Viral replication is the formation of biological viruses during the infection process in the target host cells. Viruses must first get into the cell before viral replication can occur. Through the generation of abundant copies of its genome and packaging these copies, the virus continues infecting new hosts. Replication between viruses is greatly varied and depends on the type of genes involved in them. Most DNA viruses assemble in the nucleus while most RNA viruses develop solely in cytoplasm.
42-431: Narnavirus is a genus of positive-strand RNA viruses in the family Narnaviridae . Fungi serve as natural hosts. There are two species in this genus. Member viruses have been shown to be required for sexual reproduction of Rhizopus microsporus . Narnaviruses have a na ked RNA genome without a virion and derive their name from this feature. Narnaviruses have no true virion. They do not have structural proteins or
84-571: A capsid . Narnaviruses have nonsegmented, linear, positive-sense , single-stranded RNA genomes. The genome has one open reading frame which encodes the RNA-dependent RNA polymerase (RdRp). The genome is associated with the RdRp in the cytoplasm of the fungi host and forms a naked ribonucleoprotein complex. Viral replication is cytoplasmic. Replication follows the positive-strand RNA virus replication model. Positive-strand RNA virus transcription
126-438: A genome and as messenger RNA ; it can be directly translated into protein in the host cell by host ribosomes . The first proteins to be expressed after infection serve genome replication functions; they recruit the positive-strand viral genome to viral replication complexes formed in association with intracellular membranes. These complexes contain proteins of both viral and host cell origin, and may be associated with
168-426: A competent virus is formed. This typically involves capsid modifications that are provided enzymes (host or virus-encoded). The final step in viral replication is release, which is when the newly assembled and mature viruses leave the host cell. How a virus releases from the host cell is dependent on the type of virus it is. One common type of release is budding. This occurs when viruses that form their envelope from
210-553: A sister clade in relation to Lenarviricota . The third phylum that contains +ssRNA viruses is Pisuviricota , which has been informally called the "picornavirus supergroup". The phylum contains a large assemblage of eukaryotic viruses known to infect animals, plants, fungi, and protists. The phylum contains three classes, two of which contain only +ssRNA viruses: Pisoniviricetes , which contains nidoviruses , picornaviruses , and sobeliviruses , and Stelpaviricetes , which contains potyviruses and astroviruses . The third class
252-454: Is Duplopiviricetes , whose members are double-stranded RNA viruses that are descended from +ssRNA viruses. Viral replication Viruses multiply only in living cells. The host cell must provide the energy and synthetic machinery and the low-molecular-weight precursors for the synthesis of viral proteins and nucleic acids. Virus replication occurs in seven stages: It is the first step of viral replication. Some viruses attach to
294-654: Is also one of the most-studied types of viruses, alongside the double-stranded DNA viruses. The positive-sense RNA viruses and indeed all genes defined as positive-sense can be directly accessed by host ribosomes to immediately form proteins. These can be divided into two groups, both of which replicate in the cytoplasm: Examples of this class include the families Coronaviridae , Flaviviridae , and Picornaviridae . The negative-sense RNA viruses and indeed all genes defined as negative-sense cannot be directly accessed by host ribosomes to immediately form proteins. Instead, they must be transcribed by viral polymerases into
336-413: Is defined by the removal of the virion's protein "coat" and the release of its genetic material. This step occurs in the same area that viral transcription occurs. Different viruses have various mechanisms for uncoating. Some RNA viruses such as Rhinoviruses use the low pH in a host cell's endosomes to activate their uncoating mechanism. This involves the rhinovirus releasing a protein that creates holes in
378-473: Is further disrupted by viral proteases degrading components required to initiate translation of cellular mRNA. All positive-strand RNA virus genomes encode RNA-dependent RNA polymerase , a viral protein that synthesizes RNA from an RNA template. Host cell proteins recruited by +ssRNA viruses during replication include RNA-binding proteins , chaperone proteins , and membrane remodeling and lipid synthesis proteins, which collectively participate in exploiting
420-524: Is the method of transcription. The virus exits the host cell by cell-to-cell movement. Fungi serve as the natural host. Transmission routes are parental and sexual. The genus has the following two species: Positive-strand RNA virus Positive-strand RNA viruses ( +ssRNA viruses ) are a group of related viruses that have positive-sense , single-stranded genomes made of ribonucleic acid . The positive-sense genome can act as messenger RNA (mRNA) and can be directly translated into viral proteins by
