retrovirus

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A family of viruses distinguished by three characteristics: (1) genetic information in ribonucleic acid (RNA); (2) virions possess the enzyme reverse transcriptase; and (3) virion morphology consists of two proteinaceous structures, a dense core and an envelope that surrounds the core. Some viruses outside the retrovirus family have some of these characteristics, but none has all three. Numerous retroviruses have been described; they are found in all families of vertebrates. See also Animal virus; Reverse transcriptase; Ribonucleic acid (RNA).

The genome is composed of two identical molecules of single-stranded RNA, which are similar in structure and function to cellular messenger RNA. Deoxyribonucleic acid (DNA) is not present in the virions of retroviruses. The reverse transcriptase in each virus makes a DNA copy of the RNA genome shortly after entry of the virus into the host cell. The discovery of this enzyme changed thinking in biology. Previously, the only known direction for the flow of genetic information was from DNA to RNA, yet retroviruses make DNA copies of their genome by using an RNA template. This reversal of genetic information was considered backward and hence the family name retrovirus, meaning backward virus.

Once the DNA copy of the RNA genome is made, it is inserted directly into one of the chromosomes of the host cell. This results in new genetic information being acquired by the host species. The study of reverse transcriptase has led to other discoveries of how retroviruses add a variety of new genetic information into the host. One such class of genes carried by retroviruses is oncogenes, meaning tumor genes. Retroviral oncogenes appear to be responsible for tumors in animals. See also Oncogenes; Virus classification.

Two distinct retroviruses have been discovered in humans. One is human T-cell lymphotropic virus type 1 (HTLV-1), a type C-like virus associated with adult T-cell leukemia. The other is the human acquired immune deficiency syndrome (AIDS) virus, a type E lentivirus. See also Acquired immune deficiency syndrome (AIDS); Leukemia.

A virus that is designed to avoid discovery by actively attacking the very antivirus programs attempting to detect it. See virus.

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A virus containing ribonucleic acid rather than deoxyribonucleic acid.

Retroviruses replicate inside cells they have invaded, using an enzyme called "reverse transcriptase" to transcribe RNA into DNA. In this way they can evade the body's natural immune defense mechanisms as they make new copies of themselves. The most important retrovirus is the human immunodefeciency virus (HIV). HIV invades and destroys host cells, particularly T-helper lymphocytes, which are crucially important in maintaining the body's immune defense mechanisms. Disruption of immune defense mechanisms following the destruction of T-helper lymphocytes is the main way in which HIV leads to AIDS.

(SEE ALSO: HIV/AIDS; Pathogenic Organisms)

— JOHN M. LAST

Retroviruses are RNA-containing viruses that use the enzyme reverse transcriptase to copy their RNA into the DNA of a host cell. Retroviruses have been isolated from a variety of vertebrate species, including humans, other mammals, reptiles, and fish. The family Retroviridae includes such important human pathogens as human immunodeficiency virus (HIV) and human Tlymphotropic virus (HTLV), the causes of AIDS and adult T-cell leukemia respectively. The study of this virus family has led to the discovery of oncogenes, resulting in a quantum advance in the field of cancer genetics. Retro-viruses are also valuable research tools in molecular biology and gene therapy.

Characteristics

The classification of retroviruses is based on comparisons of the size of the genome and morphologic characteristics (see Table 1). The genomic RNA of retroviruses is single-stranded and possesses "positive" polarity similar to that found in messenger RNA (mRNA). Virions (virus particles) contain two 5′ ("five prime"), end-linked, identical copies of the genome RNA, and are therefore said to be diploid.

Table 1

Three genes are universally present in the genomes of retroviruses that are capable of replication, such as murine (mouse) leukemia virus. The gag (group antigen) gene encodes proteins that make up the nucleocapsid of the virus as well as a matrix layer, the two of which surround the RNA. The pol gene (a type of polymerase) encodes reverse transcriptase, which copies the RNA into DNA, and integrase, which integrates the DNA into the host chromosome. Depending on the species, pol can also encode protease, a protein that cleaves the initial multiprotein products of retrovirus translation to make functional proteins. Some retroviruses have incorporated viral oncogene sequences. An example of this is reticuloendotheliosis virus strain T. The genome of complex retroviruses, such as HTLV, can contain several other genes that regulate genome expression or replication and are not present in simple retroviruses.

