Viral Interference
Encephalitis Viruses
Virus Replication
RNA Interference
Ear, Inner
Embryology
Labyrinth Diseases
Cochlea
Ear
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. (1/528)
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)Characterization of the major control region of Vibrio cholerae bacteriophage K139: immunity, exclusion, and integration. (2/528)
The temperate bacteriophage K139 is highly associated with pathogenic O1 Vibrio cholerae strains. The nucleotide sequence of the major control region of K139 was determined. The sequences of four (cox, cII, cI, and int) of the six deduced open reading frames and their gene order indicated that K139 is related to the P2 bacteriophage family. Two genes of the lysogenic transcript from the mapped promoter PL encode homologs to the proteins CI and Int, with deduced functions in prophage formation and maintenance. Between the cI and int genes, two additional genes were identified: orf2, which has no significant similarity to any other gene, and the formerly characterized gene glo. Further analysis revealed that Orf2 is involved in preventing superinfection. In a previous report, we described that mutations in glo cause an attenuation effect in the cholera mouse model (J. Reidl and J. J. Mekalanos, Mol. Microbiol. 18:685-701, 1995). In this report, we present strong evidence that Glo participates in phage exclusion. Glo was characterized to encode a 13.6-kDa periplasmic protein which inhibits phage infection at an early step, hence preventing reinfection of vibriophage K139 into K139 lysogenic cells. Immediately downstream of gene int, the attP site was identified. Upon analysis of the corresponding attB site within the V. cholerae chromosome, it became evident that phage K139 is integrated between the flagellin genes flaA and flaC of O1 El Tor and O139 V. cholerae lysogenic strains. (+info)Site-specific recombination of temperate Myxococcus xanthus phage Mx8: regulation of integrase activity by reversible, covalent modification. (3/528)
Temperate Myxococcus xanthus phage Mx8 integrates into the attB locus of the M. xanthus genome. The phage attachment site, attP, is required in cis for integration and lies within the int (integrase) coding sequence. Site-specific integration of Mx8 alters the 3' end of int to generate the modified intX gene, which encodes a less active form of integrase with a different C terminus. The phage-encoded (Int) form of integrase promotes attP x attB recombination more efficiently than attR x attB, attL x attB, or attB x attB recombination. The attP and attB sites share a common core. Sequences flanking both sides of the attP core within the int gene are necessary for attP function. This information shows that the directionality of the integration reaction depends on arm sequences flanking both sides of the attP core. Expression of the uoi gene immediately upstream of int inhibits integrative (attP x attB) recombination, supporting the idea that uoi encodes the Mx8 excisionase. Integrase catalyzes a reaction that alters the primary sequence of its gene; the change in the primary amino acid sequence of Mx8 integrase resulting from the reaction that it catalyzes is a novel mechanism by which the reversible, covalent modification of an enzyme is used to regulate its specific activity. The lower specific activity of the prophage-encoded IntX integrase acts to limit excisive site-specific recombination in lysogens carrying a single Mx8 prophage, which are less immune to superinfection than lysogens carrying multiple, tandem prophages. Thus, this mechanism serves to regulate Mx8 site-specific recombination and superinfection immunity coordinately and thereby to preserve the integrity of the lysogenic state. (+info)Chromosomal localization of human genes governing the interferon-induced antiviral state. (4/528)
Interferon sensitivity of different normal and aneusomic human cells and of different mouse-human hybrids cells has been compared. G21 trisomic cells are more sensitive than diploid cells; whereas, on the contrary, triploid cells are normal in their human interferon sensitivity. Among other aneusomic cell lines tested, E16 trisomic cells are significantly less sensitive. These data are in favor of the hypotheses that the G21 chromosome carries genetic information for structural proteins involved in the receptor system for interferon, that there is a regulatory mechanism governing the antiviral state, and that the E16 chromosome is a possible candidate for carrying information for such a depressive regulatory mechanism. None of the chromosome abnormalities studies are involved with interferon synthesis. (+info)Synergistic interactions of a potyvirus and a phloem-limited crinivirus in sweet potato plants. (5/528)
