae family. The virus is transmitted by biting midges of the Culicoides species and can infect various animals such as sheep, cattle, goats, and wild ruminants.

The virus has a double-stranded RNA genome and consists of ten segments that encode seven structural and four non-structural proteins. The clinical signs of Bluetongue disease in sheep include fever, salivation, swelling of the head and neck, nasal discharge, and respiratory distress, which can be severe or fatal. In contrast, cattle usually show milder symptoms or are asymptomatic, although they can serve as reservoirs for the virus.

Bluetongue virus is an important veterinary pathogen that has a significant economic impact on the global sheep industry. The disease is prevalent in many parts of the world, particularly in tropical and subtropical regions, but has also spread to temperate areas due to climate change and the movement of infected animals. Prevention and control measures include vaccination, insect control, and restricting the movement of infected animals.

Orthomyxoviridae is a family of viruses that includes influenza A, B, and C viruses, which can cause respiratory infections in humans. Orthomyxoviridae infections are typically characterized by symptoms such as fever, cough, sore throat, runny or stuffy nose, muscle or body aches, headaches, and fatigue.

Influenza A and B viruses can cause seasonal epidemics of respiratory illness that occur mainly during the winter months in temperate climates. Influenza A viruses can also cause pandemics, which are global outbreaks of disease that occur when a new strain of the virus emerges to which there is little or no immunity in the human population.

Influenza C viruses are less common and typically cause milder illness than influenza A and B viruses. They do not cause epidemics and are not usually included in seasonal flu vaccines.

Orthomyxoviridae infections can be prevented through vaccination, good respiratory hygiene (such as covering the mouth and nose when coughing or sneezing), hand washing, and avoiding close contact with sick individuals. Antiviral medications may be prescribed to treat influenza A and B infections, particularly for people at high risk of complications, such as older adults, young children, pregnant women, and people with certain underlying medical conditions.

Gene expression regulation, viral, refers to the processes that control the production of viral gene products, such as proteins and nucleic acids, during the viral life cycle. This can involve both viral and host cell factors that regulate transcription, RNA processing, translation, and post-translational modifications of viral genes.

Viral gene expression regulation is critical for the virus to replicate and produce progeny virions. Different types of viruses have evolved diverse mechanisms to regulate their gene expression, including the use of promoters, enhancers, transcription factors, RNA silencing, and epigenetic modifications. Understanding these regulatory processes can provide insights into viral pathogenesis and help in the development of antiviral therapies.

Sendai virus, also known as murine parainfluenza virus or pneumonia virus of mice, is a species of paramyxovirus that primarily infects rodents. It is an enveloped, negative-sense, single-stranded RNA virus with a nonsegmented genome. The virus is named after the city of Sendai in Japan where it was first isolated in 1952.

Sendai virus is highly contagious and can cause respiratory illness in mice, rats, and other small rodents. It replicates in the respiratory epithelium, leading to inflammation and necrosis of the airways. The virus can also suppress the host's immune response, making infected animals more susceptible to secondary bacterial infections.

In laboratory settings, Sendai virus is sometimes used as a tool for studying viral pathogenesis, immunology, and gene therapy. It has been used as a vector for delivering genes into mammalian cells, including human cells, due to its ability to efficiently infect and transduce a wide range of cell types.

It's important to note that Sendai virus is not known to infect humans or cause disease in humans, and it is not considered a significant public health concern.

The Moloney murine leukemia virus (Mo-MLV) is a type of retrovirus, specifically a gammaretrovirus, that is commonly found in mice. It was first discovered and isolated by John Moloney in 1960. Mo-MLV is known to cause various types of cancerous conditions, particularly leukemia, in susceptible mouse strains.

Mo-MLV has a single-stranded RNA genome that is reverse transcribed into double-stranded DNA upon infection of the host cell. This viral DNA then integrates into the host's genome and utilizes the host's cellular machinery to produce new virus particles. The Mo-MLV genome encodes for several viral proteins, including gag (group-specific antigen), pol (polymerase), and env (envelope) proteins, which are essential for the replication cycle of the virus.

Mo-MLV is widely used in laboratory research as a model retrovirus to study various aspects of viral replication, gene therapy, and oncogenesis. It has also been engineered as a vector for gene delivery applications due to its ability to efficiently integrate into the host genome and deliver large DNA sequences. However, it is important to note that Mo-MLV and other retroviruses have the potential to cause insertional mutagenesis, which can lead to unintended genetic alterations and adverse effects in some cases.

Virus integration, in the context of molecular biology and virology, refers to the insertion of viral genetic material into the host cell's genome. This process is most commonly associated with retroviruses, such as HIV (Human Immunodeficiency Virus), which have an enzyme called reverse transcriptase that converts their RNA genome into DNA. This DNA can then integrate into the host's chromosomal DNA, becoming a permanent part of the host's genetic material.

This integration is a crucial step in the retroviral life cycle, allowing the virus to persist within the host cell and evade detection by the immune system. It also means that the viral genome can be passed on to daughter cells when the host cell divides.

However, it's important to note that not all viruses integrate their genetic material into the host's genome. Some viruses, like influenza, exist as separate entities within the host cell and do not become part of the host's DNA.

A capsid is the protein shell that encloses and protects the genetic material of a virus. It is composed of multiple copies of one or more proteins that are arranged in a specific structure, which can vary in shape and symmetry depending on the type of virus. The capsid plays a crucial role in the viral life cycle, including protecting the viral genome from host cell defenses, mediating attachment to and entry into host cells, and assisting with the assembly of new virus particles during replication.

Yellow fever virus (YFV) is an single-stranded RNA virus belonging to the Flaviviridae family, genus Flavivirus. It is primarily transmitted to humans through the bite of infected mosquitoes, most commonly Aedes and Haemagogus species. The virus is named for the jaundice that can occur in some patients, giving their skin and eyes a yellowish color.

Yellow fever is endemic in tropical regions of Africa and South America, with outbreaks occurring when large numbers of people are infected. After an incubation period of 3 to 6 days, symptoms typically begin with fever, chills, headache, back pain, and muscle aches. In more severe cases, the infection can progress to cause bleeding, organ failure, and death.

Prevention measures include vaccination, mosquito control, and personal protective measures such as wearing long sleeves and using insect repellent in areas where yellow fever is endemic or outbreaks are occurring.

Simplexvirus is a genus of viruses in the family Herpesviridae, subfamily Alphaherpesvirinae. This genus contains two species: Human alphaherpesvirus 1 (also known as HSV-1 or herpes simplex virus type 1) and Human alphaherpesvirus 2 (also known as HSV-2 or herpes simplex virus type 2). These viruses are responsible for causing various medical conditions, most commonly oral and genital herpes. They are characterized by their ability to establish lifelong latency in the nervous system and reactivate periodically to cause recurrent symptoms.

Tobacco mosaic virus (TMV) is not typically considered in the context of medical definitions, as it's primarily known for its impact on plants rather than humans or animals. However, I will provide the botanical definition for your interest.

Tobacco mosaic virus (TMV) is a positive-sense single-stranded RNA virus that infects a wide range of plants, including tobacco, tomatoes, cucumbers, and many ornamental plants. The virus is named after its initial discovery in tobacco plants, which exhibit symptoms such as mosaic patterns of light and dark green on the leaves, leaf curling, and stunted growth. TMV is highly contagious and can be spread through mechanical means, such as touching infected plants or using contaminated tools. It's also one of the most well-studied viruses due to its impact on agriculture and its historical significance in early virology research.

Respiratory Syncytial Virus (RSV) infections refer to the clinical illnesses caused by the Respiratory Syncytial Virus. RSV is a highly contagious virus that spreads through respiratory droplets, contact with infected surfaces, or direct contact with infected people. It primarily infects the respiratory tract, causing inflammation and damage to the cells lining the airways.