Reverse Transcriptase

Retroviruses follow the same general steps in their replication cycles that are common to other viruses. The steps that differ from other viruses involve the retroviral reverse transcriptase, an enzyme discovered simultaneously by Howard Temin and David Baltimore in 1970. (Temin and Baltimore were awarded the Nobel Prize for this work in 1975.) Reverse transcriptase converts the single-stranded, positive-polarity RNA genome of retrovirus into double-stranded DNA, thereby reversing the typical flow of genetic information (which is from DNA to mRNA). The DNA copy is transported into the nucleus of the host cell, circularized, and integrated into the host chromosome.

This DNA copy of the retrovirus genome is referred to as the provirus or proviral DNA. The genomes of most vertebrates contain abundant numbers of incomplete and complete proviruses (endogenous retroviruses) that appear to represent remnants of past retroviral infections in germline cells. Proviruses contain structures called long terminal repeats (LTR) at each end. The LTRs contain promoter elements and transcriptional start sites that enable the retroviral genes to be expressed. They can also affect the expression of nearby cellular genes.

Retrovirus Replication Cycle

There are seven steps in the replication cycle of the retrovirus. The first step is attachment, in which the retrovirus uses one of its glycoproteins to bind to one or more specific cell-surface receptors on the host cell. Some retroviruses also employ a secondary receptor, referred to as the co-receptor. Some retroviral receptors and coreceptors have been identified. For example, CD4 and various members of the chemokine receptor family on human T cells (a type of white blood cell) serve as the HIV receptors and coreceptors.

The second and third steps are penetration and uncoating, respectively. Retroviruses penetrate the host cell by direct fusion of the virion envelope with the plasma membrane of the host. Continuation of this fusion process results in the release of the viral capsid directly into the host cell's cytoplasm, where it is partially disrupted.

Step four is replication, which occurs after the retrovirus has undergone partial uncoating. At this stage, the RNA genome is converted by reverse transcriptase into double-stranded DNA. Reverse transcriptase has three enzymatic activities: RNA-directed DNA polymerase makes one DNA strand, DNA-directed DNA polymerase makes the complementary strand, and RNAse H degrades the viral RNA strand. Reverse transcription is primed by a cellular transfer RNA (tRNA) that is packaged into retrovirus virions. It concludes with the synthesis of a double-stranded copy of the retroviral genome that is termed the "provirus," or proviral DNA.

This proviral DNA is circularized and transported to the host cell's nucleus, where it is integrated, apparently at random, into the genome by means of the retroviral enzyme called integrase. Following integration, the provirus behaves like a set of cellular genes, while the LTRs function as promoters that begin transcription back into mRNA. This transcription is carried out by RNA polymerases in the host cell. Transcription of the proviral DNA is also the means of generating progeny RNA. Viral proteins are made in the cytoplasm of the host cell by cellular ribosomes.

The next step (step five) is termed "assembly," in which retrovirus capsids are assembled in an immature form at various locations in the host cell. This is followed by an "egress" stage, in which the envelope proteins of retroviruses are acquired by budding from the plasma membrane (cell surface) of the host. Finally, step seven is "maturation." In this step, the Gag and Pol proteins of the retrovirus are cleaved by the retroviral protease, thus forming the mature and infectious form of the virus.

Consequences of Retroviral Infection

Retroviral infection can result in several different outcomes for the virus and the cell. Retroviruses are capable of inducing immunosuppressive, autoimmune, and neurological illnesses. Some retroviruses, such as the lentiviruses and the spumaviruses, are capable of directly killing cells. Cytopathic (cell-killing) effects in infected T cells and cells in the brain may account for the profound immune deficiencies and neurological diseases induced by HIV and related lentiviruses.

