The type species of PARVOVIRUS prevalent in mouse colonies and found as a contaminant of many transplanted tumors or leukemias.
A family of very small DNA viruses containing a single molecule of single-stranded DNA and consisting of two subfamilies: PARVOVIRINAE and DENSOVIRINAE. They infect both vertebrates and invertebrates.
Virus infections caused by the PARVOVIRIDAE.
A genus of the family PARVOVIRIDAE, subfamily PARVOVIRINAE, infecting a variety of vertebrates including humans. Parvoviruses are responsible for a number of important diseases but also can be non-pathogenic in certain hosts. The type species is MINUTE VIRUS OF MICE.
Proteins encoded by a VIRAL GENOME that are produced in the organisms they infect, but not packaged into the VIRUS PARTICLES. Some of these proteins may play roles within the infected cell during VIRUS REPLICATION or act in regulation of virus replication or VIRUS ASSEMBLY.
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 genus in the subfamily PARVOVIRINAE comprising three species: Bovine parvovirus, Canine minute virus, and HUMAN BOCAVIRUS.
Deoxyribonucleic acid that makes up the genetic material of viruses.
The outer protein protective shell of a virus, which protects the viral nucleic acid.
Viruses whose genetic material is RNA.
Established cell cultures that have the potential to propagate indefinitely.
The process by which a DNA molecule is duplicated.
Process of growing viruses in live animals, plants, or cultured cells.
Proteins that form the CAPSID of VIRUSES.
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.
The functional hereditary units of VIRUSES.
The assembly of VIRAL STRUCTURAL PROTEINS and nucleic acid (VIRAL DNA or VIRAL RNA) to form a VIRUS PARTICLE.
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.
Any of the processes by which cytoplasmic factors influence the differential control of gene action in viruses.
Proteins found in any species of virus.
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.
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.
Ribonucleic acid that makes up the genetic material of viruses.
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).
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
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.
Viruses parasitic on plants higher than bacteria.
Viruses whose nucleic acid is DNA.
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.
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.
A species of the genus PARVOVIRUS and a host range variant of FELINE PANLEUKOPENIA VIRUS. It causes a highly infectious fulminating ENTERITIS in dogs producing high mortality. It is distinct from CANINE MINUTE VIRUS, a species in the genus BOCAVIRUS. This virus can also infect cats and mink.

A premature termination codon interferes with the nuclear function of an exon splicing enhancer in an open reading frame-dependent manner. (1/280)

Premature translation termination codon (PTC)-mediated effects on nuclear RNA processing have been shown to be associated with a number of human genetic diseases; however, how these PTCs mediate such effects in the nucleus is unclear. A PTC at nucleotide (nt) 2018 that lies adjacent to the 5' element of a bipartite exon splicing enhancer within the NS2-specific exon of minute virus of mice P4 promoter-generated pre-mRNA caused a decrease in the accumulated levels of P4-generated R2 mRNA relative to P4-generated R1 mRNA, although the total accumulated levels of P4 product remained the same. This effect was seen in nuclear RNA and was independent of RNA stability. The 5' and 3' elements of the bipartite NS2-specific exon enhancer are redundant in function, and when the 2018 PTC was combined with a deletion of the 3' enhancer element, the exon was skipped in the majority of the viral P4-generated product. Such exon skipping in response to a PTC, but not a missense mutation at nt 2018, could be suppressed by frame shift mutations in either exon of NS2 which reopened the NS2 open reading frame, as well as by improvement of the upstream intron 3' splice site. These results suggest that a PTC can interfere with the function of an exon splicing enhancer in an open reading frame-dependent manner and that the PTC is recognized in the nucleus.  (+info)

Activation of promoter P4 of the autonomous parvovirus minute virus of mice at early S phase is required for productive infection. (2/280)

