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searching for Viral replication 466 found (878 total)

alternate case: viral replication

Birnaviridae (729 words) [view diff] exact match in snippet view article find links to article

concurring. The protein can not be found in the virion.[citation needed] Viral replication is cytoplasmic. Entry into the host cell is achieved by cell receptor

immunity refers to a form of innate immunity that directly restricts viral replication and assembly, thereby rendering a cell non-permissive to a specific

(Vif, Vpx, Vpr, Vpu, and Nef) carried by lentiviruses that enhances viral replication by inhibiting host antiviral factors. Vpx enhances HIV-2 replication

HIV/AIDS, hepatitis C and COVID-19. These protease inhibitors prevent viral replication by selectively binding to viral proteases (e.g. HIV-1 protease) and

sensitive test need to be performed. B-type inclusions are the sites of viral replication and are found in all poxvirus-infected cells, unlike A-type inclusions

cytoplasm of epithelial cells in humans. They are important as sites of viral replication. Morphologically there are two types of Orthopoxvirus inclusion bodies

involved in a viral replication signal which is highly conserved in citrus tristeza viruses. Replication signals are required for viral replication and are

therapeutic drugs, including a range of antiviral products used to prevent viral replication in infected cells. The most commonly used is acyclovir. Nucleotide

can act as an initial response to pathogen invasion, slowing down viral replication and increasing expression of immune signaling complexes. There are

acting as an RNA polymerase inhibitor and thereby interfering with viral replication. Bemnifosbuvir has been researched for the treatment of coronavirus

alveolar cells. Studies have linked LAMP3 with the inhibition of the viral replication of Influenza A cells. LAMP3 is a Type I integral membrane protein

X-box binding protein 1, also known as XBP1, is a protein which in humans is encoded by the XBP1 gene. The XBP1 gene is located on chromosome 22 while

Dynein and kinesin can both be exploited by viruses to mediate the viral replication process. Many viruses use the microtubule transport system to transport

abrogate the helicase activity of LTag, which is required for normal viral replication. In MCPyV, STag, rather than LTag, is the primary oncoprotein, is

25,000 base pairs long and organised into twelve segments. All the viral replication occurs in the cytoplasm. The virus is 22% RNA by weight, the other

Proton conductance by the M2 protein in influenza A is essential for viral replication. Influenza B and C viruses encode proteins with similar function dubbed

kDa) is a membrane protein which is required for viral replication and accumulates in viral replication vesicles. It mediates the interactions between replication

in a protein coding region. The element is essential for efficient viral replication and it has been suggested that the CRE is required for initiation

survive for long periods of time, sometimes greater than ten years. Viral replication is almost exclusively associated with macrophages in infected tissues;

agents given to reduce viral replication, AV-HALTs are single or combination drugs designed to reduce the rate of viral replication while, at the same time

(Alpharetroviruses and Avian type C retroviruses). dr1 is required for efficient viral replication and is thought to be involved in genomic RNA packaging although this

for minus strand RNA accumulation and is essential for efficient viral replication. Poxvirus AX element late mRNA cis-regulatory element Pillai-Nair

that both AUGs and the conserved cHP are necessary for efficient viral replication in human and mosquito cells. Clyde K, Harris E (2006). "RNA Secondary

inhibitor of the viral enzyme RNA polymerase, which is essential for viral replication. In tests on mice, JK-05 was claimed to show efficacy against a range

All stem loop structures are thought to be important for efficient viral replication and deletion of stem loop three is known to be lethal. Togavirus 5′

with a pseudoknot. Disruption of any of these elements impairs both viral replication and growth. Human rhinovirus internal cis-acting regulatory element

Cafeteria roenbergensis virus (CroV) is a giant virus that infects the marine bicosoecid flagellate Cafeteria roenbergensis, a member of the microzooplankton

intracellular parasites require factors in the host cell to support viral replication and release of progeny virions. Specifically, the host factors include

been added, VPg is able to prime the initiation of viral replication. Cres also affect viral replication through RNA-RNA interactions, specifically interactions

progeny viruses. This process is called packaging and is vital for viral replication. The packaging signal is found in the positive-sense single-stranded

polyprotein into individual proteins that will help continue the viral replication process. As soon as viral proteins have been translated and cleaved

T=31 symmetry. The diameter is around 74 nm. Genomes are circular. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

inhibitor of the viral enzyme RNA polymerase which is essential for viral replication, and in animal studies showed good oral bioavailability and protected

briefly within the first site of infection, within the muscle tissues. Viral replication then leads to viremia and the virus spreads to its secondary site

affected viral replication. In contrast, Zahler et al. found that over expression of hnRNP A1 in vitro adversely affected viral replication. As a result

interactions of proteins and RNAs involved in protein synthesis and viral replication, especially in HIV. Musier-Forsyth was born in 1962 in Dover, NJ to

diameter is around 40 nm. Genomes are linear, around 5.6kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

with viruses or bacteria. Granzymes also kill bacteria and inhibit viral replication. In NK cells and T cells, granzymes are packaged in cytotoxic granules

a group of atropisomeric alkaloid which have been found to be HIV viral replication inhibitors in vitro. It was discovered in the leaves of Ancistrocladus

are linear and non-segmented, bipartite, around 6.5kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

genome codes for two proteins, and has three open reading frames. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

cytoplasm of the fungi host and forms a naked ribonucleoprotein complex. Viral replication is cytoplasmic. Replication follows the positive-strand RNA virus

modifying enzymes. In addition, cccDNA can serve as a template for viral replication and DNA transcription for five viral RNAs which allows for the production

around 6.5–9kb in length. The genome codes for 2 to 6 proteins. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

around 5.4-9kb in length. The genome codes for 1 to 6 proteins. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

RNase L, which results in viral RNA degradation and the inhibition of viral replication. The three known members of this gene family are located in a cluster