462-664: The Retroviridae (e.g. HIV ), genome damage appears to be avoided during reverse transcription by strand switching, a form of recombination. Recombination occurs in the Coronaviridae (e.g. SARS ). Recombination in RNA viruses appears to be an adaptation for coping with genome damage. Recombination can also occur infrequently between +ssRNA viruses of the same species but of divergent lineages. The resulting recombinant viruses may sometimes cause an outbreak of infection in humans, as in
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#1733092797289504-480: The host cell's ribosomes . Positive-strand RNA viruses encode an RNA-dependent RNA polymerase (RdRp) which is used during replication of the genome to synthesize a negative-sense antigenome that is then used as a template to create a new positive-sense viral genome. Positive-strand RNA viruses are divided between the phyla Kitrinoviricota , Lenarviricota , and Pisuviricota (specifically classes Pisoniviricetes and Stelpavirictes ) all of which are in
546-685: The Circoviridae and Parvoviridae . They replicate within the nucleus, and form a double-stranded DNA intermediate during replication. A human Anellovirus called TTV is included within this classification and is found in almost all humans, infecting them asymptomatically in nearly every major organ . RNA viruses: The polymerase of RNA viruses lacks the proofreading functions found in the polymerase of DNA viruses. This contributed to RNA viruses having lower replicative fidelity compared to DNA viruses, causing RNA viruses to be highly mutagenic, which can increase their overall survival rate. RNA viruses lack
588-505: The Reoviridae and Birnaviridae . Replication is monocistronic and includes individual, segmented genomes, meaning that each of the genes codes for only one protein, unlike other viruses, which exhibit more complex translation. These viruses consist of two types, however both share the fact that replication is primarily in the cytoplasm, and that replication is not as dependent on the cell cycle as that of DNA viruses. This class of viruses
630-518: The cell membrane of the host cell and inject its DNA or RNA into the host to initiate infection. Attachment to a host cell is often achieved by a virus attachment protein that extends from the protein shell ( capsid ), of a virus. This protein is responsible for binding to a surface receptor on the plasma membrane (or membrane carbohydrates) of a host cell. Viruses can exploit normal cell receptor functions to allow attachment to occur by mimicking molecules that bind to host cell receptors. For example,
672-459: The rhinovirus uses their virus attachment protein to bind to the receptor ICAM-1 on host cells that is normally used to facilitate adhesion between other host cells. Entry, or penetration, is the second step in viral replication. This step is characterized by the virus passing through the plasma membrane of the host cell. The most common way a virus gains entry to the host cell is by receptor-mediated endocytosis , which comes at no energy cost to
714-449: The "readable" complementary positive-sense. These can also be divided into two groups: Examples in this class include the families Orthomyxoviridae , Paramyxoviridae , Bunyaviridae , Filoviridae , and Rhabdoviridae (which includes rabies ). A well-studied family of this class of viruses include the retroviruses . One defining feature is the use of reverse transcriptase to convert the positive-sense RNA into DNA. Instead of using
756-458: The RNA for templates of proteins, they use DNA to create the templates, which is spliced into the host genome using integrase . Replication can then commence with the help of the host cell's polymerases. This small group of viruses, exemplified by the Hepatitis B virus, have a double-stranded, gapped genome that is subsequently filled in to form a covalently closed circle ( cccDNA ) that serves as
798-467: The RNA is in a replicative form. Viruses may undergo two types of life cycles: the lytic cycle and the lysogenic cycle. In the lytic cycle, the virus introduces its genome into a host cell and initiates replication by hijacking the host's cellular machinery to make new copies of the virus. In the lysogenic life cycle, the viral genome is incorporated into the host genome. The host genome will undergo its normal life cycle, replicating and dividing replicating
840-478: The apparent descendants of leviviruses, which infect eukaryotes . The phylum is divided into four classes: Leviviricetes , which contains leviviruses and their relatives, Amabiliviricetes , which contains narnaviruses and their relatives, Howeltoviricetes , which contains mitoviruses and their relatives, and Miaviricetes , which contains botourmiaviruses and their relatives. Based on phylogenetic analysis of RdRp, all other RNA viruses are considered to comprise