Retroviruses are also capable of inducing latent infections, in which the virus is dormant, or persistent infections, in which low levels of the virus are continuously produced. These capabilities explain the life-long nature of retroviral infections, and render the diseases induced by these pathogens extremely difficult to treat.

Retroviruses and Cancer

Retroviruses are among several types of viruses that can induce cancer in the host organism. So-called slowly transforming viruses are exemplified by human T-lymphotropic virus (HTLV), which causes leukemia (a type of blood cancer) in humans. These viruses induce malignancy by a process called insertional mutagenesis. The initial event is thought to be retroviral integration near, and subsequent activation of, a cellular oncogene (c-onc). Examples of c-onc include genes for growth factors, protein kinases, and transcription factors. Harold Varmus and Michael Bishop won the Nobel Prize for physiology or medicine in 1989 for their contributions to the discovery of oncogenes.

When a malignancy is triggered, tumors appear only after a long latent period of months or years, and these tumors are typically clonal in origin. That is, they arise by the rare transformation of a single cell. HTLV-1 is highly prevalent in people living in Japan, the Caribbean, and Africa, areas where approximately one percent of adults are infected. About one to three percent of infected individuals will eventually develop adult T-cell leukemia after an incubation period, which is usually several decades long. HTLV stimulates T-cell proliferation that could favor mutational events leading to cell transformation.

Acutely transforming retroviruses contain a viral oncogene (v-onc) and induce polyclonal cancers (that is, many different cancer cells are derived in multiple transforming events) at high efficiency within a short time frame (weeks). The v-onc are derived by incorporation and modification (that is, by deletion of introns, mutations, and other such processes) of host-cell oncogenes. The v-onc are often expressed in great quantity, due to the highly active viral LTRs. Most acutely transforming retroviruses are replication-defective, because incorporation of the oncogene deletes an essential gene or genes. They therefore require a helper virus to propagate. An exception is Rous sarcoma virus, whose genome retains enough of the structural gene sequences to remain capable of replication.

Bibliography

Varmus, Harold E. "Form and Function of Retroviral Proviruses." Science 216, no. 4548 (1982): 812-820.

Weinberg, Robert A. "How Cancer Arises." Scientific American 275, no. 3 (1996): 62-70.

—Robert Garry

A virus, such as HIV, whose RNA codes for DNA, which is then inserted into some part of the host's DNA. This virus comes with its own special enzyme, called reverse transcriptase, which facilitates this insertion.

A member of the family Retroviridae.

• defective r. — a virus unable to replicate independently; commonly the result of loss of part of the envelope gene when leukosis viruses acquire an oncogene. Propagation is achieved by coinfection with a leukosis virus able to provide the envelope for the defective virus.
• endogenous r. — one transmitted in germ-line DNA from an infected parent to offspring.
• exogenous r. — one transmitted horizontally.
• rapidly transforming r. — characterized by rapid oncogenesis attributable to the v-onc gene which they carry.
• slowly transforming r. — weakly oncogencic after a long incubation period. They do not carry the v-onc gene.

This article may be too technical for most readers to understand. Please improve this article to make it accessible to non-experts, without removing the technical details. (November 2009)

Retroviruses
Virus classification
Group:	Group VI (ssRNA-RT)
Family:	Retroviridae
Genera
Subfamily: Orthoretrovirinae Alpharetrovirus Betaretrovirus Gammaretrovirus Deltaretrovirus Epsilonretrovirus Lentivirus Subfamily: Spumaretrovirinae Spumavirus

A retrovirus is an RNA virus that is replicated in a host cell via the enzyme reverse transcriptase to produce DNA from its RNA genome. The DNA is then incorporated into the host's genome by an integrase enzyme. The virus thereafter replicates as part of the host cell's DNA. Retroviruses are enveloped viruses that belong to the viral family Retroviridae.

The virus itself stores its nucleic acid in the form of a +mRNA (including the 5'cap and 3'PolyA inside the virion) genome and serves as a means of delivery of that genome into cells it targets as an obligate parasite, and constitutes the infection. Once in the host's cell, the RNA strands undergo reverse transcription in the cytosol and are integrated into the host's genome, at which point the retroviral DNA is referred to as a provirus. It is difficult to detect the virus until it has infected the host.