34 nm. Genomes are linear and non-segmented, around 4.4kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

pathogen within an infected cell for critical viral replication resources, reducing the viral replication rate and resulting in reduced pathogenesis. But

infection causes disease. Viral disease is the sum of the effects of viral replication on the host and the host's subsequent immune response against the

in both viral and endogenous RNA degradation and the inhibition of viral replication. The three known members of this gene family are located in a cluster

in a viral genome that are expressed at the same time during the viral replication cycle. Five of the human DNA viral families have multiple kinetic

linear, around 6.8kb in length. The genome has 2 open reading frames. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

Genomes are linear dsDNA and non-segmented, around 20–30kb in length. Viral replication is cytoplasmic. DNA-templated transcription is the method of transcription

Self-complementary adeno-associated virus (scAAV) is a viral vector engineered from the naturally occurring adeno-associated virus (AAV) to be used as

is around 26-35 nm. Genomes are linear and segmented, tripartite. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

and annotated in 1997, and the necessity of most of its genes in viral replication was characterized by random transposon mutagenesis. Alpha-, beta-

round geometries, and T=1 symmetry. The diameter is around 18–19 nm. Viral replication is nuclear. Entry into the host cell is achieved by penetration into

nucleus. Little is understood as to how the polymerase assists in both viral replication and transcription and how these processes can be regulated. The encoded

helicase proteins. These inclusion bodies are thought to be sites of viral replication and assembly, making then an important factor in the viral lifecycle

polymerase. Some totiviruses contain a third small potential ORF. Viral replication is cytoplasmic. Replication follows the double-stranded RNA virus

endothelial cells, primary fibroblasts, and monocyte-derived macrophages. Viral replication is highly cytopathic, but susceptible to type-I and -II interferon

Black beetle virus (BBV) is a virus that was initially discovered in the North Island of New Zealand in Helensville in dead New Zealand black beetles (Heteronychus

Genomes are linear and non-segmented, bipartite, around 20kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

single capsid protein (ORF4) is translated from a subgenomic RNA. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

host exhibiting many symptoms. Once the warmer months roll around, viral replication rates dramatically lower to the point of little to no replication

They are propagated during cell division and hyphal anastomosis. Viral replication occurs in the cytoplasm. It follows the double-stranded RNA virus

to the 5' UTR lies the cHP structure, which is essential for the viral replication. The first structural element is termed 5'SLA and comprises three

replication and infectivity. The precore region is not necessary for viral replication. Precore mutants can replicate. They are readily detectable by HBV

human immunodeficiency virus (HIV)-host interactions that govern viral replication and persistence. Cohen graduated from Collège Jean-de-Brébeuf of Montréal

genome encodes 5 proteins. From left to right these proteins are: the viral replication protein that consists of a capping enzyme domain, a helicase-like

including the coronavirus SARS-CoV-2. It has been shown to inhibit viral replication in silico and in vitro. 3CLpro-1 Ebselen GC376 Shanker AK, Bhanu D

species. The genome is relatively cytosine rich.[citation needed] Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

the putative nucleocapsid protein and RNA-dependent RNA polymerase. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

to be an important cellular factor for HIV-1 gene expression and viral replication. It also associates transiently with U6 and U4/U6 snRNPs during the

the virus in a selective manner from the host cytoplasmic membrane. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

Rio Negro virus is an alphavirus that was first isolated in Argentina in 1980. The virus was first called Ag80-663 but was renamed to Rio Negro virus in

very important to viral replication. This enzyme shuts off protein synthesis in the host, degrades host mRNA, helps in viral replication, and regulates gene

cytoplasm of the fungi host and forms a naked ribonucleoprotein complex. Viral replication is cytoplasmic. Replication follows the positive-strand RNA virus

85–390 nm. Genomes are linear and segmented, around 6.7kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

currently 59 species in this family, divided among seven genera. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

of a total length of 16.1 kbp. The genome codes for four proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

been associated with some pleomorphic cytoplasmic membrane vesicles. Viral replication is cytoplasmic. The viral replicative form of the Endornaviridae is

able to replicate and spread to multiple organs within the host. Viral replication causes an increase in vascular permeability, which leads to the lesions

the virus and the ants allows the ants to serve as a reservoir for viral replication to occur. Chronic bee paralysis virus is also similar to slow bee

The carrot yellow-leaf virus (CYLV) infects carrots, particularly the carrot root cells. There are viruses that are similar to CYLV which affect hogweed

pleomorphic, enveloped and about 80 nm (range 50–125 nm) in diameter. Viral replication is cytoplasmic. DNA-templated transcription is the method of transcription

kDa γ protein, at a conserved Asn/Ala site during virus assembly. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

reading frames that encode for at least six structural proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by virus attaches

NS2B, NS3, NS4A, NS4B, and NS5. These proteins mainly assist with viral replication or act as proteases. The nonstructural proteins are located near the

Alternative start codons are common in the avian species.[citation needed] Viral replication is nuclear. Entry into the host cell is achieved by penetration into

host factors involved in RNA processing could potentially impede viral replication. Aberrations in splicing processes may lead to abnormal protein production

Genomes are linear and non-segmented, around 8.8-9.7kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

(Q04350) cleaves into a p48 C8 protease and the RNA replicase–helicase. Viral replication is cytoplasmic. Replication follows the double-stranded RNA virus

Georgian and viricetes is an official suffix for a virus class). Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

diagnostic tool is limited by the amount of the virus present in the CSF. Viral replication tends to peak early and then decline to undetectable levels in CNS

diameter is around 150-200 nm. Genomes are linear and non-segmented. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

families Fuselloviridae, Thaspiviridae, Halspiviridae and Clavaviridae. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

3'-N-P-M-G-NV-L-5'. Viral replication occurs at both 15 °C and 28 °C in cell line derived from snakehead and carp, although the optimal temperature range for viral replication

carry high quantities of a protein called APOBEC3G that disrupts viral replication in cells. APOBEC3G, or "A3" for short, is a protein that sabotages

150-200 nm. Genomes are linear and non-segmented, around 134kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

diameter is around 150-200 nm. Genomes are linear and non-segmented. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

150-200 nm. Genomes are linear and non-segmented, around 180kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

Banerjea AC (2015). "HIV-1 Rev downregulates Tat expression and viral replication via modulation of NAD(P)H:quinine oxidoreductase 1 (NQO1)". Nat. Commun

further 15% by weight. Carbohydrates are not present.[citation needed] Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