Autonomous parvoviruses are tightly dependent on host cell factors for various steps of their life cycle. In particular, DNA replication and gene expression of the prototype strain of the minute virus of mice (MVMp) are closely linked to the onset of host cell DNA replication, pointing to the involvement of an S-phase-specific cellular factor(s) in parvovirus multiplication. The viral nonstructural protein NS-1 is absolutely required for parvovirus DNA replication and is able to transcriptionally regulate parvoviral and heterologous promoters. We previously showed that the promoter P4, which directs the transcription unit encoding the NS proteins, is activated at the onset of S phase. This activation is dependent on an E2F motif in the proximal region of promoter P4. An infectious MVM DNA clone was mutated in the E2F motif of P4. The wild type and the E2F mutant derivative were tested for their ability to produce progeny viruses after transfection of permissive cells. In the context of the whole MVMp genome, the E2F mutation abolished P4 induction in S phase and inactivated the infectious molecular clone, which failed to become amplified and generate progeny particles. The virus could be rescued when NS proteins were supplied in trans, showing that P4 hyperactivity in S is needed to reach a level of NS-1 expression that is sufficient to drive the viral replication cycle. These data show that E2F-mediated P4 activation at the early S phase is a limiting factor for parvovirus production. The primary barrier to parvovirus gene expression in G1 is thought to be promoter formation rather than activation, due to the poor conversion of the parental single-strand genome to a duplex form. The S dependence of P4 activation may therefore be a sign of the virus adaptation to life in the S-phase host cell. If the conversion block in G1 were to be leaky, the S induction of promoter P4 could be envisioned as a safeguard against the production of toxic NS proteins until cells reach the S phase and provide the full machinery for parvovirus replication.  (+info)

Inclusion of the NS2-specific exon in minute virus of mice mRNA is facilitated by an intronic splicing enhancer that affects definition of the downstream small intron. (3/280)

Alternative splicing of pre-mRNAs plays a critical role in maximizing the coding capacity of the small parvovirus genome. The small-intron region of minute virus of mice (MVM) pre-mRNAs undergoes an unusual pattern of overlapping alternative splicing, using two donors, D1 and D2, and two acceptors, A1 and A2, within a region of 120 nucleotides, that governs the steady-state ratios of the various viral mRNAs. In a previous report we demonstrated that a complex interaction between both donor and acceptor sequences, as well as the constraints of size, defines the small intron and governs its alternative splicing. We also identified a G-rich intronic splicing enhancer sequence (IES) that appeared to function as both an intron- and an exon-defining element. In this report we further examined the components that govern MVM small-intron splicing. In fully processed wild-type mRNAs, A1 is used preferentially over A2. In this report, we show that in the context of the wild-type small intron the position of the downstream acceptor A2 was preferred, and the primary sequence of A1 must be stronger for it to be utilized at wild-type efficiency. Use of A2 in generation of the minor spliced forms D2/A2 required the IES because of a weak A2 polypyrimidine tract and because of the relative strength of A1. The small size of the intron and the relative position of the IES were also shown to play a critical role in donor and acceptor site selection. Finally, we have further characterized how the IES functions as an intronic enhancer of upstream exon definition. When the small intron was expanded, upstream exon inclusion was dependent upon the position of the IES. Within the context of the small intron, alterations of the small intron that overcame the requirement for the IES for splicing to A2 also permitted wild-type levels of upstream exon inclusion in the absence of the IES, suggesting that, in its natural context, the IES facilitates upstream exon inclusion by affecting small-intron definition.  (+info)

Phosphorylation of the viral nonstructural protein NS1 during MVMp infection of A9 cells. (4/280)

The major nonstructural protein of parvovirus MVMp, NS1, is an 83-kDa nuclear phosphoprotein which exerts a variety of functions during a viral infection. These multiple tasks range from its major involvement in viral DNA amplification and promoter regulation to the cytotoxic action on the host cell. Since these most divergent functions are exerted in an orderly fashion, it has been proposed that NS1 is regulated by posttranslational modifications, in particular phosphorylation. So far it has been shown that the capacity of NS1 for initiation of replication is regulated in vitro by phosphorylation through members of the protein kinase C family, most likely as a result of control of the DNA unwinding activity (J. P. F. Nuesch et al., 1998, J. Virol. 72, 9966-9977). To substantiate these in vitro findings in vivo, we investigated NS1 phosphorylation during an MVMp infection in a natural host cell, A9 fibroblasts, with reference to characteristic features of the virus cycle. The NS1 phosphorylation pattern was found to change throughout the infection, raising the possibility that distinct tasks of NS1 might be achieved through differential phosphorylation of the polypeptide. In addition, we present in vivo evidence that a phosphorylated form of NS1 is able to initiate viral DNA replication and becomes covalently attached to replicated DNA. Moreover, NS1 was found to be phosphorylated in vivo within the helicase domain, showing alignment with at least one phosphopeptide generated by an "activating" kinase in vitro. These data suggest that phosphorylation-mediated regulation of NS1 for replicative functions as observed in vitro may also take place during a natural virus infection.  (+info)