Contents 1 Virion structure 2 Multiplication 3 Genes 4 Provirus 5 Development 6 Gene therapy 7 Cancer 8 Classification 8.1 Exogenous 8.2 Endogenous 8.3 Group VI 8.4 Group VII 9 Treatment 10 Treatment of Veterinary Retroviruses 11 References 12 External links

Virion structure

Virions of retroviruses consist of enveloped particles about 100 nm in diameter. The virions also contain two identical single-stranded RNA molecules 7-10 kilobases (kb) in length. Although virions of different retroviruses do not have the same morphology or biology, all the virion components are very similar.^[1]

The main virion components are:

• Envelope: composed of a lipid bilayer, which is obtained from the host plasma membrane during budding process.

• RNA: consisted of a dimer RNA. It has a cap at 5' end and polyadenyle at 3' end. The RNA genome also has terminal noncoding regions, which are important in replication and internal regions that encode virion proteins for gene expression. The 5' end includes four regions, which are R, U5, PBS, and L. R region is a short repeated sequence at each end of the genome during the reverse transcription in order to ensure correct end-to-end transfer in growing chain. U5, on the other hand, is a short unique sequence between R and PBS. PBS (primer binding site) consists of 18 bases complementary to 3' end of tRNA primer. L region is an untranslated leader region that gives signal for packaging of genome RNA. The 3' end includes 3 regions, which are PPT (polypurine tract), U3, and R. PPT is primer for plus-strand DNA synthesis during reverse transcription. U3 is a sequence between PPT and R, which has signal that provirus can use in transcription. R is the terminal repeated sequence at 3' end.

• Proteins: consisted of gag proteins, protease (PR), pol proteins and env proteins. Gag proteins are major components of the viral capsid, which are about 2000-4000 copies per virion. Protease, on one hand, is expressed differently in different viruses. It functions in proteolytic cleavages during virion maturation to make mature gag and pol proteins. Pol proteins are responsible for synthesis of viral DNA and integration into host DNA after infection. Finally, env proteins play role in association and entry of virion into the host cell.^[2]

Multiplication

When retroviruses have integrated their own genome into the germ line, their genome is passed on to a following generation. These endogenous retroviruses (ERVs), contrasted with exogenous ones, now make up 5-8% of the human genome.^[3] Most insertions have no known function and are often referred to as "junk DNA". However, many endogenous retroviruses play important roles in host biology, such as control of gene transcription, cell fusion during placental development in the course of the germination of an embryo, and resistance to exogenous retroviral infection. Endogenous retroviruses have also received special attention in the research of immunology-related pathologies, such as autoimmune diseases like multiple sclerosis, although endogenous retroviruses have not yet been proven to play any causal role in this class of disease. The role of endogenous retroviruses in human gene evolution is explored in a 2005 peer-reviewed article.^[4]

While transcription was classically thought to only occur from DNA to RNA, reverse transcriptase transcribes RNA into DNA. The term "retro" in retrovirus refers to this reversal (making DNA from RNA) of the central dogma of molecular biology. Reverse transcriptase activity outside of retroviruses has been found in almost all eukaryotes, enabling the generation and insertion of new copies of retrotransposons into the host genome. These inserts are transcribed by enzymes of the host into new RNA molecules that enter the cytosol. Next, some of these RNA molecules are translated into viral proteins. For example, the gag gene is translated into molecules of the capsid protein, the pol gene is transcribed into molecules of reverse transcriptase, and the env gene is translated into molecules of the envelope protein. It is important to note that a retrovirus must "bring" its own reverse transcriptase in its capsid, otherwise it is unable to utilize the enzymes of the infected cell to carry out the task, due to the unusual nature of producing DNA from RNA.