Genomes are linear and non-segmented, around 220-231kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

Bigot Y (2009). "Ascoviruses: Superb Manipulators of Apoptosis for Viral Replication and Transmission". Lesser Known Large dsDNA Viruses. Current Topics

circular, around 3.2kb in length. The genome codes for 7 proteins. Viral replication is nucleo-cytoplasmic. Replication follows the dsDNA(RT) replication

clustered together. Genome replication is bidirectional.[citation needed] Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

are circular and non-segmented. The genome codes for 5 proteins. Viral replication is nuclear/cytoplasmic. Replication follows the dsDNA (RT) replication

around 50 nm. Genomes are circular. The genome codes for 8 proteins. Viral replication is nuclear/cytoplasmic. Replication follows the dsDNA(RT) replication

Genomes are linear and segmented, bipartite, around 24-7kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

Genomes are linear and segmented, bipartite, around 24-7kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

non-segmented, around 7.7kb in length. The genome has 3 open reading frames. Viral replication is nuclear/cytoplasmic. Replication follows the dsDNA(RT) replication

"Temperature-dependent innate defense against the common cold virus limits viral replication at warm temperature in mouse airway cells", investigates the relationship

150-200 nm. Genomes are linear and unsegmented, around 152kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

120-200 nm. Genomes are linear and non-segmented, around 150kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

GM-CSF gene and deletion of the thymidine kinase gene which limits viral replication to cells with high levels of thymidine kinase, typically seen in cancer

which are encoded by retroviruses such as HIV and are required for viral replication. In eukaryotes, ribonuclease H1 is involved in DNA replication of

non-segmented, around 35-36kb in length. The genome codes for 40 proteins. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

150-200 nm. Genomes are linear and non-segmented, around 134kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

Genomes are linear and non-segmented, around 134-248kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

transcription. Introduction of nucleus localized HBx protein seams to restore viral replication to cells infected by HBx-deficient virus. In a study purifying cancerous

circular, around 3.2kb in length. The genome codes for 7 proteins. Viral replication is nucleo-cytoplasmic. Replication follows the dsDNA(RT) replication

achieved by penetration into the host cell. Once in the host cell, viral replication is cytoplasmic. Replication follows the double-stranded RNA virus

encapsidated together. RNA-1 and RNA-2 are thought to be involved in viral replication while RNA-3 has a role in the spread of infection throughout the plant

ITPase or HAM1) are protein domains identified in atypical members. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

be directly translated into viral proteins (e.g., those needed for viral replication). Therefore, in positive-sense RNA viruses, the viral RNA genome can

double stranded DNA. Like most giant viruses, Pandoraviruses have a viral replication cycle. They lack the ability to make their own proteins, rely on the

the virion measures 28–35 nm in diameter, and it is not enveloped. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

reverse transcriptase for viral cDNA synthesis and thus prevents viral replication. SAMHD1 has also shown nuclease activity. Although a ribonuclease

the bacteria by adsorption on its pilus and then membrane fusion. Viral replication is cytoplasmic. Replication follows the double-stranded RNA virus

150-200 nm. Genomes are linear and non-segmented, around 180kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

150-200 nm. Genomes are linear and non-segmented, around 230kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

cellular and viral proteases into the 10 smaller proteins that allow viral replication within the host cell, or assemble into the mature viral particles

kbp in length, while the total genome length is around 3.0–4.8 kbp. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

indicating active viral replication, suggest MWPyV prevalence in the range of 1-10% of children, with low or no detection of active viral replication in adults

linked with cholesterol control, cancer development and inhibition of viral replication. Its function relies on introducing a stop codon into apolipoprotein

non-coding RNA found in the hepatitis delta virus that is necessary for viral replication. Hepatitis delta virus is the only known human virus that utilizes

150-200 nm. Genomes are linear and non-segmented, around 180kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

diameter is around 200 nm. Genomes are linear, around 145kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

lentiviral Vif. Vif1 is a 23-kilodalton protein that is essential for viral replication. Vif1 inhibits the cellular protein APOBEC3G from entering the virion

packaged in capsid proteins. They are around 2.0–31kb in length. Viral replication is nuclear. DNA-templated transcription is the method of transcription

of the capsid shell. It is a double-stranded enveloped DNA virus Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

Badnaviruses and Tungroviruses have bacilliform virus particles. Viral replication is nuclear/cytoplasmic. Entry into the host cell is achieved by attachment

inhibitor, targeting the RSV-F protein on the viral surface to prevent viral replication. Sisunatovir has been granted Fast Track designation by the U.S. Food

The genome is linear and non-segmented, around 134kb in length. Viral replication is nuclear, and is lysogenic. DNA templated transcription is the method

diameter is around 29 nm. Genomes are linear and have three segments. Viral replication is cytoplasmic and lysogenic. Entry into the host cell is achieved

The genome is linear and non-segmented, around 212kb in length. Viral replication is nuclear. DNA-templated transcription is the method of transcription

across the M2 channel. Rimantadine is believed to inhibit influenza's viral replication, possibly by preventing the uncoating of the virus's protective shells

drug-resistant mutants in untreated patients, the impact of disease stage and viral replication on the rates of viral evolution, and the independent evolution of

150-200 nm. Genomes are linear and non-segmented, around 200kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

initiated by the virus encoded endonuclease P12.[citation needed] Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

the virion superhelix. Genomes are linear, up to 40 kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

Genomes are linear and segmented, bipartite, around 24-7kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

Caulimoviruses are para-retroviruses with a DNA genome; thus, part of their viral replication takes place in the nucleus, where the host replication machinery is

non-segmented, around 30kb in length. The genome codes for 30 proteins. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

diameter is around 29 nm. Genomes are linear and segmented, tripartite. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

such as replication protein A and Nbs1. The OBD is required for viral replication. The zinc-binding and ATPase domains together comprise the helicase

Genomes are linear and non-segmented, around 140-240kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

Other parvoviruses replicate only when the host cell is in S phase: viral replication results in the death of the host cell. This pattern has not yet been