When infecting alone, Sweet potato feathery mottle virus (SPFMV, genus Potyvirus) and Sweet potato chlorotic stunt virus (SPCSV, genus Crinivirus) cause no or only mild symptoms (slight stunting and purpling), respectively, in the sweet potato (Ipomoea batatas L. ). In the SPFMV-resistant cv. Tanzania, SPFMV is also present at extremely low titers, though plants are systemically infected. However, infection with both viruses results in the development of sweet potato virus disease (SPVD) characterized by severe symptoms in leaves and stunting of the plants. Data from this study showed that SPCSV remains confined to phloem and at a similar or slightly lower titer in the SPVD-affected plants, whereas the amounts of SPFMV RNA and CP antigen increase 600-fold. SPFMV was not confined to phloem, and the movement from the inoculated leaf to the upper leaves occurred at a similar rate, regardless of whether or not the plants were infected with SPCSV. Hence, resistance to SPFMV in cv. Tanzania was not based on restricted virus movement, neither did SPCSV significantly enhance the phloem loading or unloading of SPFMV. It is also noteworthy that SPVD is an unusual synergistic interaction in that the potyvirus component is not the cause of synergism but is the beneficiary. It is hypothesized that SPCSV is able to enhance the multiplication of SPFMV in tissues other than where it occurs itself, perhaps by interfering with systemic phloem-dependent signaling required in a resistance mechanism directed against SPFMV. (+info)Identification and characterization of a shared TNFR-related receptor for subgroup B, D, and E avian leukosis viruses reveal cysteine residues required specifically for subgroup E viral entry. (6/528)
Genetic and receptor interference data have indicated the presence of one or more cellular receptors for subgroup B, D, and E avian leukosis viruses (ALV) encoded by the s1 allele of the chicken tvb locus. Despite the prediction that these viruses use the same receptor, they exhibit a nonreciprocal receptor interference pattern: ALV-B and ALV-D can interfere with infection by all three viral subgroups, but ALV-E only interferes with infection by subgroup E viruses. We identified a tvb(s1) cDNA clone which encodes a tumor necrosis factor receptor-related receptor for ALV-B, -D, and -E. The nonreciprocal receptor interference pattern was reconstituted in transfected human 293 cells by coexpressing the cloned receptor with the envelope (Env) proteins of either ALV-B or ALV-E. This pattern of interference was also observed when soluble ALV surface (SU)-immunoglobulin fusion proteins were bound to this cellular receptor before viral challenge. These data demonstrate that viral Env-receptor interactions can account for the nonreciprocal interference between ALV subgroups B, D, and E. Furthermore, they indicate that a single chicken gene located at tvb(s1) encodes receptors for these three viral subgroups. The TVB(S1) protein differs exclusively at residue 62 from the published subgroup B- and D-specific receptor, encoded by the s3 allele of tvb. Residue 62 is a cysteine in TVB(S1) but is a serine in TVB(S3), giving TVB(S1) an even number of cysteines in the extracellular domain. We present evidence for a disulfide bond requirement in TVB(S1) for ALV-E infection but not for ALV-B infection. Thus, ALV-B and ALV-E interact in fundamentally different ways with this shared receptor, a finding that may account for the observed biological differences between these two ALV subgroups. (+info)Role of the intracellular domain of the human type I interferon receptor 2 chain (IFNAR2c) in interferon signaling. Expression of IFNAR2c truncation mutants in U5A cells. (7/528)
A human cell line (U5A) lacking the type I interferon (IFN) receptor chain 2 (IFNAR2c) was used to determine the role of the IFNAR2c cytoplasmic domain in regulating IFN-dependent STAT activation, interferon-stimulated gene factor 3 (ISGF3) and c-sis-inducible factor (SIF) complex formation, gene expression, and antiproliferative effects. A panel of U5A cells expressing truncation mutants of IFNAR2c on their cell surface were generated for study. Janus kinase (JAK) activation was detected in all mutant cell lines; however, STAT1 and STAT2 activation was observed only in U5A cells expressing full-length IFNAR2c and IFNAR2c truncated at residue 462 (R2.462). IFNAR2c mutants truncated at residues 417 (R2. 