RSV infections can lead to a range of respiratory illnesses, from mild, cold-like symptoms to more severe conditions such as bronchiolitis (inflammation of the small airways in the lungs) and pneumonia (infection of the lung tissue). The severity of the infection tends to depend on factors like age, overall health status, and presence of underlying medical conditions.

In infants and young children, RSV is a leading cause of bronchiolitis and pneumonia, often resulting in hospitalization. In older adults, people with weakened immune systems, and those with chronic heart or lung conditions, RSV infections can also be severe and potentially life-threatening.

Symptoms of RSV infection may include runny nose, cough, sneezing, fever, wheezing, and difficulty breathing. Treatment typically focuses on managing symptoms and providing supportive care, although hospitalization and more aggressive interventions may be necessary in severe cases or for high-risk individuals. Preventive measures such as hand hygiene, wearing masks, and avoiding close contact with infected individuals can help reduce the spread of RSV.

Myxoma virus (MYXV) is a member of the Poxviridae family, specifically in the Leporipoxvirus genus. It is a double-stranded DNA virus that naturally infects European rabbits (Oryctolagus cuniculus) and causes a fatal disease called myxomatosis. The virus is transmitted through insect vectors such as mosquitoes and fleas, and it replicates in the cytoplasm of infected cells.

Myxoma virus has been studied extensively as a model organism for viral pathogenesis and host-pathogen interactions. It has also been explored as a potential oncolytic virus for cancer therapy due to its ability to selectively infect and kill certain types of cancer cells while leaving normal cells unharmed. However, it is important to note that the use of Myxoma virus in humans is still experimental and requires further research and development before it can be considered safe and effective for therapeutic purposes.

Virus inactivation is the process of reducing or eliminating the infectivity of a virus, making it no longer capable of replicating and causing infection. This can be achieved through various physical or chemical methods such as heat, radiation, chemicals (like disinfectants), or enzymes that damage the viral genome or disrupt the viral particle's structure.

It is important to note that virus inactivation does not necessarily mean complete destruction of the viral particles; it only implies that they are no longer infectious. The effectiveness of virus inactivation depends on factors such as the type and concentration of the virus, the inactivation method used, and the duration of exposure to the inactivating agent.

Virus inactivation is crucial in various settings, including healthcare, laboratory research, water treatment, food processing, and waste disposal, to prevent the spread of viral infections and ensure safety.