Genomes are linear and segmented, bipartite, around 24-7kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

(2015), who gave average dimensions of 92 x 40 nm with a 12 nm tail. Viral replication is cytoplasmic. Entry into the host cell is achieved by virus attachment

transports them into the cell before they can uncoat. This stage of viral replication can be inhibited in two ways: Using agents which mimic the virus-associated

guanine/cytosine content is usually around 52%.[citation needed] Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

immune-phenotype of prolonged lung-specific viral replication was described debunking the notion that viral replication ended after the first week of symptoms

the research suggest previously undocumented cases of infection and viral replication followed by an abortive infection. This could indicate that people

linear, around 33kb in length. The genome codes for 45 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

linear, around 7.5-8.0kb in length. The genome codes for 3 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

non-segmented, around 35-36kb in length. The genome codes for 40 proteins. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

non-segmented, around 35-36kb in length. The genome codes for 25 proteins. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

proteins are imported to the nucleus to further increase the rate of viral replication and form RNPs. HA, NA, and M2 proteins are trafficked with the aid

(fibrosis) is often evident in surviving dogs. Myofibers are the site of viral replication within cells. The disease may or may not be accompanied with the signs

genomes with a terminal protein covalently attached to each end. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

Increases in gp120 variability result in significantly elevated levels of viral replication, indicating an increase in viral fitness in individuals infected by

Recombinant Snakehead Rhabdovirus: the NV Protein Is Not Required for Viral Replication". Journal of Virology. 74 (5): 2343–50. doi:10.1128/JVI.74.5.2343-2350

which is flanked by repetitive DNA sequences called terminal repeats. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

caliciviruses remain unclassified, including the chicken calicivirus. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

minute virus NP1 has been shown to be essential for an early step in viral replication and is also required for the read through of an internal polyadenylation

individually encapsidated forming small icosahedral virions (18–20 nm). Viral replication is nuclear. Entry into the host cell is achieved by penetration into

centrally located DNA binding domain. The Bet protein is required for viral replication, as it counteracts the innate antiretroviral activity of APOBEC3 family

criss-cross pattern. Genomes are linear, around 130–150kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

200-300 nm. Genomes are linear and bipartite, around 23.5-3.8kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

virus genome is incorporated as prophage and a repressor prevents viral replication. Nonetheless, a temperate phage can escape repression to replicate

utilize alkanes as a carbon source. AlkB domains are present within viral replication-associated proteins of plant RNA viruses of the families Closteroviridae

wide and 90-900 nm long. Genomes are circular and non-segmented. Viral replication is nuclear/cytoplasmic. Entry into the host cell is achieved by attachment

Because NS5A exerts functionally essential effects in regulation of viral replication, assembly and egress, it has been considered a potential drug target

trunk for Elephants) on its host - often leading to death afterwards. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

linear, around 6277kb in length. The genome has 2 open reading frames. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

localized to the viral replication compartments and that some of these inhibit viral replication while some are essential for viral replication. He discovered

Chk2-mediated response. It is not known if viral proteins or active viral replication activate the DDR, but UV-inactivated MVM does not induce a response

diameter is around 18-26 nm. Genomes are linear, around 6kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment to

(Mpro) protein of the SARS-CoV-2 virus, a crucial enzyme required for viral replication, potentially offering another therapeutic avenue against COVID-19

(Mpro) protein of the SARS-CoV-2 virus, a crucial enzyme required for viral replication, potentially offering another therapeutic avenue against COVID-19

conserved across the family and may be useful for phylogenetic analysis. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

genome. This gene is transcribed and is an essential gene involved in viral replication. Porcine circovirus is a replicating entity with one of the smallest

fact that IL-21 stimulated CD8 or NK cells are able to inhibit HIV viral replication in vitro, show that this cytokine could potentially be useful for

able to replicate. A virus may only replicate in a permissive cell. Viral replication will therefore occur in a susceptible cell which is also a permissive

brick-shaped geometries. Genomes are linear, around 154 kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

linear, around 7.6kb in length. The genome codes for 5 proteins. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

Genomes are circular and non-segmented, around 3.0kb in length. Viral replication is nuclear. Entry into the host cell is achieved by penetration into

linear, monopartite or bipartite, and around 9.3-10.0kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

treatment of chronic hepatitis B in adults with evidence of active viral replication and either evidence of persistent elevations in serum aminotransferases

diameter is around 30 nm. Genomes are linear, around 6.3kb in length. Viral replication is cytoplasmic and lysogenic. Entry into the host cell is achieved

Genomes are circular and non-segmented, around 3.0kb in length. Viral replication is nuclear. Entry into the host cell is achieved by penetration into

long. Cytorhabdovirus genomes are linear and around 13 kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

Genomes are linear and segmented, bipartite, around 23.9kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

120–200 nm. Genomes are linear and non-segmented, around 175kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved

Genomes are circular and non-segmented, around 3.0kb in length. Viral replication is nuclear. Entry into the host cell is achieved by penetration into

functions as the RNA-dependent RNA polymerase. NS1 is important in the viral replication process. NS2A interacts with NS3 and NS5, helps in viral assembly

are linear, around 7kb in length. The genome codes for 5 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

diameter is around 26 nm. Genomes are linear and segmented, tripartite. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

significantly increased survival rates, inhibited weight loss, and suppressed viral replication in aged mice. A retrospective study conducted between November 2022

30 nm. Genomes are linear and nonsegmented, around 6.7 kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

800 nm. Genomes are linear and non-segmented, around 11kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

brick-shaped geometries. Genomes are linear, around 160kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

around 120-150 nm. Genomes are linear, around 150-350kb in length. Viral replication is nucleo-cytoplasmic, and is lysogenic. Replication follows the DNA

leaves. On the other hand, the 'M' strain produces only mottling. Viral replication is nuclear/cytoplasmic. Replication follows the dsDNA(RT) replication

30 nm. Genomes are linear and non-segmented, around 7.5kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

around 15–16 kb in length. The genome codes for eight proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by virus attaching