Industrial drugs that are designed as protease and reverse transcriptase inhibitors can quickly be proved ineffective because the gene sequences that code for the protease and the reverse transcriptase can undergo many substitutions. These substitutions of nitrogenous bases, which make up the DNA strand, can make either the protease or the reverse transcriptase difficult to attack. The amino acid substitution enables the enzymes to evade the drug regiments because mutations in the gene sequences can cause physical or chemical change, which makes them harder to detect by the drug. When the drugs that are supposed to attack enzymes, such as protease, are designed, the manufacturers target specific sites on the enzyme. One way to attack these targets can be through hydrolysis of molecular bonds, which means that the drug will add molecules of H₂O (water) to specific bonds. By adding molecules of water at a site on the virus, the drug breaks the previous bonds that were linked to each other. If several of these breaks occur, the result can lead to lysis, the death of the virus.^[5]

Because reverse transcription lacks the usual proofreading of DNA replication, a retrovirus mutates very often. This enables the virus to grow resistant to antiviral pharmaceuticals quickly, and impedes the development of effective vaccines and inhibitors for the retrovirus.^[6]

Genes

Retrovirus genomes commonly contain these three open reading frames that encode for proteins that can be found in the mature virus:

• group-specific antigen (gag) codes for core and structural proteins of the virus;
• polymerase (pol) codes for reverse transcriptase, protease and integrase; and,
• envelope (env) codes for the retroviral coat proteins.

Provirus

This DNA can be incorporated into host genome as a provirus that can be passed on to progeny cells. The provirus DNA is inserted at random into the host genome. Because of this, it can be inserted into oncogenes. In this way some retroviruses can convert normal cells into cancer cells. Some provirus remains latent in the cell for a long period of time before it is activated by the change in cell environment.

Development

Studies of retroviruses led to the first demonstrated synthesis of DNA from RNA templates, a fundamental mode for transferring genetic material that occurs in both eukaryotes and prokaryotes. It has been speculated that the RNA to DNA transcription processes used by retroviruses may have first caused DNA to be used as genetic material. In this model, the RNA world hypothesis, cellular organisms adopted the more chemically stable DNA when retroviruses evolved to create DNA from the RNA templates. Retroviruses are proving to be valuable research tools in molecular biology and have been used successfully in gene delivery systems.^[7]

Gene therapy

Gammaretroviral and lentiviral vectors for gene therapy have been developed that mediate stable genetic modification of treated cells by chromosomal integration of the transferred vector genomes. This technology is of use, not only for research purposes, but also for clinical gene therapy aiming at the long-term correction of genetic defects, e.g., in stem and progenitor cells. Retroviral vector particles with tropism for various target cells have been designed. Gammaretroviral and lentiviral vectors have so far been used in more than 300 clinical trials, addressing treatment options for various diseases.^[7][8]

Cancer

Retroviruses that cause tumor growth include Rous sarcoma virus and mouse mammary tumor virus. Cancer can be triggered by proto-oncogenes that were mistakenly incorporated into proviral DNA or by the disruption of cellular proto-oncogenes. Rous sarcoma virus contains the src gene that triggers tumor formation. Later it was found that a similar gene in cells is involved in cell signaling, which was most likely excised with the the proviral DNA. Nontransforming viruses can randomly insert their DNA into proto-oncogenes, disrupting the expression of proteins that regulate the cell cycle. The promoter of the provirus DNA can also cause over expression of regulatory genes.

Classification

Phylogeny of Retroviruses

Exogenous

The following genera are included here:

• Genus Alpharetrovirus; type species: Avian leukosis virus; others include Rous sarcoma virus
• Genus Betaretrovirus; type species: Mouse mammary tumour virus
• Genus Gammaretrovirus; type species: Murine leukemia virus; others include Feline leukemia virus
• Genus Deltaretrovirus; type species: Bovine leukemia virus; others include the cancer-causing Human T-lymphotropic virus
• Genus Epsilonretrovirus; type species: Walleye dermal sarcoma virus
• Genus Lentivirus; type species: Human immunodeficiency virus 1; others include Simian, Feline immunodeficiency viruses
• Genus Spumavirus; type species: Simian foamy virus

These were previously divided into three subfamilies (Oncovirinae, Lentivirinae, and Spumavirinae), but with current knowledge of retroviruses, this is no longer appropriate. (The term oncovirus is still commonly used, though.)