Page for Tombus virus defective interfering (DI) RNA region 3 at Rfam v t e (Cis-regulatory RNA elements, Tombusviridae, All ... Tombus virus defective interfering (DI) RNA region 3 is an important cis-regulatory region identified in the 3' UTR of ... Infectious bronchitis virus D-RNA Red clover necrotic mosaic virus translation enhancer elements Ray D, White KA (2003). "An ... Defective interfering RNAs are small sub-viral replicons which are non-coding deletion mutants of the virus that maintain cis- ...
Despite the inability to isolate them, von Magnus discovered defective interfering particles (DIPs) using the "influenza virus ... Huang, Alice S.; Baltimore, David (1977). "2. Defective Interfering Animal Viruses". In Fraenkel-Conrat, Heinz; Wagner, Robert ... He warned however, that such viruses were stable and easily cultured and therefore the emergence of a new virus with a more ... "Incomplete Forms of Influenza Virus", in Kenneth M. Smith and Max A. Lauffer's Advances in Virus Research, Volume 2, Academic ...
In other words, defective and non-defective viruses replicate simultaneously, but when defective particles increase, the amount ... Defective interfering particles (DIPs), also known as defective interfering viruses, are spontaneously generated virus mutants ... 2012). "Cloned defective interfering influenza virus protects ferrets from pandemic 2009 influenza A virus and allows ... Pathak KB, Nagy PD (December 2009). "Defective Interfering RNAs: Foes of Viruses and Friends of Virologists". Viruses. 1 (3): ...
Hepatitis D virus (HDV) is an example of a replication defective, helper dependent ssRNA virus because it requires Hepatitis B ... Gonçalves, Manuel AFV (2005). "Adeno-associated virus: From defective virus to effective vector". Virology Journal. 2: 43. doi: ... The term satellite virus has been given to a large group of viruses that all require the presence of another virus to replicate ... 1965). "Adenovirus-Associated Defective Virus Particles". Science. 149 (3685): 754-6. Bibcode:1965Sci...149..754A. doi:10.1126/ ...
It is, therefore, a defective virus. Although hepatitis delta virus genome may replicate independently once inside a host cell ... A virus has either a DNA or an RNA genome and is called a DNA virus or an RNA virus, respectively. The vast majority of viruses ... Other viruses, such as rabies virus, can infect different species of mammals and are said to have a broad range. The viruses ... Quote: "Virus: virus (s.n. II), gen. sing. viri, nom. pl. vira, gen. pl. vīrorum (to be distinguished from virorum, of men)." ...
Hovav, Anat (August 2005). "Capital market reaction to defective IT products". Computers and Security. 24 (5): 409-424. doi: ... A macro virus (or "document virus") is a virus that is written in a macro language and embedded into these documents so that ... The virus will eventually be activated by the "trigger" which states which event will execute the virus. Not all viruses have ... Some viruses, called polymorphic viruses, will employ a means of encryption inside an executable in which the virus is ...
"Generation of Replication-Defective Virus-Based Vaccines That Confer Full Protection in Sheep against Virulent Bluetongue Virus ... His research in the early 1970s was in the field of plant viruses, including tobacco rattle virus and tobacco necrosis virus, ... Minson's group called the resulting virus a "disabled infectious single cycle" (DISC) virus; similarly disabled viruses are ... Such replication-impaired viruses unite many of the advantages of both live and killed virus vaccines, and are much less likely ...
Gonçalves, M (2005). "Adeno-associated virus: from defective virus to effective vector". Virology Journal. 2 (1): 43-60. doi: ... They are only limited by the virus they must infect with, also known as the helper virus. These helper viruses are necessary ... Dependoparvovirus (formerly Dependovirus or Adeno-associated virus group) is a genus in the subfamily Parvovirinae of the virus ... 2009). "Directed evolution of adeno-associated virus to an infectious respiratory virus". Proceedings of the National Academy ...
They called it "Hepatitis Delta Virus" (HDV). This new virus was found to be defective. HDV needed HBV to act as a helper ... Agents of this virus resemble that of plant viroids. It is still hard to tell how many stereotypes exist because HDV is under ... Flu viruses can be directly transmitted (via droplets from sneezing or coughing) from pigs to people, and vice versa. These ... Human Immunodeficiency virus (HIV) can cause AIDS which is an acronym for Acquired Immunodeficiency Syndrome (AIDS), a ...
... termini of RNA from vesicular stomatitis virus and its defective interfering particles". Proceedings of the National Academy of ... and rabies virus (RABV), members of the Rhabdoviridae family of viruses, and for Ebola virus and Marburg virus from the broader ... "The origins of defective interfering particles of the negative-strand RNA viruses". Cell. 26 (2): 145-154. doi:10.1016/0092- ... He identified the origins of defective interfering particles of negative-strand RNA viruses. Through combinatorial studies of ...
Viruses selectively infect tumor cells because of their defective anti-viral response. Imlygic, an attenuated herpes simplex ... an oncolytic herpes virus which is a modified herpes simplex virus, became the first oncolytic virus to be approved for use in ... Herpes simplex virus (HSV) was one of the first viruses to be adapted to attack cancer cells selectively, because it was well ... An oncolytic virus is a virus that preferentially infects and kills cancer cells. As the infected cancer cells are destroyed by ...
Aaskov J, Buzacott K, Thu HM, Lowry K, Holmes EC (January 2006). "Long-term transmission of defective RNA viruses in humans and ... Additional examples of complementation among RNA viruses have been reported. Complementation is a means to maintain defective ... A founder virus can introduce a different phenotype for the ensuing evolution. Evolution of viruses in nature and as disease ... Attenuated RNA virus vaccines can revert to virulent forms. RNA viruses released in nature for pest control purposes can mutate ...
"Characterization of temperature sensitive influenza virus mutants defective in neuraminidase". Virology. 61 (2): 397-410. doi: ... Liu C, Eichelberger MC, Compans RW, Air GM (February 1995). "Influenza type A virus neuraminidase does not play a role in viral ... The enzymatic mechanism of influenza virus sialidase has been studied by Taylor et al., shown in Figure 1. The enzyme catalysis ... Article includes a good clear line drawing of a neuraminidase on an influenza virus. Portal: Biology (CS1: long volume value, ...
MR of HSV appears to partially depend on the host cell recombinational repair machinery since skin fibroblast cells defective ... adenovirus simian virus 40, vaccinia virus, reovirus, poliovirus and herpes simplex virus. When HSV particles are exposed to ... Animal herpes viruses all share some common properties. The structure of herpes viruses consists of a relatively large, double- ... All virus genes are transcribed by host RNA polymerase II. Although host proteins are sufficient for virus transcription, viral ...
"Utilizing fowlpox virus recombinants to generate defective RNAs of the coronavirus infectious bronchitis virus". The Journal of ... "Presence of an encephalomyocarditis virus internal ribosome entry site sequence in avian infectious bronchitis virus defective ... The Infectious bronchitis virus D-RNA is an RNA element known as defective RNA or D-RNA. This element is thought to be ... Tombus virus defective interfering (DI) RNA region 3 Dalton K, Casais R, Shaw K, Stirrups K, Evans S, Britton P, Brown TD, ...
"Ambivalent effects of defective DNA in beet curly top virus-infected transgenic sugarbeet plants". Virus Research. 158 (1-2): ... Wikispecies has information related to Beet curly top virus. ICTVdB-The Universal Virus Database: Beet curly top virus Family ... Beet curly top virus was first discovered in 1888 in the Western parts of the United States. The virus wasn't fully recognized ... Beet curly top virus (BCTV) is a pathogenic plant virus of the family Geminiviridae, containing a single-stranded DNA. The ...
"Biased hypermutation and other genetic changes in defective measles viruses in human brain infections". Cell. 55 (2): 255-265. ... influenza virus, lymphocytic choriomeningitis virus, polyomavirus, hepatitis delta virus, and hepatitis C virus. Although ADAR1 ... ADAR1's A to I editing has been found in many viruses including measles virus, ... ADAR1 is an interferon ( IFN )-inducible protein (one released by a cell in response to a pathogen or virus), able to assist in ...
The von Magnus phenomenon describes the generation of defective interfering particles (DIPs) by viruses. It was first observed ... Kristen Ann Stauffer Thompson (2008). Quantitative Effects of Defective Interfering Virus-like Particles on the Growth and ... Gard, S. (1952). "Studies on the sedimentation of influenza virus". Archiv für die Gesamte Virusforschung. 4 (5): 591-611. doi: ... by Preben von Magnus in influenza viruses, after the serial passage of undiluted allantoic fluid in eggs. ...