The genome codes for 4 proteins, and has 3 open reading frames. Viral replication is nuclear. Entry into the host cell is achieved by penetration into

Genomes are linear and non-segmented, around 6.8-7kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

permitting viral entry. Availability of transcription factors involved in viral replication. The molecular nature of the viral tropogen or virus surface, such

Genomes are linear and non-segmented, around 6.8-7kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

260-300 nm. Genomes are linear and segmented, around 3.5-3.6kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

around 80-180kb in length. The genome codes for 100 to 180 proteins. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

30 nm. Genomes are linear and non-segmented, around 9kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

diameter is around 30 nm. Genomes are linear, around 4.4kb in length. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

is around 100-220 nm. Genomes are linear, around 295kb in length. Viral replication is nucleo-cytoplasmic. Replication follows the DNA strand displacement

vein enation virus Grapevine enamovirus 1 Pea enation mosaic virus 1 Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

around 15.3.2-3.5kb in length. The genome codes for 5 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

84.5kb in total length (8600–11300 nucleotides for each length). Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

diameter is around 60 nm. Genomes are linear, around 40-42kb in length. Viral replication is cytoplasmic. DNA templated transcription is the method of transcription

there is limited viral replication in the nasal cavity in the first 24 hours after infection, followed by later viral replication in other tissues. The

segments, around 2.7-3.4kb in length. The genome codes for 6 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

circular, around 82-86kb in length. The genome codes for 90 proteins. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

linear, around 17.9kb in length. The genome codes for 13 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

diameter is around 30 nm. Genomes are circular, around 6.1kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by pilus-mediated

84.5kb in total length (8600–11300 nucleotides for each length). Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

around 170-245kb in length. The genome codes for 300 to 415 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

diameter is around 60 nm. Genomes are circular, around 8kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

diameter is around 28-34 nm. Genomes are linear, around 4.1kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

circular, around 2.1kb in length. The genome has 2 open reading frames. Viral replication is nuclear. Entry into the host cell is achieved by penetration into

diameter is around 30 nm. Genomes are linear, around 8.4kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

around 80-180kb in length. The genome codes for 100 to 180 proteins. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

kbp. The genome has eleven segments and codes for twelve proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

Genomes are circular and non-segmented, around 3.0kb in length. Viral replication is nuclear. Entry into the host cell is achieved by penetration into

Demonstrates that Rotavirus Nonstructural Protein NSP6 Is Not Essential for Viral Replication in Cell Culture". Journal of Virology. 91 (21): e00695-17. doi:10

Genomes are linear and segmented, tripartite, around 123kb in length. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

is around 28-34 nm. Genomes are linear, around 4-5.4kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

supports viral replication. HDAg-L, in contrast, is produced during the later stages of an infection, acts as an inhibitor of viral replication, and is

diameter is around 30 nm. Genomes are circular, around 4.5kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by pilus-mediated

linear, around 11.2 kb in length. The genome codes for 7 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

segmented, around 15.8kb in length. The genome codes for 11 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

around 124kb in length. The genome has 108 open reading frames. Viral replication is nuclear. DNA-templated transcription is the method of transcription

lysis – selective viral replication in permissive cancer cells leading to tumor cell lysis; Innate immune response – viral replication resulting in a cascade

indicative of lysogeny. Genomes are linear, around 45kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

circular, around 8kb in length. The genome has 7 open reading frames. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

a regular surface structure and are composed of 17% nucleic acid. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

diameter is around 34 nm. Genomes are linear, around 4kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

circular, around 8kb in length. The genome has 7 open reading frames. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

RNA-dependent RNA polymerase located at the 5' end of the genome. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

Inhibits Autophagic Flux via Disruption of the SNARE Complex to Enhance Viral Replication". Cell Reports. 22 (12): 3292–3303. doi:10.1016/j.celrep.2018.02.090

are linear, around 15kb in length. The genome codes for 8 proteins. Viral replication is cytoplasmic. Entry into the host cells is achieved after viral

around 28 nm in diameter. Genomes are linear, around 4kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

Genomes are linear and non-segmented, around 7.5-8.3kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

30 nm. Genomes are linear and non-segmented, around 7.6kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

30 nm. Genomes are linear and non-segmented, around 7.3kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

linear, around 6.5kb in length. The genome codes for 3 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

the putative nucleocapsid protein and RNA-dependent RNA polymerase. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

Genomes are linear and segmented, bipartite, around 21.4kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

around 9kb in length. The genome has three open reading frames. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

25-30 nm. Genomes are linear and non-segmented, around 9kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

diameter is around 30 nm. Genomes are circular, around 6.1kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by pilus-mediated

28 nm. Genomes are linear and non-segmented, around 7.5kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

35 nm. Genomes are linear and non-segmented, around 8.3kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

around 100-170 nm. Genomes are linear, around 120-485kb in length. Viral replication is nucleo-cytoplasmic. Replication follows the DNA strand displacement

circular, around 100kb in length. The genome codes for 100 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

diameter is around 18-26 nm. Genomes are linear, around 6kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment to

around 190kb in length. The genome has 160 open reading frames. Viral replication is nuclear. DNA-templated transcription is the method of transcription

30 nm. Genomes are linear and non-segmented, around 7.7kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

around 130-160kb in length. The genome codes for 190 to 230 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

cell cycle, wherein the DNA polymerases of cell origin needed for viral replication are available. If either fetal or adult bovine serum is incorporated

around 190kb in length. The genome has 160 open reading frames. Viral replication is nuclear. DNA-templated transcription is the method of transcription

linear, around 8.7kb in length. The genome has 3 open reading frames. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

cell cycle, wherein the DNA polymerases of cell origin needed for viral replication are available. If either fetal or adult bovine serum is incorporated

hypovirulence or debilitation. Genomes are linear, around 5.5kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

viral infections Antiviral protein, produced by cells to inhibit viral replication and spread Antivirus software, program designed to prevent, detect

the functions of the other proteins are unknown.[citation needed] Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

circular, around 59kb in length. The genome codes for 100 proteins. Viral replication is cytoplasmic. The virus attaches to the host cell using its terminal