417) and 346 (R2.346) or IFNAR2c mutant lacking tyrosine residues in its cytoplasmic domain (R2.Y-F) render the receptor inactive. A similar pattern was observed for IFN-inducible STAT activation, STAT complex formation, and STAT-DNA binding. Consistent with these data, IFN-inducible gene expression was ablated in U5A, R2.Y-F, R2.417, and R2.346 cell lines. The implications are that tyrosine phosphorylation and the 462-417 region of IFNAR2c are independently obligatory for receptor activation. In addition, the distal 53 amino acids of the intracellular domain of IFNAR2c are not required for IFN-receptor mediated STAT activation, ISFG3 or SIF complex formation, induction of gene expression, and inhibition of thymidine incorporation. These data demonstrate for the first time that both tyrosine phosphorylation and a specific domain of IFNAR2c are required in human cells for IFN-dependent coupling of JAK activation to STAT phosphorylation, gene induction, and antiproliferative effects. In addition, human and murine cells appear to require different regions of the cytoplasmic domain of IFNAR2c for regulation of IFN responses. (+info)Transport in bacteriophage P22-infected Salmonella typhimurium. (8/528)
There was rapid efflux of L-leucine, L-phenylalanine, and alpha-methyl-D-glucoside after infection of Salmonella typhimurium with the clear plaque mutant C1 of phage P22. The efflux was similar to that observed with cyanide or arsenate treatment except that there was partial recovery in the case of phage infection and almost complete recovery under the condition of lysogeny. There was no efflux after infection with the temperature-sensitive mutant ts16C1 at nonpermissive temperature. Superinfection of superinfection exclusion negative lysogen (sie A minus sie B minus) with C1 led to efflux, whereas the efflux was much less on superinfection of sie A+ Sie B+ lysogen. These results indicate that an effective injection process is enough to cause depression in the cellular transport processes. (+info)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.
Encephalitis viruses are a group of viruses that can cause encephalitis, which is an inflammation of the brain. Some of the most common encephalitis viruses include:
1. Herpes simplex virus (HSV) type 1 and 2: These viruses are best known for causing cold sores and genital herpes, but they can also cause encephalitis, particularly in newborns and individuals with weakened immune systems.
2. Varicella-zoster virus (VZV): This virus causes chickenpox and shingles, and it can also lead to encephalitis, especially in people who have had chickenpox.
3. Enteroviruses: These viruses are often responsible for summertime meningitis outbreaks and can occasionally cause encephalitis.
4. Arboviruses: These viruses are transmitted through the bites of infected mosquitoes, ticks, or other insects. Examples include West Nile virus, St. Louis encephalitis virus, Eastern equine encephalitis virus, and Western equine encephalitis virus.
5. Rabies virus: This virus is transmitted through the bite of an infected animal and can cause encephalitis in its later stages.
6. Measles virus: Although rare in developed countries due to vaccination, measles can still cause encephalitis as a complication of the infection.
7. Mumps virus: Like measles, mumps is preventable through vaccination, but it can also lead to encephalitis as a rare complication.
8. Cytomegalovirus (CMV): This virus is a member of the herpesvirus family and can cause encephalitis in people with weakened immune systems, such as those with HIV/AIDS or organ transplant recipients.
9. La Crosse virus: This arbovirus is primarily transmitted through the bites of infected eastern treehole mosquitoes and mainly affects children.
10. Powassan virus: Another arbovirus, Powassan virus is transmitted through the bites of infected black-legged ticks (also known as deer ticks) and can cause severe encephalitis.
It's important to note that many of these viruses are preventable through vaccination or by avoiding exposure to infected animals or mosquitoes. If you suspect you may have been exposed to one of these viruses, consult a healthcare professional for proper diagnosis and treatment.
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.
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.
RNA interference (RNAi) is a biological process in which RNA molecules inhibit the expression of specific genes. This process is mediated by small RNA molecules, including microRNAs (miRNAs) and small interfering RNAs (siRNAs), that bind to complementary sequences on messenger RNA (mRNA) molecules, leading to their degradation or translation inhibition.
RNAi plays a crucial role in regulating gene expression and defending against foreign genetic elements, such as viruses and transposons. It has also emerged as an important tool for studying gene function and developing therapeutic strategies for various diseases, including cancer and viral infections.