However, the virus has a bug that causes it to delete only .EXE files. Because it is defective and easy to track, it has been ... The virus can be removed with an antivirus program, or by rebooting in Safe Mode and manually removing the infected files. " ... "Eliza Virus". VSUM. Retrieved 13 February 2013. "Eliza Description , F-Secure Labs". Retrieved 2020-07-05. v ... It has been reported that it is defective, yet destroys the .EXE files it creates. The .COM files are not deleted. To avoid ...
Natural selection and dynamical coexistence of defective and complementing virus segments. Journal of theoretical biology 157, ...
"Yeast as a model host to study replication and recombination of defective interfering RNA of Tomato bushy stunt virus". ... Tomato bushy stunt virus (TBSV) is a virus of the tombusvirus family. It was first reported in tomatoes in 1935 and primarily ... Yamamura, Y; Scholthof, HB (1 September 2005). "Tomato bushy stunt virus: a resilient model system to study virus-plant ... Martelli, G.P.; Russo, M.; Rubino, L. (December 2001). "Tomato bushy stunt virus". Descriptions of Plant Viruses. Association ...
Alice Huang's research focused on defective interfering particles (DIPs) which can be utilized to combat viruses. DIPs are ... An RNA polymerase in the virion." This paper went on to show that "the virions of vesicular stomatitis virus contain an enzyme ... These DIPs will interfere in replication of the virus because they are reproduced at the expense of a standard viral particle. ... Baltimore unraveled that RNA viruses were different and used RNA polymerase to replicate its RNA genome, but they discovered an ...
"Detection and enumeration of transformation-defective strains of avian sarcoma virus with molecular hybridization". Virology. ... It belongs to a family of Src family kinases and is similar to the v-Src (viral Src) gene of Rous sarcoma virus. It includes an ... It is believed that at one point an ancestral virus mistakenly incorporated the c-Src gene of its cellular host. Eventually ... "Uninfected vertebrate cells contain a protein that is closely related to the product of the avian sarcoma virus transforming ...
Much of his research focused on the molecular biology of the vesicular stomatitis virus. With student Alice S. Huang, Wagner ... characterized what are now known as defective interfering particles. Emerson, Suzanne U. (1 April 2002). "Obituary". Archives ... His research focused on the vesicular stomatitis virus. Wagner died of cancer in 2001. Wagner attended Columbia College as an ...
Some components of GIs are lysogenic or defective phages; one of these widespread GIs encodes virus-derived mismatch repair and ... May 2021). "A Novel Broad Host Range Phage Infecting Alteromonas". Viruses. 13 (6): 987. doi:10.3390/v13060987. PMC 8228385. ...
ISBN 978-0-07-174271-9. Carter, M. J.; Willcocks, M. M.; Ter Meulen, V. (1983). "Defective translation of measles virus matrix ... SSPE is caused by the wild-type virus, not by vaccine strains. SSPE is characterized by a history of primary measles infection ... As a result, infectious particles like the M protein are not produced, and the virus is able to survive persistently without ... SSPE should not be confused with acute disseminated encephalomyelitis, which can also be caused by the measles virus, but has a ...
"Detection and enumeration of transformation-defective strains of avian sarcoma virus with molecular hybridization". Virology. ... The causative agent in the liquid was a virus, this is now called the Rous sarcoma virus (RSV). Further research done later on ... v-Src is a gene found in Rous sarcoma virus (RSV) that encodes a tyrosine kinase that causes a type of cancer in chickens. The ... Francis Peyton Rous first proposed that viruses can cause cancer. He proved it in 1911 and was later awarded the Nobel prize in ...
It has also been found that upon persistent infection with EFV, the viral genome replication system becomes defective. Like ... Equine foamy virus (EFV), also called foamy virus (FV), is virus in the genus Equispumavirus. It shares similarities, with ... Additionally, these viruses have been identified in animals that most often carry lentiviruses. The name foamy virus can be ... Foamy viruses are the only viruses of the Retroviridae that reside in the subfamily Spumaretrovirinae. The remainder of the ...
... effectively creating an attenuated virus. The result is a defective vaccine strain that is similar to the current virus strain ... This produces a viral strain that is still live, but not pathogenic to humans, as these viruses are rendered defective in that ... Reverse genetics systems can also allow the recovery and generation of infectious or defective viruses with desired mutations. ... Attenuated viruses are created by propagating a live virus under novel conditions, such as a chicken's egg. ...
One noteworthy study used amber mutants defective in the gene encoding the major head protein of phage T4. This experiment ... Escherichia virus T4 is a species of bacteriophages that infect Escherichia coli bacteria. It is a double-stranded DNA virus in ... Surviving T4 virus released from multicomplexes show no increase in mutation, indicating that MR of UV irradiated virus is an ... The time it takes for DNA replication in a living cell was measured as the rate of virus T4 DNA elongation in virus-infected E ...
Page for Tombus virus defective interfering (DI) RNA region 3 at Rfam v t e (Cis-regulatory RNA elements, Tombusviridae, All ... Tombus virus defective interfering (DI) RNA region 3 is an important cis-regulatory region identified in the 3 UTR of ... Infectious bronchitis virus D-RNA Red clover necrotic mosaic virus translation enhancer elements Ray D, White KA (2003). "An ... Defective interfering RNAs are small sub-viral replicons which are non-coding deletion mutants of the virus that maintain cis- ...
... the influenza virus generates genetically defective viruses. These are found in natural infections as part of the virus ... Influenza defective interfering (DI) viruses have long been considered promising antiviral candidates because of their ability ... To better determine the mechanisms underlying the protective effects of these defective interfering (DI) viruses, we tested a ... Wang C, Honce R, Salvatore M, Chow D, Randazzo D,. Influenza Defective Interfering Virus Promotes Multiciliated Cell ...
... were found to support the replication of defective interfering (DI) RNA in Saccharomyces cerevisiae cells. Two yeast strains ... The replicase proteins p33 and p92 of Cymbidium ringspot virus (CymRSV) ... Pantaleo V., Rubino L., Russo M. 2003; Replication of Carnation Italian ringspot virus defective interfering RNA in ... Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures Richard E. ...
Although the exact origins of vaccinia virus are uncertain, vaccinia may represent a hybrid of the variola and cowpox viruses. ... Vaccination with vaccinia virus has been directly responsible for the successful eradication of smallpox (variola). ... Replication-defective attenuated vaccinia viruses. Modified versions of vaccinia virus have been developed for use as ... Whether vaccinia virus is the product of genetic recombination, a species derived from cowpox virus or variola virus by ...
Defective interfering influenza A virus protects in vivo against disease caused by a heterologous influenza B virus. J Gen ... mechanisms involved in virus-host and virus-virus interactions. Viruses. 2021;13:139. DOIPubMedGoogle Scholar ... influenza A virus [IAV] and respiratory syncytial virus [RSV]) (3). The type of virusvirus interaction (negative or positive) ... pdm09 virus) (1). Negative virusvirus interaction can be homologous or heterologous depending on whether the 2 viruses belong ...
Defective Viruses / genetics * Defective Viruses / physiology * HIV Infections / drug therapy * HIV Infections / virology* ... However, none of the 75 expanded T cell clones assayed contained intact virus. In contrast, the cells bearing single ... The data indicate that dividing clonally expanded T cells contain defective proviruses and that the replication-competent ...
Subclinical infections in mice resulting from the modulation of a lethal dose of Semliki Forest virus with defective ... infections in mice resulting from the modulation of a lethal dose of Semliki Forest virus with defective interfering viruses: ... interfering viruses: Neurochemical abnormalities in the central nervous system. A. D.T. Barrett, A. J. Cross, T. J. Crow, J. A ...
Influenza A Virus Infection Induces Viral and Cellular Defective Ribosomal Products Encoded by Alternative Reading Frames.. ... 1 register of NS1 mRNA in the influenza A virus (IAV). NS1-ARF21-8 elicits a robust, highly functional CD8+ T cell response in ... which potentially has important implications for virus-induced autoimmunity. ...
... play a key role in the adaptability of viruses to changing environments and the fate of the population as a whole. Mutant ... Holland JJ (1990) Defective viral genomes. In Fields BM, Knipe DM (eds) Virology. Raven, New York, pp 151-165 ... García-Arriaza J, Domingo E, Escarmís C (2005) A segmented form of foot-and-mouth disease virus interferes with standard virus ... Novella IS (2003) Contributions of vesicular stomatitis virus to the understanding of RNA virus evolution. Curr Opin Microbiol ...
Generation of "OP7 chimera" defective interfering influenza A particle preparations free of infectious virus that show ... Frequency of respiratory virus-associated infection among children and adolescents from a tertiary-care hospital in Mexico City ... Respiratory syncytial virus in pediatric patients with severe acute respiratory infections in Senegal: findings from the 2022 ...