30 nm. Genomes are linear and non-segmented, around 9kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

diameter is around 52-55 nm. Genomes are circular, around 8kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

40 nm. Genomes are linear and bipartite, around 2.5kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

linear, around 11.1 kb in length. The genome codes for 5 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

segmented. There are nine segments which code for nine proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

around 8.8-9.5kb in length. The genome has 2 open reading frames. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

diameter is around 30 nm. Genomes are circular, around 6.1 kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by pilus-mediated

52-55 nm. Genomes are circular. The genome has 22 open reading frames. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

around 27–30 kbp in total length. The genome codes for 11 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

capable of modulating cellular signals such that cell proliferation and viral replication occur at the appropriate times in the viral life cycle. "Viral Zone"

clover mottle virus Turnip rosette virus Velvet tobacco mottle virus Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

30 nm. Genomes are linear and non-segmented, around 6-8kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

circular, around 78kb in length. The genome has 7 open reading frames. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

parts weighing about 28 and 33 kDa). The genome codes for 6 proteins. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

circular, around 8kb in length. The genome codes for 6 proteins. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

linear and segmented, tripartite, around 38.43.23.1kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

Genomes are circular and non-segmented, around 2.86kb in length. Viral replication is nuclear. Entry into the host cell is achieved by penetration into

6–14.8 kb in length. The genome codes for five to nine proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

30 nm. Genomes are linear and non-segmented, around 7-8kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

pairs (total size around 26 kb). The genome codes for 12 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

Genomes are linear and non-segmented, around 9.7-10.3kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

one segment is about 7kb and the second segment is 4.6 to 5.4kb. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

are linear, around 15kb in length. The genome codes for 8 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by virus attaches

Holland Cheng; Tatsuo Miyamura (2008). Structure-based Study of Viral Replication: With CD-ROM. World Scientific. pp. 13–. ISBN 978-981-279-085-9. Richard

diameter is around 21-22 nm. Genomes are linear, around 4kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment to

diameter is around 52-55 nm. Genomes are circular, around 8kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

linear, around 32kb in length. The genome codes for 51 proteins. Viral replication is cytoplasmic, and entry into the host cell is achieved by adsorption

linear, around 6.5-7.5kb in length. The genome codes for 3 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

split in two segments RNA1 and RNA2 that together encode three genes. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

proteins E6 and E7 induce the S-phase in the lower epithelial layers. Viral replication proteins E1 and E2 are also required to form the papilloma and keep

is around 25-35 nm. Genomes are linear and segmented, tripartite. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

negative-sense RNA viruses, the genomic RNA alone is not infectious and the viral replication machinery is required to initiate infection within a host cell. Genomic

receptors, which mediates clathrin-mediated endocytosis. The main viral replication process happens in host cytoplasm. Replication follows the positive

linear, around 20kb in length. The genome codes for 40 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

non-segmented, around 8.8kb in length. The genome has 2 open reading frames. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

The genome codes for 6 proteins, and has 6, 8 open reading frames. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

through probably horizontal gene transfer mechanism.[citation needed] Viral replication is nucleo-cytoplasmic. DNA-templated transcription is the method of

diameter is around 21-22 nm. Genomes are linear, around 5kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment to

are linear and non-segmented, bipartite, around 8.0kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

30 nm. Genomes are linear and segmented, around 2.8kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

nucleotides, with 60 proteins. The complete genome is available here Viral replication is cytoplasmic. The virus attaches to the host cell's adhesion receptors

28-34 nm. Genomes are linear and non-segmented, around 4kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

linear, around 8.4-9.3kb in length. The genome codes for 5 proteins. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

through probably horizontal gene transfer mechanism.[citation needed] Viral replication is nucleo-cytoplasmic. DNA-templated transcription is the method of

are linear and non-segmented, bipartite, around 8.0kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

morphogenesis, lysis and integration). Genomes are around 40kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

around 4.6-6.7kb in length. The genome has 2 open reading frames. Viral replication is cytoplasmic. Entry into the host cell is achieved by virus remains

diameter is around 30 nm. Genomes are linear, around 12kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

(March 2007). "A dengue fever viremia model in mice shows reduction in viral replication and suppression of the inflammatory response after treatment with

not alter their infectivity. No lipids have so far been reported. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

COVID-19 drug development is the research process to develop preventative therapeutic prescription drugs that would alleviate the severity of coronavirus

repeats are sometimes referred to as "b sequence" and "c sequence". Viral replication is nuclear and lysogenic. Entry into the host cell is achieved by

geometries. Genomes are circular and segmented, around 6.0-20kb in length. Viral replication is nuclear. DNA-templated transcription is the method of transcription

inhibits the NS3 Helicase protein of the Zika virus, thus reducing viral replication by up to 86%; a FightAIDS@home paper on the discovery of new vulnerabilities

Viruses in Luteovirus also lack polyadenylation at the 3' terminus. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

is around 250 nm. Genomes are linear, around 260-370kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

diameter is around 21-22 nm. Genomes are linear, around 4kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment to

30 nm. Genomes are linear and non-segmented, around 8.5kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

30 nm. Genomes are linear and non-segmented, around 8.5kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

termed the "cytopathic vacuole" (CPV) which can serve as a site for viral replication and possible transcription. The relationship between the CPV and RER

diameter is around 60 nm. Genomes are circular, around 8kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

Infectious Laryngotracheitis Virus during In Vivo Coinfection Parallels Viral Replication and Arises from Recombination Hot Spots within the Genome". Applied

the action of virus-derived proteins on the cell membrane. During viral replication in T lymphoid cells, large amounts of viral envelope Glycoprotein

has a terminal knob. Psimunavirus is currently unlisted by NCBI. Viral replication is cytoplasmic. The virus attaches to the host cell's adhesion receptors

which is involved in packaging, morphogenesis, lysis and integration. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

circular, around 7kb in length. The genome has 6 open reading frames. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

diameter is around 52-55 nm. Genomes are circular, around 8kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

is around 230 nm. Genomes are linear, around 250-380kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

diameter is around 60 nm. Genomes are circular, around 8kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

diameter is around 28 nm. Genomes are linear, around 4kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

segmented, around 2.7-3kb in length. The genome codes for 5 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

dephosphorylation by a herpes simplex virus protein and inhibits viral replication. eIF2α phosphorylation is cytoprotective during endoplasmic reticulum

diameter is around 60 nm. Genomes are circular, around 8kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

linear, around 16-17kb in length. The genome codes for 10 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

to abnormal T-cell and B-Cell function that decreases control of viral replication and host defense. Anti-viral therapeutic drugs which also reduce inflammation