Endogenous

Main article: endogenous retrovirus

Endogenous retroviruses are not formally included in this classification system, and are broadly classified into three classes, on the basis of relatedness to exogenous genera:

• Class I are most similar to the gammaretroviruses
• Class II are most similar to the betaretroviruses and alpharetroviruses
• Class III are most similar to the spumaviruses

Group VI

All members of Group VI use virally encoded reverse transcriptase, an RNA-dependent DNA polymerase, to produce DNA from the initial virion RNA genome. This DNA is often integrated into the host genome, as in the case of retroviruses and pseudoviruses, where it is replicated and transcribed by the host.

Group VI includes:

• Family Metaviridae
• Family Pseudoviridae
• Family Retroviridae - Retroviruses, e.g. HIV

Group VII

Both families in Group VII have DNA genomes contained within the invading virus particles. The DNA genome is transcribed into both mRNA, for use as a transcript in protein synthesis, and pre-genomic RNA, for use as the template during genome replication. Virally encoded reverse transcriptase uses the pre-genomic RNA as a template for the creation of genomic DNA.

Group VII includes:

• Family Hepadnaviridae - e.g. Hepatitis B virus
• Family Caulimoviridae - e.g. Cauliflower mosaic virus

Treatment

Main article: Antiretroviral drug

Antiretroviral drugs are medications for the treatment of infection by retroviruses, primarily HIV. Different classes of antiretroviral drugs act at different stages of the HIV life cycle. Combination of several (typically three or four) antiretroviral drugs is known as highly active anti-retroviral therapy (HAART).

Treatment of Veterinary Retroviruses

Feline Leukemia Virus and Feline immunodeficiency virus infections are treated with biologics, including Lymphocyte T-Cell Immune Modulator (LTCI)^[9] marketed by IMULAN BioTherapeutics, LLC.

References

1. ^ Jhon M. Coffin (1992). "Structure and Classification of Retroviruses". in Jay A. Levy. The Retroviridae (1st ed.). New York: Plenum Press. pp. 20. ISBN 0-306-44074-1. 
2. ^ Jhon M. Coffin (1992). "Structure and Classification of Retroviruses". in Jay A. Levy. The Retroviridae (1st ed.). New York: Plenum Press. pp. 26–34. ISBN 0-306-44074-1. 
3. ^ Robert Belshaw; Pereira V; Katzourakis A; Talbot G; Paces J; Burt A; Tristem M. (April 2004). "Long-term reinfection of the human genome by endogenous retroviruses". Proc Natl Acad Sci USA 101 (14): 4894–99. doi:10.1073/pnas.0307800101. PMID 15044706. http://www.pubmedcentral.com/articlerender.fcgi?artid=387345. 
4. ^ Medstrand P, van de Lagemaat L, Dunn C, Landry J, Svenback D, Mager D (2005). "Impact of transposable elements on the evolution of mammalian gene regulation". Cytogenet Genome Res 110 (1-4): 342–52. doi:10.1159/000084966. PMID 16093686. 
5. ^ Teklemariam, Ephrem. "HIV drug resistance and its impact on public health". http://mason.gmu.edu/~eteklema/Researchfinal.html. 
6. ^ Svarovskaia ES; Cheslock SR; Zhang WH; Hu WS; Pathak VK. (January 2003). "Retroviral mutation rates and reverse transcriptase fidelity.". Front Biosci. 8: 117–134. doi:10.2741/957. http://www.ncbi.nlm.nih.gov/pubmed/12456349. 
7. ^ ^{a b} Kurth, R; Bannert, N (editors) (2010). Retroviruses: Molecular Biology, Genomics and Pathogenesis. Caister Academic Press. ISBN 978-1-904455-55-4. 
8. ^ Desport, M (editors) (2010). Lentiviruses and Macrophages: Molecular and Cellular Interactions. Caister Academic Press. ISBN 978-1-904455-60-8. 
9. ^ Gingerich DA (2008). "Lymphocyte T-cell immunomodulator (LTCI): Review of the immunopharmacology of a new biologic". Intern J Appl Res Vet Med 6 (2): 61-68. http://jarvm.com/articles/Vol6Iss2/Vol6Iss2Gingerich61-68.pdf. 