Evaluation of vertebrate-specific replication-defective zika virus, a novel single-cycle arbovirus vaccine, in a mouse model. ... Evaluation of vertebrate-specific replication-defective zika virus, a novel single-cycle arbovirus vaccine, in a mouse model. ... Evaluation of vertebrate-specific replication-defective zika virus, a novel single-cycle arbovirus vaccine, in a mouse model. ... Evaluation of vertebrate-specific replication-defective zika virus, a novel single-cycle arbovirus vaccine, in a mouse model. ...
Protection and Defective IgA B-Cell Memory in Experimental Infection of Adults with Respiratory Syncytial Virus ... Impaired Antibody-mediated Protection and Defective IgA B-Cell Memory in Experimental Infection of Adults with Respiratory ...
The Hepatitis Delta Virus (HDV) is a RNA defective virus; and an infection with HDV only occurs in the presence of acute or ... Co-infection with hepatitis D virus (HDV) in persons with acute or chronic hepatitis B virus (HBV) infection can lead to ... Hepatitis viruses constitute a major public health problem because of the morbidity and mortality associated with the acute and ... New immunization strategies have been developed to eliminate the spread of HBV and hepatitis A virus (HAV) in the United States ...
Immunodeficiency following hereditary defective response to Epstein-Barr virus D82.4 Hyperimmunoglobulin E [IgE] syndrome ...
Hepatitis D Virus (HDV). Background. Hepatitis D virus (HDV) is a defective virus requiring HBsAg for transmission [15]. ... Hepatitis E Virus (HEV). Background. Hepatitis E virus (HEV) infection causes acute viral hepatitis and is transmitted by the ... Hepatitis C Virus (HCV). Background. Hepatitis C virus (HCV) infection can lead to a chronic, generally asymptomatic viral ... Mixson-Hayden, T., et al., Hepatitis B virus and hepatitis C virus infections in United States-bound refugees from Asia and ...
As compared to the parental virus, the two reporter-expressing ZIKVs grew to lower titers with slower growth kinetics and ... is an enveloped virus with an ~10.8 kb plus-strand RNA genome that can cause neurological disease. To facilitate the ... they displayed a genome-wide viral protein expression profile identical to that of the parental virus, except for two ... Zika virus (ZIKV), a mosquito-borne transplacentally transmissible flavivirus, ...
We discuss their parasitic lifestyle as bona fide viruses of the giant virus factories, genetic parasites of their genomes, and ... In addition, the isolation of virophages has led us to discover previously unknown features displayed by their host viruses and ... The discovery of giant viruses and a distinct new class of viral agents that parasitize their viral factories, the virophages. ... but also the relevant ecological impact of these small viruses and their potential role in the dynamics of the microbial ...
Papadopoulos NG, Stanciu LA, Papi A, et al. A defective type 1 response to rhinovirus in atopic asthma. Thorax2002;57:328-32. ... Direct detection of respiratory syncytial virus, parainfluenza virus, and adenovirus in clinical respiratory specimens by a ... Marin J, Jeler-Kacar D, Levstek V, et al. Persistence of viruses in upper respiratory tract of children with asthma. J Infect ... We hypothesised that respiratory viruses as well as C pneumoniae, M pneumoniae, and B pertussis are present in the airways of ...
Defective Epstein-Barr virus in chronic active infection and haematological malignancy. Okuno Y, Murata T, Sato Y, Muramatsu H ...
... and H9N2 influenza viruses, through binding to a highly conserved epitope in the influenza hemagglutinin stem region. To ... and H9N2 influenza viruses, through binding to a highly conserved epitope in the influenza hemagglutinin stem region. To ... Adeno-associated virus: from defective virus to effective vector. Virol J. (2005) 2:43. ... For TCID50 determination, a 10-4 dilution of influenza virus was made and diluted ten-fold across the plate. Virus dilutions ...
How can the same flu virus be a mild infection in some people and a killer in others? The answer may lie in your genes ... What makes the same flu virus deadly for some people but not much more than an excuse for a duvet day for others? A French girl ... Their daughter, however, inherited two defective copies, one from each parent. So neither her immune cells nor her lung cells ... Nor has she succumbed to any other severe viruses, suggesting that IRF7 isnt a widely used antiviral defence in people. If it ...
... attorneys represent clients in faulty medical devices and consumer product liability claims involving a full range of defective ... Office Air Conditioning Can Spread COVID-19 Virus: Lessons from Toxic Chemical Defective Product Lawsuits. June 9, 2020. By ... But the virus spreads through droplets and micro droplets. Typically, the virus attaches to particles or droplets which should ... Office Air Conditioning Can Spread COVID-19 Virus: Lessons from Toxic Chemical Defective Product Lawsuits ...
"Defective viral genomes as determinants of virus and host fate during viral infections". Carolina B. Lopez, Ph.D.. Associate ... "Rift Valley fever virus NSs: A new role in co-packaging of viral genome segments and vaccine development". Kaori Terasaki, PhD ...
"Characterization of Ebola Virus Defective Genomes". Rebecca Johnson, Griffiths Lab. and. "Advancement of a Small Molecule ... "Investigating a Virus that Doesnt Exist: Generating a Minigenome System for Lloviu Virus". and. "The Effect of Adjuvants on ... Vaccinia virus hijacks EGFR signalling to enhance virus spread through rapid and directed infected cell motility. Nat. ... "Investigating the Role of Virus-Encoded Small RNAs in Ebola Virus Transcription Initiation". Stephen Ross, Cifuentes & ...
Did Wyden plant a virus to kill a morally defective bill?. » All Related Discussion ...
A viruses to humans1,2. Influenza A viruses contain a segmented negative-sense RNA genome, which is transcribed and ... Structures of RNA polymerase of human and avian influenza A viruses reveal that the interface of the RNA polymerase dimer ... viruses at a resolution of 3.0-4.3 Å, in the presence or absence of a cRNA or vRNA template. In solution, FluPolA ... A virus has previously been reported6, there are no complete structures available for human and avian FluPolA. Furthermore, the ...
Hepatitis B virus infection: Defective surface antigen expression and pathogenesis. World J Gastroenterol 2018; 24(31): 3488- ...
2. A transformation-defective mutant of Abelson murine leukemia virus lacks protein kinase activity Witte, Owen N.; Goff, ... Interactions of Host Proteins with the Murine Leukemia Virus Integrase Studamire, Barbara; Goff, Stephen P. 2010 Articles ... 1. Synthesis of a 600-nucleotide-long plus-strand DNA by virions of Moloney murine leukemia virus Mitra, Sudha W.; Goff, ... Mouse leukemia virusesRetroviruses--GeneticsRecombinant proteinsBiochemistryInsertional mutagenesis 8. Linker insertion ...
defective (nonfunctional): 8% co-opted RNA viruses: ,0.1% b. bCo-opted RNA viruses are defective integrated virus genomes that ... Viruses (9% junk). DNA viruses. active (functional): ,0.1% defective DNA viruses: ~1% RNA viruses active (functional): ,0.1% ... RNA viruses are viruses that contain RNA instead of DNA. When the RNA molecule is injected into the cell it serves immediately ... We try to explain that half of our genome is composed of defective transposons and viruses-often fragments of the intact genes ...
... which protects the body from autoimmune disorders also helps secretly usher in some viruses by changing their look. ... When the ADAR1 gene is defective, it cant transform some double-stranded RNA produced by the body into single-stranded RNA. ... The measles virus stores its genetic information in RNA instead of DNA. And though the virus usually makes single-stranded RNA ... also helps secretly usher in viruses by making them undetectable. But how the story ends depends on how much virus is trying to ...
  • Defective interfering RNAs are small sub-viral replicons which are non-coding deletion mutants of the virus that maintain cis-acting RNA elements necessary for replication of the host virus. (
  • The mechanisms involved in viral interference have been evaluated in differentiated airway epithelial cells and in animal models susceptible to the respiratory viruses of interest. (
  • Heterologous viral interference relies on induction of a nonspecific innate immune response by a first virus that reduces or prevents infection and replication of a second virus (e.g., influenza A virus [IAV] and respiratory syncytial virus [RSV]) ( 3 ). (
  • The more probable mechanism of negative viral interactions relies on the induction of a transient innate immunity by the interfering virus. (
  • Influenza A Virus Infection Induces Viral and Cellular Defective Ribosomal Products Encoded by Alternative Reading Frames. (
  • During viral infections, the complex and dynamic distributions of variants, termed viral quasispecies, play a key role in the adaptability of viruses to changing environments and the fate of the population as a whole. (