A premature termination codon in either exon of minute virus of mice P4 promoter-generated pre-mRNA can inhibit nuclear splicing of the intervening intron in an open reading frame-dependent manner. (5/280)

How premature translation termination codons (PTCs) mediate effects on nuclear RNA processing is unclear. Here we show that a PTC at nucleotide (nt) 385 in the NS1/2 shared exon of P4-generated pre-mRNAs of the autonomous parvovirus minute virus of mice caused a decrease in the accumulated levels of doubly spliced R2 relative to singly spliced R1, although the total accumulated levels of R1 plus R2 remained the same. The effect of this PTC was evident within nuclear RNA, was mediated by a PTC and not a missense transversion mutation at this position, and could be suppressed by improvement of the large intron splice sites and by mutation of the AUG that initiated translation of R1 and R2. In contrast to the PTC at nt 385, the reading frame-dependent effect of the PTC at nt 2018 depended neither on the initiating AUG nor the normal termination codon for NS2; however, it could be suppressed by a single nucleotide deletion mutation in the upstream NS1/2 common exon that shifted the 2018 PTC out of the NS2 open reading frame. This suggested that there was recognition and communication of reading frame between exons on a pre-mRNA in the nucleus prior to or concomitant with splicing.  (+info)

DNA unwinding functions of minute virus of mice NS1 protein are modulated specifically by the lambda isoform of protein kinase C. (6/280)

The parvovirus minute virus of mice NS1 protein is a multifunctional protein involved in a variety of processes during virus propagation, ranging from viral DNA replication to promoter regulation and cytotoxic action to the host cell. Since NS1 becomes phosphorylated during infection, it was proposed that the different tasks of this protein might be regulated in a coordinated manner by phosphorylation. Indeed, comparing biochemical functions of native NS1 with its dephosphorylated counterpart showed that site-specific nicking of the origin and the helicase and ATPase activities are remarkably reduced upon NS1 dephosphorylation while site-specific affinity of the protein to the origin became enhanced. As a consequence, the dephosphorylated polypeptide is deficient for initiation of DNA replication. By adding fractionated cell extracts to a kinase-free in vitro replication system, the combination of two protein components containing members of the protein kinase C (PKC) family was found to rescue the replication activity of the dephosphorylated NS1 protein upon addition of PKC cofactors. One of these components, termed HA-1, also stimulated NS1 helicase function in response to acidic lipids but not phorbol esters, indicating the involvement of atypical PKC isoforms in the modulation of this NS1 function (J. P. F. Nuesch, S. Dettwiler, R. Corbau, and J. Rommelaere, J. Virol. 72:9966-9977, 1998). The present study led to the identification of atypical PKClambda/iota as the active component of HA-1 responsible for the regulation of NS1 DNA unwinding and replicative functions. Moreover, a target PKClambda phosphorylation site was localized at S473 of NS1. By site-directed mutagenesis, we showed that this residue is essential for NS1 helicase activity but not promoter regulation, suggesting a possible modulation of NS1 functions by PKClambda phosphorylation at residue S473.  (+info)

Nuclear export factor CRM1 interacts with nonstructural proteins NS2 from parvovirus minute virus of mice. (7/280)

The nonstructural NS2 proteins of autonomous parvoviruses are known to act in a host cell-dependent manner and to play a role in viral DNA replication, efficient translation of viral mRNA, and/or encapsidation. Their exact function during the parvovirus life cycle remains, however, still obscure. We report here the characterization of the interaction with the NS2 proteins from the parvovirus minute virus of mice (MVM) and rat as well as mouse homologues of the human CRM1 protein, a member of the importin-beta family recently identified as an essential nuclear export factor. Using the two-hybrid system, we could detect the interaction between the carboxy-terminal region of rat CRM1 and each of the three isoforms of NS2 (P [or major], Y [or minor], and L [or rare]). NS2 proteins were further shown to interact with the full-length CRM1 by coimmunoprecipitation experiments using extracts from both mouse and rat cell lines. Our data show that CRM1 preferentially binds to the nonphosphorylated isoforms of NS2. Moreover, we observed that the treatment of MVM-infected cells with leptomycin B, a drug that specifically inhibits the CRM1-dependent nuclear export pathway, leads to a drastic accumulation of NS2 proteins in the nucleus. Both NS2 interaction with CRM1 and nuclear accumulation upon leptomycin B treatment strongly suggest that these nonstructural viral proteins are actively exported out of the nuclei of infected cells via a CRM1-mediated nuclear export pathway.  (+info)