Labyrinthitis is a medical condition characterized by inflammation of the labyrinth, which is the inner ear's balance- and hearing-sensitive system. It is often caused by an infection, such as a viral or bacterial infection, that spreads to the inner ear. The inflammation can affect the delicate structures of the labyrinth, leading to symptoms such as vertigo (a spinning sensation), dizziness, imbalance, hearing loss, and tinnitus (ringing in the ears). Labyrinthitis can be a serious condition that requires medical attention and treatment.
The inner ear is the innermost part of the ear that contains the sensory organs for hearing and balance. It consists of a complex system of fluid-filled tubes and sacs called the vestibular system, which is responsible for maintaining balance and spatial orientation, and the cochlea, a spiral-shaped organ that converts sound vibrations into electrical signals that are sent to the brain.
The inner ear is located deep within the temporal bone of the skull and is protected by a bony labyrinth. The vestibular system includes the semicircular canals, which detect rotational movements of the head, and the otolith organs (the saccule and utricle), which detect linear acceleration and gravity.
Damage to the inner ear can result in hearing loss, tinnitus (ringing in the ears), vertigo (a spinning sensation), and balance problems.
Embryology is the branch of biology that deals with the formation, growth, and development of an embryo. It is a scientific study that focuses on the structural and functional changes that occur during the development of a fertilized egg or zygote into a mature organism. Embryologists study the various stages of embryonic development, including gametogenesis (the formation of sperm and eggs), fertilization, cleavage, gastrulation, neurulation, and organogenesis. They also investigate the genetic and environmental factors that influence embryonic development and may use this information to understand and prevent birth defects and other developmental abnormalities.
Anatomy is the branch of biology that deals with the study of the structure of organisms and their parts. In medicine, anatomy is the detailed study of the structures of the human body and its organs. It can be divided into several subfields, including:
1. Gross anatomy: Also known as macroscopic anatomy, this is the study of the larger structures of the body, such as the organs and organ systems, using techniques such as dissection and observation.
2. Histology: This is the study of tissues at the microscopic level, including their structure, composition, and function.
3. Embryology: This is the study of the development of the embryo and fetus from conception to birth.
4. Neuroanatomy: This is the study of the structure and organization of the nervous system, including the brain and spinal cord.
5. Comparative anatomy: This is the study of the structures of different species and how they have evolved over time.
Anatomy is a fundamental subject in medical education, as it provides the basis for understanding the function of the human body and the underlying causes of disease.
Labyrinth diseases refer to conditions that affect the inner ear's labyrinth, which is the complex system of fluid-filled channels and sacs responsible for maintaining balance and hearing. These diseases can cause symptoms such as vertigo (a spinning sensation), dizziness, nausea, hearing loss, and tinnitus (ringing in the ears). Examples of labyrinth diseases include Meniere's disease, labyrinthitis, vestibular neuronitis, and benign paroxysmal positional vertigo. Treatment for these conditions varies depending on the specific diagnosis but may include medications, physical therapy, or surgery.
The cochlea is a part of the inner ear that is responsible for hearing. It is a spiral-shaped structure that looks like a snail shell and is filled with fluid. The cochlea contains hair cells, which are specialized sensory cells that convert sound vibrations into electrical signals that are sent to the brain.
The cochlea has three main parts: the vestibular canal, the tympanic canal, and the cochlear duct. Sound waves enter the inner ear and cause the fluid in the cochlea to move, which in turn causes the hair cells to bend. This bending motion stimulates the hair cells to generate electrical signals that are sent to the brain via the auditory nerve.
The brain then interprets these signals as sound, allowing us to hear and understand speech, music, and other sounds in our environment. Damage to the hair cells or other structures in the cochlea can lead to hearing loss or deafness.
The ear is the sensory organ responsible for hearing and maintaining balance. It can be divided into three parts: the outer ear, middle ear, and inner ear. The outer ear consists of the pinna (the visible part of the ear) and the external auditory canal, which directs sound waves toward the eardrum. The middle ear contains three small bones called ossicles that transmit sound vibrations from the eardrum to the inner ear. The inner ear contains the cochlea, a spiral-shaped organ responsible for converting sound vibrations into electrical signals that are sent to the brain, and the vestibular system, which is responsible for maintaining balance.
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