  • On the contrary, current evidence indicates that mutant spectra contribute to viral pathogenesis, can modulate the expression of phenotypic traits by subpopulations of viruses, can include memory genomes that reflect the past evolutionary history of the viral lineage, and, furthermore, can participate in viral extinction through lethal mutagenesis. (
  • Arias A, Agudo R, Ferrer-Orta C, Pérez-Luque R, Airaksinen A, Brocchi E, Domingo E, Verdaguer N, Escarmis C (2005) Mutant viral polymerase in the transition of virus to error catastrophe identifies a critical site for RNA binding. (
  • Charpentier C, Dwyer DE, Mammano F, Lecossier D, Clavel F, Hance AJ (2004) Role of minority populations of human immunodeficiency virus type 1 in the evolution of viral resistance to protease inhibitors. (
  • Many viral infections can cause liver inflammation, but the term viral hepatitis usually refers to infections with one of the five hepatotropic viruses (viruses known to target the human liver): HAV, HBV, HCV, HDV, and HEV. (
  • The last decade has been marked by two eminent discoveries that have changed our perception of the virology field: The discovery of giant viruses and a distinct new class of viral agents that parasitize their viral factories, the virophages. (
  • 1 In that study picornaviruses (mostly rhinoviruses) accounted for two thirds of the viral infections, with coronavirus causing less severe asthma exacerbations than other respiratory viruses. (
  • To overcome this obstacle, conditional oncolytic viruses (such as conditional replication adenovirus (CRAD)) are developed to specifically target prostate without (or with minimal) systemic toxicity due to viral self-replication. (
  • E1-deleted (including E1a-deleted) adenoviruses are replication defective and are commonly used as viral vectors to carry therapeutic genes for gene therapy. (
  • DARPA says it wants to harness TIPs - tiny virus-like entities with engineered genetic material that encodes defective viral proteins. (
  • In a cell infected with both a flu virus and a TIP, the cell makes copies of the TIP genome that compete for viral proteins. (
  • It also exhaustively introduces the concrete mechanism of invading GC cells and the viral genome composition of adenovirus and herpes simplex virus type 1 (HSV-1). (
  • Defective genomes arise when the viral polymerases lose processivity during virus replication at high titers. (
  • Working with Sendai and influenza viruses in mice, Carolina López and colleagues show that defective viral genomes accumulate during acute viral respiratory infections. (
  • Previously, chronic ethanol consumption was shown to prolong inflammation and delay viral clearance in respiratory syncytial virus (RSV)-infected mice. (
  • These proteins may be prematurely degraded by MMP-9 in the lung, leading to defective immunity and reduced viral clearance. (
  • Here, we demonstrated the interferon (IFN)-independent protection conferred by the influenza DI virus against homologous virus infection in mice deficient in type I and III IFN signaling. (
  • Inoculation with vaccina virus produces a localized skin infection. (
  • Infection by a first virus could enhance or reduce infection and replication of a second virus, resulting in positive (additive or synergistic) or negative (antagonistic) interaction. (
  • At the host level, the course of infection of 1 virus might be influenced by prior or concurrent infection by another virus. (
  • Positive virus‒virus interaction corresponds to a co-infection that might result in an increased disease severity and pathogenesis (e.g., severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2] and influenza A[H1N1]pdm09 virus) ( 1 ). (
  • Homologous virus‒virus interaction implies that cross-reactive immunity against a first virus prevents infection with a second virus (e.g., among different influenza subtypes or lineages) ( 2 ). (
  • The type of virus‒virus interaction (negative or positive) is probably dependent on the respiratory viruses involved, the timing of each infection, and the interplay between the response of the host to each virus. (
  • Induction of ISGs by a first virus might limit infection and replication of a second virus, especially if they show a differential ability to induce an IFN response or different degrees of susceptibility to immune mediators. (
  • We further show that IAV infection enhances a model cellular ARF translation, which potentially has important implications for virus -induced autoimmunity . (
  • Co-infection with hepatitis D virus (HDV) in persons with acute or chronic hepatitis B virus (HBV) infection can lead to fulminant hepatitis. (
  • Recommendations have also been developed for the prevention and control of hepatitis C virus (HCV) infection. (
  • Because of the high rate of asymptomatic infection with these viruses, information about the prevalence of these diseases is needed to monitor prevention efforts. (
  • NHANES testing for markers of infection with hepatitis viruses will be used to determine secular trends in infection rates across most age and racial/ethnic groups, and will provide a national picture of the epidemiologic determinants of these infections. (
  • Routine screening for hepatitis D virus (HDV) infection is not recommended. (
  • Defective Epstein-Barr virus in chronic active infection and haematological malignancy. (
  • Hepatitis B virus infection: Defective surface antigen expression and pathogenesis. (
  • Dowd JB, Palermo T, Brite J, McDade TW, Aiello A. Seroprevalence of Epstein-Barr virus infection in U.S. children ages 6-19, 2003-2010. (
  • Behavioral, virologic, and immunologic factors associated with acquisition and severity of primary Epstein-Barr virus infection in university students. (
  • Dunmire SK, Verghese PS, Balfour HH Jr. Primary Epstein-Barr virus infection. (
  • Okuno Y, Murata T, Sato Y, Muramatsu H. Defective Epstein-Barr virus in chronic active infection and haematological malignancy. (
  • The goal is for harmless TIPs to outnumber flu virus genetic elements so infected cells would generate relatively few infectious viruses and a bumper crop of "dud viruses" with TIP genes, rapidly diluting the harmful viruses and halting the infection, according to DARPA. (
  • Rzew is classified by our malware research team as the DJVU virus infection. (
  • The acute and chronic consequences of hepatitis B virus (HBV) infection are major health problems in the United States. (
  • Human immunodeficiency virus (HIV) infection results from 1 of 2 similar retroviruses (HIV-1 and HIV-2) that destroy CD4+ lymphocytes and impair cell-mediated immunity, increasing risk of certain infections and cancers. (
  • Human Immunodeficiency Virus (HIV) Infection in Infants and Children Human immunodeficiency virus (HIV) infection is caused by the retrovirus HIV-1 (and less commonly by the related retrovirus HIV-2). (
  • Newly acquired symptomatic hepatitis B virus (HBV) infection. (
  • Newly acquired symptomatic hepatitis C virus (HCV) infection. (
  • This lymphomalike stage is precipitated by viruses, particularly by infection by the Epstein-Barr virus. (
  • Moreover, The use of animals as surrogate rine host, can provide a platform for animal models for tumour viruses in hosts for the study of human tu- in vivo infection. (
  • For the first time in virology, Fabris and her team will use imaging tools with gold nanoparticles to monitor mutations in the influenza virus, with unprecedented sensitivity, when it enters cells. (
  • The genomes of other chlorella virus isolates are probably co-linear with PBCV-1 and appear to share many, but not all, genes. (
  • Respiratory specimens were analysed by RT-PCR for rhinovirus, enterovirus and respiratory syncytial virus and by PCR for adenovirus, Chlamydia pneumoniae , Mycoplasma pneumoniae and Bordetella pertussis . (
  • The idea behind this study is to place the Ad5 E1 region in cis complementation (i.e., use E1 as a transgene) back into an E1-deleted, replication-defective adenovirus under the control of a prostate-specific promoter (PSP). (
  • This protein boosts the production of a virus-fighting molecule called interferon. (
  • It's a monkey virus coming out of a monkey cell line and that's the problem, but the spike protein is clearly [causing] the disease. (
  • Foot-and-mouth disease virus (FMDV) nonstructural protein 3A plays important roles in virus replication, virulence, and host range. (
  • Substitution of Val 113 in Sendai virus (SeV) M protein generates non-functional polypeptides, characterized by their exclusion from virus particles and by their ability to interfere with virus particle production. (
  • Analysis of the Sendai virus M gene and protein. (
  • Sendai virus M protein is found in two distinct isoforms defined by monoclonal antibodies. (
  • Thus, E1 protein expression will be confined strictly to the prostate tissues and render this a conditional oncolytic virus (CRAD) within the prostate. (
  • A number of PSPs have been defined over the years that include, but not limited to, promoters of prostate-specific antigen (PSA), probasin (PB), mouse mammary tumor virus (MMTV LTR), prostate-specific membrane antigen (PSMA), human glandular kallikrein 2 (hK2), and prostatic steroid-binding protein C3. (
  • Many of these genes encode proteins (e.g., enzymes involved in protein glycosylation) rarely associated with viruses. (
  • Analysis of two highly expressed genes from Chlorella virus PBCV-1: Protein characterization and the DNA sequences of the major capsid protein gene and the early/late 33-kDa protein gene. (