All have extended highly conserved terminal sequences at both ends. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

linear and around 15 kb in length. The genome codes for 8 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by virus attaches

genomes for dozens of other similar, unclassified virus strains. Viral replication is cytoplasmic. The virus attaches to the host cell using its terminal

Not all the cases reach this stage, depending on the efficiency of viral replication at the different stages and the degree of virus spread. The California

30 nm. Genomes are linear and non-segmented, around 8kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

yellow leaf virus Tobacco vein distorting virus Turnip yellows virus Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

diameter is around 52-55 nm. Genomes are circular, around 7kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

brick-shaped geometries. Genomes are linear, around 175 kilobases in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

well as several similar unclassified strains are available from [1] Viral replication is cytoplasmic. The virus attaches to the host cell using its terminal

chromosome in a process called prophage induction. After induction, viral replication begins via the lytic cycle. In the lytic cycle, the virus commandeers

around 4.6-4.9kb in length. The genome has 2 open reading frames. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

complete genome for Vibrio phage VH7D, an unclassified virus strain. Viral replication is cytoplasmic. The virus attaches to the host cell using its terminal

Orf3a induced high mobility group box 1 (HMGB1) release and inhibits viral replication: An active ingredient Glycyrrhizin in Mulethi (liquorice)—a commonly

linear, around 135kb in length. The genome codes for 126 proteins. Viral replication is nucleo-cytoplasmic. Entry into the host cell is achieved by attachment

double-stranded DNA genome occurs at the host cell nucleus within specialized viral replication compartments. Nearly 75% of the genes encoded by HCMV strain AD169

diameter is around 60 nm. Genomes are circular, around 8kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

double-stranded DNA genome occurs at the host cell nucleus within specialized viral replication compartments. Nearly 75% of the genes encoded by HCMV strain AD169

and replicate in red blood cell precursors such as reticulocytes. Viral replication in reticulocytes causes apoptosis (cell death) of affected cells.

linear and segmented, segments are about 5.9 and 4.8kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

BioCryst Pharmaceuticals, Inc. (June 10, 2020). "Galidesivir Stops Zika Viral Replication in Primate Model". GlobeNewswire News Room (Press release). Clinical

geometries, and T=pseudo3 symmetry. The diameter is around 30 nm. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

linear, around 17 kb in length. The genome codes for 9 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

geometries, and T=3 symmetry. Genomes are linear and non-segmented. Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

linear, around 11.1 kb in length. The genome codes for 5 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

°C, however for most isolates, warmer temperature result in faster viral replication. A combination of this optimal growth temperature along with shifts

guanine/cytosine content of 53–59%. The genome codes for 40 proteins. Viral replication is nuclear. Entry into the host cell is achieved by attachment of

with 17 to 35 proteins. The complete genomes are available here Viral replication is cytoplasmic. The virus attaches to the host cell adhesion receptors

sequenced. They have about 41-42k nucleotides, with 53 and 55 proteins. Viral replication is cytoplasmic. The virus attaches to the host cell's adhesion receptors

viral DNA into the host cytoplasm via contraction of its tail sheath. Viral replication is cytoplasmic. DNA-templated transcription is the method of transcription

diameter is around 250 nm. Genomes are linear, around 225kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

The genome codes for 15 proteins and has 4 open reading frames. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

disease. A number of drugs have been investigated to either reduce viral replication or provide neuroprotection in cell lines or studies in mice. None

HAM1) is an atypical protein domain identified in some ipomoviruses. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

around 23 kbp in total length. The genome codes for 12 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

therapy. In studies involving individuals with chronic HIV infection, viral replication also resumes when study subjects are taken off therapy. As with drugs

Genomes are linear and segmented, bipartite, around 23.4kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

are linear, around 9kb in length. The genome codes for 6 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

linear dsDNA genome (with terminal repeats) in the range of 70-75kb. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

withheld. Its active metabolite, cidofovir diphosphate, inhibits viral replication by selectively inhibiting viral DNA polymerases. It also inhibits

Genomes are linear and segmented, bipartite, around 25.4kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

nucleotides, with 185 proteins. The complete genome is available here Viral replication is cytoplasmic. The virus attaches to the host cell's adhesion receptors

proteins, and suggest that this is true for the entire genus.: 388  Viral replication is cytoplasmic, and is lysogenic. Entry into the host cell is achieved

diameter is around 21-22 nm. Genomes are linear, around 6kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment to

and 220-300 nm long. Genomes are linear, around 190kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

viral DNA into the host cytoplasm via contraction of its tail sheath. Viral replication is cytoplasmic. DNA-templated transcription is the method of transcription

linear, around 7.5kb in length. The genome codes for 6 proteins. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

segmented. The three segments are about 6, 3.5, and 3kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

coordinated steps of RNA transcription, processing, and release. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

precise mechanism underlying the switch in polymerase function during viral replication remained unknown. Chandipura virus is transmitted by sandflies, mosquitoes

is around 28-34 nm. Genomes are linear, around 4–5.4kb in length. Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration

lysis – selective viral replication in permissive cancer cells leading to tumor cell lysis; Innate immune response – viral replication resulting in a cascade

and is divided into 12 segments, which are termed Seg-1 to Seg-12. Viral replication in infected cells is associated with characteristic cytoplasmic granular

decreased. EBNA1 binds to sequence-specific sites at the origin of viral replication (oriP) within the viral episome. The oriP has four EBNA1 binding sites

several additional "unclassified" virus genomes, are available at [1] Viral replication is cytoplasmic. The virus attaches to the host cell using its tail

several additional "unclassified" virus genomes, are available here Viral replication is cytoplasmic. The virus attaches to the host cell using its tail

plant cells to reenter the cell cycle from a quiescent state so that viral replication can occur. The only protein encoded in the viral genome that is essential