882-423: The capacity to identify and repair mismatched or damaged nucleotides, and thus, RNA genomes are prone to mutations introduced by mechanisms intrinsic and extrinsic to viral replication. RNA viruses present a therapeutic double-edged sword: RNA viruses can withstand the challenge of antiviral drugs, cause epidemics, and infect multiple host species due to their mutagenic nature, making them difficult to treat. However,
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#1733092797289924-739: The case of SARS and MERS. Positive-strand RNA viruses are common in plants. In tombusviruses and carmoviruses , RNA recombination occurs frequently during replication. The ability of the RNA-dependent RNA polymerase of these viruses to switch RNA templates suggests a copy choice model of RNA recombination that may be an adaptive mechanism for coping with damage in the viral genome. Other +ssRNA viruses of plants have also been reported to be capable of recombination, such as Brom mosaic bromovirus and Sindbis virus . Positive-strand RNA viruses are found in three phyla: Kitrinoviricota , Lenarviricota , and Pisuviricota , each of which are assigned to
966-665: The cell to forcefully undergo cell division , which may lead to transformation of the cell and, ultimately, cancer . An example of a family within this classification is the Adenoviridae . There is only one well-studied example in which a class 1 family of viruses does not replicate within the nucleus. This is the Poxvirus family, which comprises highly pathogenic viruses that infect vertebrates . Viruses that fall under this category include ones that are not as well-studied, but still do pertain highly to vertebrates. Two examples include
1008-453: The cell's secretory pathway for viral replication. Numerous positive-strand RNA viruses can undergo genetic recombination when at least two viral genomes are present in the same host cell. The capability for recombination among +ssRNA virus pathogens of humans is common. RNA recombination appears to be a major driving force in determining genome architecture and the course of viral evolution among Picornaviridae (e.g. poliovirus). In
1050-519: The coronaviruses and rhinoviruses that cause the common cold . Positive-strand RNA virus genomes usually contain relatively few genes, usually between three and ten, including an RNA-dependent RNA polymerase. Coronaviruses have the largest known RNA genomes, between 27 and 32 kilobases in length, and likely possess replication proofreading mechanisms in the form of an exoribonuclease within nonstructural protein nsp14. Positive-strand RNA viruses have genetic material that can function both as
1092-414: The corresponding cellular machinery for said genetic material. Viruses that contain double-stranded DNA (dsDNA) share the same kind of genetic material as all organisms, and can therefore use the replication enzymes in the host cell nucleus to replicate the viral genome. Many RNA viruses typically replicate in the cytosol , and can directly access the host cell's ribosomes to manufacture viral proteins once
1134-446: The endosome, and allows the virus to release its genome through the holes. Many DNA viruses travel to the host cells nucleus and release their genetic material through nuclear pores. The fourth step in the viral cycle is replication, which is defined by the rapid production of the viral genome. How a virus undergoes replication relies on the type of genetic material the virus possesses. Based on their genetic material, viruses will hijack
1176-406: The host nucleus before it is able to replicate. Some of these viruses require host cell polymerases to replicate their genome , while others, such as adenoviruses or herpes viruses, encode their own replication factors. However, in either case, replication of the viral genome is highly dependent on a cellular state permissive to DNA replication and, thus, on the cell cycle . The virus may induce
1218-426: The host membrane, and after entry, the virion becomes uncoated, and its genomic material is then transferred into the cytoplasm. Cell-to-cell fusion: Some viruses prompt specific protein expression on the surfaces of infected cells to attract uninfected cells. This interaction causes the uninfected cell to fuse with the infected cell at lower pH levels to form a multinuclear cell known as a syncytium. Endocytic routes:
1260-436: The host's plasma membrane bend the membrane around the capsid. As the virus bends the plasma membrane it begins to wrap around the whole capsid until the virus is no longer attached to the host cell. Another common way viruses leave the host cell is through cell lysis , where the viruses lyse the cell causing it to burst which releases mature viruses that were in the host cell. Viruses are split into seven classes, according to
1302-539: The kingdom Orthornavirae and realm Riboviria . They are monophyletic and descended from a common RNA virus ancestor. In the Baltimore classification system, +ssRNA viruses belong to Group IV. Positive-sense RNA viruses include pathogens such as the Hepatitis C virus , West Nile virus , dengue virus , and the MERS , SARS , and SARS-CoV-2 coronaviruses , as well as less clinically serious pathogens such as