  • RNA viruses like influenza are coated by a protein-studded membrane envelope, Fabris noted. (
  • Ideally, the TIPs will be introduced into influenza virus populations and compete for protein, so the virus will starve and not be able to reproduce," she said. (
  • The findings, published March 26 in the open-access journal PLOS One , offer what the Johns Hopkins teams says is a first-of-its-kind evidence that a protein that specializes in bacterial detection is also turned on when it sniffs out a virus from the DNA family. (
  • What if people with Crohn's disease were susceptible to CMV not just because of immunosuppressive therapy but because of this defective protein, Boger wondered. (
  • Viruses which lack a complete genome so that they cannot completely replicate or cannot form a protein coat. (
  • These are found in natural infections as part of the virus population within the infected host. (
  • Hepatitis viruses constitute a major public health problem because of the morbidity and mortality associated with the acute and chronic consequences of these infections. (
  • Infections caused by these viruses vary in their epidemiologic features and natural history, including incubation period, routes of transmission, geographic and demographic distribution, patterns of clinical disease, and propensity for becoming chronic. (
  • Because chronic HBV and HCV infections are asymptomatic and refugees often come from settings where these viruses are endemic, it is important to consider these infections during the domestic medical screening for newly arrived refugees. (
  • Molecular Analysis of Soybean Dwarf Virus Isolates in the Eastern United States Confirms the Presence of Both D and Y Strains and Provides Evidence of Mixed Infections and Recombination. (
  • The new research provides first-of-its-kind evidence that this receptor also helps fight DNA viruses, known to cause lifelong infections. (
  • DNA viruses are known for their ability to cause chronic infections. (
  • They present recurrent sinopulmonary and herpes simplex virus infections and poor responses to immunization. (
  • To reduce the risk of an increasing antibiotic resistance, it is important to avoid unnecessary use of antibiotics, for example, during virus infections and simple bacterial infections. (
  • One gene, which protects the body from autoimmune disorders (in which the body attacks itself), also helps secretly usher in viruses by making them undetectable. (
  • This gene, called the adenosine deaminase acting on RNA 1, or ADAR1, protects the body from large amounts of the virus, but invites it in if only a small number of viruses knock on the door, the scientists found. (
  • When the ADAR1 gene is defective, it can't transform some double-stranded RNA produced by the body into single-stranded RNA. (
  • They then infected cells with either the functioning gene or the deleted gene with different amounts of a measles virus. (
  • Although virus-based gene therapy is a promising strategy to combat advanced prostate cancer, its current effectiveness is limited partially due to inefficient cellular transduction in vivo . (
  • Transgenic mice bearing PB promoter fused to simian virus 40 large tumor antigen gene all consistently develop prostate adenocarcinoma [ 13 ]. (
  • People with a specific mutation (called Δ32) on the CCR5 gene develop defective receptors, so the HIV virus can't enter the cell. (
  • Putative Gene Promoter Sequences in the Chlorella Viruses. (
  • The treatment uses a virus to insert a functional piece of DNA into the eyes to override a defective gene. (
  • In this case, it's the RPE65 gene, and the virus is directly injected into the eyes. (
  • Swine inoculated with 109 pfu of a control Ad5 virus lacking the IFN gene and challenged 24 hours later with FMDV developed typical signs of FMD including fever, vesicular lesions, and viremia. (
  • Once modified, retroviruses can be used for gene therapy as we can use them to target defective genes. (
  • Influenza defective interfering (DI) viruses have long been considered promising antiviral candidates because of their ability to interfere with replication-competent viruses and induce antiviral immunity. (
  • Some versions of these defective viruses are thought to have protective effects through their interference with replication-competent viruses and induction of antiviral immunity. (
  • In a pandemic, a new influenza virus emerges and infects the human population which has little or no pre-existing immunity ( 2 , 3 ). (
  • Tombus virus defective interfering (DI) RNA region 3 is an important cis-regulatory region identified in the 3' UTR of Tombusvirus defective interfering particles (DI). (
  • The replication of cymbidium ringspot tombusvirus defective interfering-satellite RNA hybrid molecules. (
  • Swine given one inoculation of this recombinant virus and then challenged with virulent FMDV one day postinoculation were completely protected from clinical signs of disease and viremia. (
  • Infectious bronchitis virus D-RNA Red clover necrotic mosaic virus translation enhancer elements Ray D, White KA (2003). (
  • A prospective clinical study of Epstein-Barr virus and host interactions during acute infectious mononucleosis. (
  • Vetsika EK, Callan M. Infectious mononucleosis and Epstein-Barr virus. (
  • Acute kidney injury in symptomatic primary Epstein-Barr virus infectious mononucleosis: Systematic review. (
  • Preliminary results from in vivo experiments indicated that virus with the N27D mutation is infectious at near wt NC levels. (
  • Infectious transcripts and cDNA clones of RNA viruses. (
  • On my homepage blog , I gave an update on the Ebola virus which included its definition, its transmission, how it's infectious but not contagious, and conventional treatments. (
  • Retroviruses are viruses that contain RNA, the cousin of DNA, which encodes for genes that helps it insert itself into the host DNA. (
  • Zika virus (ZIKV), a mosquito-borne transplacentally transmissible flavivirus, is an enveloped virus with an ~10.8 kb plus-strand RNA genome that can cause neurological disease. (
  • Replication-competent viruses, also known as oncolytic viruses, replicate within transduced cells and force these cells into a lytic cycle. (
  • This review integrates most experimental studies and clinical trials of various oncolytic viruses (OVs) in the diagnosis and treatment of GC. (
  • The ancient viruses that are in our DNA are considered human endogenous retroviruses (HERV) and they were once retroviruses that invaded ancestor DNA. (
  • Retroviruses are enveloped RNA viruses defined by their mechanism of replication via reverse transcription to produce DNA copies that integrate into the host cell's genome. (
  • Multiple respiratory viruses can concurrently or sequentially infect the respiratory tract and lead to virus‒virus interactions. (
  • Several respiratory viruses can circulate during the same period and can concurrently or sequentially infect the respiratory tract, leading to virus‒virus interactions. (
  • Released virus is then able to infect neighboring cells until all susceptible cells are eliminated. (
  • Research in my lab focuses on the chlorella viruses that infect chlorella-like algae. (
  • Sequence and Annotation of the 314-Kb MT325 and the 321-kb FR483 Viruses That Infect Chlorella Pbi. (
  • Sequence and annotation of the 369-kb NY-2A and the 345-kb AR158 viruses that infect Chlorella NC64A. (
  • For this reason, the infect humans, this virus can infect cordance between humans and ex- question about tumour site concor- several other species - including perimental animals. (
  • The replicase proteins p33 and p92 of Cymbidium ringspot virus (CymRSV) were found to support the replication of defective interfering (DI) RNA in Saccharomyces cerevisiae cells. (
  • Results from two other forms of HIV-1 NC (NCp9 and NCp15) and NC proteins from Simian Immunodeficiency Virus and Murine Leukemia Virus are also reported. (
  • Here, we investigated a new single-cycle flavivirus vaccine, a vertebrate-specific replication-defective ZIKV (VSRD-ZIKV), in a mouse model. (
  • Arias A, Lázaro E, Escarmís C, Domingo E (2001) Molecular intermediates of fitness gain of an RNA virus: characterization of a mutant spectrum by biological and molecular cloning. (
  • Molecular cloning and characterization of a Sendai virus internal deletion defective RNA. (
  • Although antiviral drugs such as Oseltamivir are available to control the spread of the virus their effectiveness is limited in treating patients with influenza ( 5 , 6 ). (
  • Nor has she succumbed to any other severe viruses, suggesting that IRF7 isn't a widely used antiviral defence in people. (
  • We have previously described R1a-B6, an alpaca-derived single domain antibody (nanobody), that is capable of potent cross-subtype neutralization in vitro of H1N1, H5N1, H2N2, and H9N2 influenza viruses, through binding to a highly conserved epitope in the influenza hemagglutinin stem region. (
  • Therefore, strategies to use conditional oncolytic virus, or the so-called attenuated replication-competent viruses, to specifically target prostate tissue have been developed [ 2 - 4 ]. (
  • Once the sanitary restrictions are lifted, circulation of seasonal respiratory viruses is expected to resume and will offer the opportunity to study their interactions, notably with severe acute respiratory syndrome coronavirus 2. (