88 to 127 proteins. The complete genomes are available from here. Viral replication is cytoplasmic. The virus attaches to the host cell using its terminal

Totiviruses can have satellite RNAs encoding a toxin.[citation needed] Viral replication is cytoplasmic. Entry into the host cell is achieved by virus remains

transformation-competent. These two findings gave rise to the notion that viral replication and malignant transformation are separate processes in RSV. Rous was

movement P3 Viral replication function 6K1 Unknown CI Cytoplasmic inclusion protein, RNA helicase activity 6K2 Unknown (involved in viral replication) NIa VPg

then capable of using the residue E. coli proteins to assist with viral replication. Enterobacter virus CC31 has most of the genes responsible for coding

its tail fibers, and ejects the viral DNA into the host periplasm. Viral replication is cytoplasmic. DNA-templated transcription is the method of transcription

inhibits an important viral phosphoprotein, NS5A, which is involved in viral replication, assembly, and secretion. Sofosbuvir, on the other hand, is metabolized

several additional "unclassified" virus genomes, are available at [1] Viral replication is cytoplasmic. The virus attaches to the host cell using its tail

the virus in a selective manner from the host cytoplasmic membrane. Viral replication is cytoplasmic. Entry into the host cell is achieved by adsorption

specifically with the hepatitis B virus X protein, a protein critical to viral replication. In addition, this subunit is involved in regulating hepatitis virus

regulating the switch from mRNA synthesis to antigenome synthesis. Viral replication is cytoplasmic. Entry into the host cell is achieved by viral attachment

ability of tumor cells to fight off viruses make them advantageous for viral replication compared to non-tumorous cells. The replication of viruses in tumor

the genus Phikmvvirus is classified within the Autographiviridae. Viral replication is cytoplasmic. Entry into the host cell is achieved by absorption

diameter is around 18-26 nm. Genomes are linear, around 6kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment to

made from four capsid proteins encoded by the virus. Picornavirus viral replication typically takes place in the cytoplasm of the cell. Picornavirus +ssRNA

"A cellular homolog of hepatitis delta antigen: implications for viral replication and evolution". Science. 274 (5284): 90–4. Bibcode:1996Sci...274.

proteins, Drosha and Dicer, which leads to a significant enhancement of viral replication in PBMCs from HIV-1-infected patients. Thus, Drosha, in conjunction

several additional "unclassified" virus genomes, are available here Viral replication is cytoplasmic. The virus attaches to the host cell adhesion receptors

suggests that viral mRNA synthesis and crucial steps that occur during viral replication are not necessary for induction of apoptosis in infected cells. Disregarding

follow-up report in NEJM concludes "a likely explanation for control of viral replication in this patient is genetic background, regardless of intervention

geometries, and T=169 symmetry. The diameter is around 104-118 nm. Viral replication is nucleo-cytoplasmic. Replication follows the DNA strand displacement

length. The genome codes for 6 proteins (3' to 5': N-P-X-M-G-L). Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

unique to the Bocaparvovirus genus, appears to be critical for optimal viral replication, as the NP1 knockout mutant of MVC suffers from severe impairment

are surprisingly small, with diameters ranging from 17 up to 22 nm. Viral replication is nuclear. Entry into the host cell is achieved by penetration. Replication

side being the location of internal ribosomal entry site (IRES). Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

DNA into the host cytoplasm via long flexible tail ejection system. Viral replication is cytoplasmic. Replication follows the replicative transposition

nucleotides, with 37 to 39 proteins. Complete genomes are available here Viral replication is cytoplasmic. The virus attaches to the host cell's adhesion receptors

single linear single-stranded DNA genome around 4.8 kb in length. Viral replication is nuclear. Entry into the host cell is achieved by attachment to

the virions are transmitted in a non-persistent fashion means that viral replication does not occur within the aphid vector and that, unless the aphid

arrangement is clearly visible. Capsid with 32 cup-shaped depressions. Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment

enrichment of genetically targeted cells. Complementing efforts to control viral replication, immunotherapies that may assist in the recovery of the immune system

monoclonal antibody, can stop HIV from entering the cell and stop viral replication. It prevents the virus-cell binding at a distinct site in the CCR5

well as two other similar, unclassified genomes are available here. Viral replication is cytoplasmic. The virus attaches to the host cell's adhesion receptor

of HBeAg in a host's serum is associated with much higher rates of viral replication and enhanced infectivity; however, variants of the hepatitis B virus

molecules into smaller fragments. HIV protease is vital for both viral replication within the cell and release of mature viral particles from an infected

oral NS3 serine protease inhibitor of hepatitis C virus. It inhibits viral replication in infected host cells. The mechanism of inhibition involves reversible

to premature host cell death during the lytic cycle, thus limiting viral replication. E1B-19k mimics MCL1, which is a cellular antiapoptotic protein. In

nuclear import is able to proceed as normal which may be important for viral replication. This means that eVP24 prevents the activation of an immune response

via the fecal–oral route, meaning that one ingests the virus and viral replication occurs in the gastrointestinal tract. Virus is shed in the feces of

Viral replication and transcription of associated virus orthomyxovirus

promoter transcription factor interacts with HIV-1 Tat and stimulates viral replication in human microglial cells". The Journal of Biological Chemistry. 275

(e.g., HIV-1) may find that a candidate drug functions to prevent viral replication in an in vitro setting (typically cell culture). However, before this

infection. Studies of the presence of viral DNA, indicating active viral replication, suggest STLPyV prevalence in the range of 1-2% of children. Lim,

Tube and can function like Tube by activating the NF-κB pathway. Viral replication is nuclear; DNA-templated transcription is its method. The virus infects

in the genomes of certain viruses (E.g. HSV, vaccinia) and allow viral replication in quiescent(non-replicating) cells, so if they are inactivated by

of viral replication take weeks. Researchers hypothesized that vaccines designed to maintain activated effector memory T cells might impair viral replication