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1344-423: The kingdom Orthornavirae in the realm Riboviria . In the Baltimore classification system, which groups viruses together based on their manner of mRNA synthesis, +ssRNA viruses are group IV. The first +ssRNA phylum is Kitrinoviricota . The phylum contains what have been referred to as the " alphavirus supergroup" and " flavivirus supergroup" along with various other short-genome viruses. Four classes in
1386-451: The membranes of a variety of organelles βoften the rough endoplasmic reticulum , but also including membranes derived from mitochondria , vacuoles , the Golgi apparatus , chloroplasts , peroxisomes , plasma membranes , autophagosomal membranes , and novel cytoplasmic compartments. The replication of the positive-sense RNA genome proceeds through double-stranded RNA intermediates, and
1428-419: The other steps, how a particular virus is assembled is dependent on what type of virus it is. Assembly can occur in the plasma membrane, cytosol, nucleus, golgi apparatus, and other locations within the host cell. Some viruses only insert their genome into a capsid once the capsid is completed, while in other viruses the will capsid will wrap around the genome as it is being copied. This is the final step before
1470-451: The phylum are recognized: Alsuviricetes , the alphavirus supergroup, which contains a large number of plant viruses and arthropod viruses; Flasuviricetes , which contains flaviviruses, Magsaviricetes , which contains nodaviruses and sinhaliviruses ; and Tolucaviricetes , which primarily contains plant viruses. Lenarviricota is the second +ssRNA phylum. It contains the class Leviviricetes , which infect prokaryotes , and
1512-401: The plasma membrane and can spread within the host via fusion or cell-cell fusion. Viruses attach to proteins on the host cell surface known as cellular receptors or attachment factors to aid entry. Evidence shows that viruses utilize ion channels on the host cells during viral entry. Fusion: External viral proteins promote the fusion of the virion with the plasma membrane. This forms a pore in
1554-418: The process by which an intracellular vesicle is formed by membrane invagination, which results in the engulfment of extracellular and membrane-bound components, in this context, a virus. Non-endocytic routes: the process by which viral particles are released into the cell by fusion of the extracellular viral envelope and the membrane of the host cell. Uncoating is the third step in viral replication. Uncoating
1596-528: The purpose of replication in these membranous invaginations may be the avoidance of cellular response to the presence of dsRNA. In many cases subgenomic RNAs are also created during replication. After infection, the entirety of the host cell's translation machinery may be diverted to the production of viral proteins as a result of the very high affinity for ribosomes by the viral genome's internal ribosome entry site (IRES) elements; in some viruses, such as poliovirus and rhinoviruses , normal protein synthesis
1638-510: The reverse transcriptase protein that often comes with the RNA virus can be used as an indirect target for RNA viruses, preventing transcription and synthesis of viral particles. (This is the basis for anti-AIDs and anti-HIV drugs ) Like most viruses with RNA genomes, double-stranded RNA viruses do not rely on host polymerases for replication to the extent that viruses with DNA genomes do. Double-stranded RNA viruses are not as well-studied as other classes. This class includes two major families,
1680-668: The type of genetic material and method of mRNA production, each of which has its own families of viruses, which in turn have differing replication strategies themselves. David Baltimore , a Nobel Prize -winning biologist, devised a system called the Baltimore Classification System to classify different viruses based on their unique replication strategy. There are seven different replication strategies based on this system (Baltimore Class I, II, III, IV, V, VI, VII). The seven classes of viruses are listed here briefly and in generalities. This type of virus usually must enter
1722-502: The viral genome along with its own. The viral genome can be triggered to begin viral production via chemical and environmental stimulants. Once a lysogenic virus enters the lytic life cycle, it will continue in the viral production pathways and proceed with transcription / mRNA production. (ex: Cold sores, herpes simplex virus (HSV)-1, lysogenic bacteriophages, etc.) Assembly is when the newly manufactured viral proteins and genomes are gathered and put together to form immature viruses. Like
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1764-460: The virus, only the host cell. Receptor-mediated endocytosis occurs when a molecule (in this case a virus) binds to receptor on the membrane of the cell. A series of chemical signals from this binding causes the cell to wrap the attached virus in the plasma membrane around it forming a virus-containing vesicle inside the cell. Viruses enter host cells using a variety of mechanisms, including the endocytic and non-endocytic routes. They can also fuse at
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