Screening of protective antigens of Japanese encephalitis virus by DNA immunization: a comparative study with conventional viral vaccines. (8/280)

In this study, we evaluated the relative role of the structural and nonstructural proteins of the Japanese encephalitis virus (JEV) in inducing protective immunities and compared the results with those induced by the inactivated JEV vaccine. Several inbred and outbred mouse strains immunized with a plasmid (pE) encoding the JEV envelope protein elicited a high level of protection against a lethal JEV challenge similar to that achieved by the inactivated vaccine, whereas all the other genes tested, including those encoding the capsid protein and the nonstructural proteins NS1-2A, NS3, and NS5, were ineffective. Moreover, plasmid pE delivered by intramuscular or gene gun injections produced much stronger and longer-lasting JEV envelope-specific antibody responses than immunization of mice with the inactivated JEV vaccine did. Interestingly, intramuscular immunization of plasmid pE generated high-avidity antienvelope antibodies predominated by the immunoglobulin G2a (IgG2a) isotype similar to a sublethal live virus immunization, while gene gun DNA immunization and inactivated JEV vaccination produced antienvelope antibodies of significantly lower avidity accompanied by a higher IgG1-to-IgG2a ratio. Taken together, these results demonstrate that the JEV envelope protein represents the most critical antigen in providing protective immunity.  (+info)

The Minute Virus of Mice (MVM) is a small, single-stranded DNA parvovirus that primarily infects laboratory mice. It was so named because of its extremely small size and the minimal cytopathic effect it causes in infected cells. MVM is not known to cause disease in humans or other animals. However, it has been used as a model system for studying parvovirus biology and pathogenesis due to its ability to efficiently infect and replicate in many types of mammalian cells. There are three strains of MVM (MVMp, MVMi, and MVMc) that vary in their host range and tissue tropism.

Parvoviridae is a family of small, non-enveloped viruses that infect a wide range of hosts, including humans, animals, and birds. These viruses have a single-stranded DNA genome and replicate in the nucleus of infected cells. They are resistant to heat, acid, and organic solvents, making them difficult to inactivate.

The family Parvoviridae is divided into two subfamilies: Parvovirinae and Densovirinae. Parvovirinae infect vertebrates, while Densovirinae infect invertebrates. The subfamily Parvovirinae includes several genera that infect various hosts, such as humans, dogs, cats, and primates.

Parvovirus B19 is a well-known member of this family that causes a variety of clinical manifestations in humans, including fifth disease (slapped cheek syndrome), arthralgia, and occasionally more severe diseases in immunocompromised individuals or those with certain hematological disorders.

In animals, parvoviruses can cause serious diseases such as canine parvovirus infection in dogs and feline panleukopenia in cats, which can be fatal if left untreated.

Parvoviridae infections refer to diseases caused by viruses belonging to the Parvoviridae family. These viruses are known to infect a wide range of hosts, including humans, animals, and insects. The most well-known member of this family is the human parvovirus B19, which is responsible for a variety of clinical manifestations such as:

1. Erythema infectiosum (Fifth disease): A common childhood exanthem characterized by a "slapped cheek" rash and a lace-like rash on the extremities.
2. Transient aplastic crisis: A sudden and temporary halt in red blood cell production, which can lead to severe anemia in individuals with underlying hematologic disorders.
3. Hydrops fetalis: Intrauterine death due to severe anemia caused by parvovirus B19 infection in pregnant women, leading to heart failure and widespread fluid accumulation in the fetus.

Parvoviruses are small, non-enveloped viruses with a single-stranded DNA genome. They primarily infect and replicate within actively dividing cells, making them particularly harmful to rapidly proliferating tissues such as bone marrow and fetal tissues. In addition to parvovirus B19, other Parvoviridae family members can cause significant diseases in animals, including cats, dogs, and livestock.