External links

• ViralZone A Swiss Institute of Bioinformatics resource for all viral families, providing general molecular and epidemiological information (follow links for "Retro-transcribing viruses")
• Retrovirus Animation (Flash Required)
• Retrovirology Scientific journal
• Retrovirus life cycle chapter From Kimball's Biology (online biology textbook pages)
• NCBI retrovirus book online
• Annals of Science: Darwin’s Surprise, New Yorker Dec 3 2007

v • d • e Microbiology: Virus Components Viral envelope · Capsid · Viral protein Viral life cycle Viral entry · Viral replication · Viral shedding · Virus latency Genetics Reassortment · Antigenic shift · Antigenic drift · Phenotype mixing Other Virus disease · Laboratory diagnosis of viral infections · Antiviral drug · Bacteriophage · Neurotropic virus · Oncovirus

v • d • e Virus: Retroviruses SsRNA-RT virus/ retroviridae Alpharetrovirus Avian Sarcoma Leukosis Virus · Rous sarcoma virus Betaretrovirus Mouse mammary tumor virus Gammaretrovirus Murine leukemia virus · Abelson murine leukemia virus · Feline leukemia virus  · Xenotropic murine leukemia virus-related virus Deltaretrovirus Human T-lymphotropic virus (HTLV-1, HTLV-2) · Bovine leukemia virus Epsilonretrovirus Walleye epidermal hyperplasia virus Lentivirus HIV  · SIV  · FIV  · Puma lentivirus  · EIA  · Bovine immunodeficiency virus  · Caprine arthritis encephalitis virus  · Visna/maedi virus Spumavirus SFV · HFV Other Metaviridae · Pseudoviridae DsDNA-RT virus Hepadnaviridae (Hepatitis B virus) Other Endogenous retrovirus

v • d • e Baltimore (virus classification) DNA   I: dsDNA viruses Caudovirales Myoviridae · Podoviridae · Siphoviridae enveloped: Herpesviridae · Poxviridae nonenveloped: Adenoviridae · Papovaviridae (obsolete) · Papillomaviridae · Polyomaviridae ungrouped: Ascoviridae · Asfarviridae · Baculoviridae · Coccolithoviridae · Corticoviridae · Fuselloviridae · Guttaviridae · Iridoviridae · Lipothrixviridae · Nimaviridae  · Phycodnaviridae · Plasmaviridae · Rudiviridae · Tectiviridae   II: ssDNA viruses non-enveloped: Parvoviridae (Parvovirus B19) ungrouped: Circoviridae · Geminiviridae · Inoviridae · Microviridae · Nanoviridae RNA   III: dsRNA viruses Birnaviridae · Chrysoviridae · Cystoviridae · Hypoviridae · Partitiviridae · Reoviridae (Rotavirus) · Totiviridae   IV: (+)ssRNA viruses (primarily icosahedral) Nidovirales Arteriviridae · Coronaviridae · Roniviridae Astroviridae · Barnaviridae · Bromoviridae · Caliciviridae · Closteroviridae · Comoviridae · Dicistroviridae · Flaviviridae · Flexiviridae · Leviviridae · Luteoviridae · Marnaviridae · Narnaviridae · Nodaviridae · Picornaviridae (Enterovirus, Rhinovirus) · Potyviridae · Sequiviridae · Tetraviridae · Togaviridae (Rubella virus) · Tombusviridae · Tymoviridae   V: (-)ssRNA viruses (primarily helical) Mononegavirales Bornaviridae · Filoviridae · Paramyxoviridae · Rhabdoviridae Arenaviridae · Bunyaviridae · Orthomyxoviridae RT   VI: ssRNA-RT viruses Metaviridae · Pseudoviridae · Retroviridae   VII: dsDNA-RT viruses Hepadnaviridae · Caulimoviridae

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