  • Structural components of viruses are sensed by pattern recognition receptors in epithelial and immune cells ( Figure ) ( 4 ). (
  • The data indicate that dividing clonally expanded T cells contain defective proviruses and that the replication-competent reservoir is primarily found in CD4(+) T cells that remain relatively quiescent. (
  • In addition, the isolation of virophages has led us to discover previously unknown features displayed by their host viruses and cells. (
  • So neither her immune cells nor her lung cells were able to crank out interferon when exposed to the flu virus. (
  • We also show that a nanobody (a single-domain antibody) that interferes with FluPol A dimerization inhibits the synthesis of vRNA and, consequently, inhibits virus replication in infected cells. (
  • Eventually, however, cells began using DNA, while viruses predominantly began encoding genetic information in RNA. (
  • The team also infected the cells with a mutated measles virus that carried more double-stranded RNA and watched what happened. (
  • I think the most surprising aspect of this virus is that it causes vasculitis , but not because it reproduces itself in the endothelial cells that line blood vessels. (
  • TIPs, like viruses, can enter cells, but they don't replicate unless the cells are also infected with the virus. (
  • Her role will be to provide imaging and quantification methods to study, in cells and eventually animals, which parts of the influenza virus genome have mutated and to what degree. (
  • We demonstrated that cells infected with these viruses express high levels of biologically active IFN. (
  • Mice that were infected with a mix of wild-type influenza and DI viruses had less intense inflammatory and innate immune responses than did mice that were infected with the wild-type virus only, even when type I or III interferons, which are cytokines that play a prominent role in defending the respiratory epithelial barrier, were absent. (
  • Borrego B, Novella IS, Giralt E, Andreu D, Domingo E (1993) Distinct repertoire of antigenic variants of foot-and-mouth disease virus in the presence or absence of immune selection. (
  • More than this and the immune system notices the virus. (
  • Measles is not the only virus that can hijack the immune system, and Cattaneo said he hopes to determine the activation thresholds for other viruses, such as the yellow fever virus and the Chikungunya virus (which are both spread by mosquitoes). (
  • Although healthy adults who carry the virus rarely exhibit symptoms, CMV can cause serious problems in people with certain immune-deficiency disorders, those with advanced HIV, and in patients receiving immunosuppressive therapy to treat cancer or prevent organ rejection. (
  • Patients are also often more susceptible than others because of their weaker immune systems, defective defence barriers or changes in their normal bacterial flora. (
  • In their Pearl, James Wynne and Lin-Fa Wang focus on bat viruses that have caused zoonotic disease outbreaks in humans and domestic animals. (
  • Typically, the virus attaches to particles or droplets which should be filtered by a MERV 13 filter. (
  • In the United States, Dryvax became the first approved vaccinia virus vaccine in 1931. (
  • Vaccinia virus is the species now characterized as the constituent of smallpox vaccine. (
  • Chumakov KM, Powers LB, Noonan KE, Roninson IB, Levenbook IS (1991) Correlation between amount of virus with altered nucleotide sequence and the monkey test for acceptability of oral poliovirus vaccine. (
  • I think when you have no commercial experience with a vaccine strategy and you're using that as a way to try to stop a new virus, there will be something of a learning curve. (
  • So you have this difficult-to-characterize, elusive virus that you are now about to meet with a handful of vaccine strategies for which you have no commercial experience. (
  • Treasury Sec. Steve Mnuchin, who we hope is working on mass distribution of the ~vaccine~ and not the virus. (
  • For more on word-substitution errors like Mnuchin's virus for vaccine , see " Defendants wrongly committed of a crime ", 8/4/2011. (
  • Plus, it must be the virus he's talking about, because there's no vaccine to distribute to the masses, yet. (
  • Some are host-dependent defectives, meaning they can replicate only in cell systems which provide the particular genetic function which they lack. (
  • Others, called SATELLITE VIRUSES, are able to replicate only when their genetic defect is complemented by a helper virus. (
  • During the coronavirus disease pandemic, nonpharmacologic interventions have prevented the circulation of most respiratory viruses. (
  • IMPORTANCE During replication, the influenza virus generates genetically defective viruses. (
  • Wang C, Honce R, Salvatore M, Chow D, Randazzo D,. Influenza Defective Interfering Virus Promotes Multiciliated Cell Differentiation and Reduces the Inflammatory Response in Mice . (
  • To better determine the mechanisms underlying the protective effects of these defective interfering (DI) viruses, we tested a DI that we previously identified in vitro with mice. (
  • . S-adenosylhomocysteine hydrolase inhibitors have been found to have complete mortality protection in mice infected with a lethal dose of Ebola virus (30). (
  • An association between MMP-9 and impaired T cell migration in ethanol-fed BALB/c mice infected with respiratory syncytial virus-2A. (
  • One exception is hu- humanized SCID mice, the use of al oncogenic viruses that are strictly man T-cell lymphotropic virus type 1 surrogate hosts has not proven very species-specific, causing cancer in (HTLV-1): in addition to its ability to useful for defining tumour site con- humans only. (
  • For instance, mice are able to reconstitute most lymphomas in monkeys and humans woodchuck hepatitis virus induces major components of the human provides strong support for a direct hepatocellular carcinoma (HCC) haematolymphoid system including oncogenic role of EBV in vivo. (
  • These results demonstrate, for the first time, that a single inoculation of an Ad5-interferon virus can be used as a tool to immediately control FMD in emergency outbreak situations. (
  • The variola virus causes smallpox and may have begun infecting humans approximately 10,000 years ago. (
  • HIV-1 originated in Central Africa in the first half of the 20th century, when a closely related chimpanzee virus first infected humans. (
  • For other human tumour virus- primate species are related to the hu- tween data in humans and in experi- es, the use of humanized severe man tumour viruses, the incidence of mental animals is not obvious. (
  • In addition, NHANES provides the means to better define the epidemiology of other hepatitis viruses. (
  • Epstein-Barr Virus Epidemiology, Serology, and Genetic Variability of LMP-1 Oncogene Among Healthy Population: An Update. (
  • 1. The Ebola virus was named after the Ebola River where it was first recognized. (
  • Interestingly, the Ebola virus is inactivated by UV radiation.12 It certainly isn't the first time sunlight has been shown to be beneficial in the fight against disease, although bacteria appears to be more susceptible to UV radiation than viruses. (
  • They're called TIPs and their task would be to infiltrate and outcompete influenza , HIV , Ebola and other viruses. (
  • So far, efforts to develop effective drugs against these viruses have failed, and typical therapy usually relies on symptomatic treatment. (
  • They also highlight questions about the interactions between bat viruses and their flying mammalian hosts. (
  • Nevertheless, while Q44R led to recovery of viruses that maintained the mutation, Q44D resulted in selection of infective viruses with substitution D44E with acidic charge but with structural features similar to those of the parental virus, suggesting that Q44 is involved in functions other than 3A dimerization. (
  • Here, using crystallography and cryo-electron microscopy, we determine the structures of FluPol A from human influenza A/NT/60/1968 (H3N2) and avian influenza A/duck/Fujian/01/2002 (H5N1) viruses at a resolution of 3.0-4.3 Å, in the presence or absence of a cRNA or vRNA template. (
  • Negative virus‒virus interaction can be homologous or heterologous depending on whether the 2 viruses belong to the same family or to different serotypes or families. (
  • Briones C, Domingo E, Molina-París C (2003) Memory in retroviral quasispecies: experimental evidence and theoretical model for human immunodeficiency virus. (
  • Human immunodeficiency virus (HIV) is a retrovirus. (
  • Animal models for human tumour mental animals is not easy to answer does induce adult T-cell leukaemia/ viruses that make use of animal virus- for these agents, because cancer bi- lymphoma (ATLL), albeit in monkeys es are scarce. (
  • These in vitro, and their expression in these human tumour virus. (
  • Vaccines produced by chemical inactivation of virus are available, but there are concerns about their safety and they do not induce protection prior to about 7 days postvaccination. (
  • The A312L 5'-UTR of Chlorella Virus PBVC-1 is a Translational Enhancer in Arabidopsis Thaliana. (
  • These individuals are not benefiting from our scientific discoveries and may continue to transmit the virus to others because their virus is not undetectable. (