Parvovirus is a type of virus that is known to cause diseases in various animals, including dogs and humans. The most common strain that infects humans is called Parvovirus B19. This particular strain is responsible for the illness known as Fifth disease, which primarily affects young children and causes symptoms such as fever, rash, and joint pain.

Parvovirus B19 spreads through respiratory droplets, such as when an infected person coughs or sneezes. It can also be transmitted through blood or contaminated objects. Once the virus enters the body, it typically targets and infects rapidly dividing cells, particularly those found in the bone marrow and the fetal heart.

In dogs, a different strain of parvovirus called Canine Parvovirus (CPV) is responsible for a highly contagious and often fatal gastrointestinal illness. CPV primarily affects puppies between 6 weeks and 6 months old, but older dogs can also be infected if they haven't been vaccinated.

It is essential to maintain good hygiene practices and ensure proper vaccination to prevent parvovirus infections in both humans and animals.

Viral nonstructural proteins (NS) are viral proteins that are not part of the virion structure. They play various roles in the viral life cycle, such as replication of the viral genome, transcription, translation regulation, and modulation of the host cell environment to favor virus replication. These proteins are often produced in large quantities during infection and can manipulate or disrupt various cellular pathways to benefit the virus. They may also be involved in evasion of the host's immune response. The specific functions of viral nonstructural proteins vary depending on the type of virus.

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.

Bocavirus is a type of virus that belongs to the Parvoviridae family. It is specifically classified under the genus Bocaparvovirus. This virus is known to infect humans and animals, causing respiratory and gastrointestinal illnesses. In humans, human bocavirus (HBoV) has been identified as a cause of acute respiratory tract infections, particularly in young children. There are four species of HBoV (HBoV1-4), but HBoV1 is the most common and best studied. It can be detected in nasopharyngeal swabs or washes, and it is often found as a co-infection with other respiratory viruses.

The medical definition of Bocavirus refers to this specific virus and its associated illnesses. The name "Bocavirus" comes from the initials of two diseases it causes in cattle: bovine parvovirus (BPV) and bovine rhinitis (BRSV) complex. In addition to humans, Bocaviruses have been identified in various animals, including dogs, cats, pigs, and non-human primates.

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 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.

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 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.

DNA replication is the biological process by which DNA makes an identical copy of itself during cell division. It is a fundamental mechanism that allows genetic information to be passed down from one generation of cells to the next. During DNA replication, each strand of the double helix serves as a template for the synthesis of a new complementary strand. This results in the creation of two identical DNA molecules. The enzymes responsible for DNA replication include helicase, which unwinds the double helix, and polymerase, which adds nucleotides to the growing strands.

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.

Capsid proteins are the structural proteins that make up the capsid, which is the protective shell of a virus. The capsid encloses the viral genome and helps to protect it from degradation and detection by the host's immune system. Capsid proteins are typically arranged in a symmetrical pattern and can self-assemble into the capsid structure when exposed to the viral genome.

The specific arrangement and composition of capsid proteins vary between different types of viruses, and they play important roles in the virus's life cycle, including recognition and binding to host cells, entry into the cell, and release of the viral genome into the host cytoplasm. Capsid proteins can also serve as targets for antiviral therapies and vaccines.

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.

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.

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.

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.

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.

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 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.

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.

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.

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.

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.

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 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.

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.

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.

Canine Parvovirus (CPV) is a small, non-enveloped, single-stranded DNA virus that belongs to the family Parvoviridae and genus Parvovirus. It is highly contagious and can cause severe gastrointestinal illness in dogs, particularly in puppies between 6 weeks and 6 months old.

The virus primarily attacks rapidly dividing cells in the body, such as those found in the intestinal lining, leading to symptoms like vomiting, diarrhea (often bloody), lethargy, loss of appetite, and fever. CPV can also cause damage to the bone marrow, which can result in a decrease in white blood cell counts and make the dog more susceptible to secondary infections.

Canine parvovirus is highly resistant to environmental factors and can survive for long periods of time on surfaces, making it easy to transmit from one dog to another through direct contact with infected dogs or their feces. Fortunately, there are effective vaccines available to prevent CPV infection in dogs.

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