Polyomaviridae

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Polyomaviridae
Polyomavirus.jpg
Micrograph showing a polyomavirus infected cell—large (blue) cell below-center-left. Urine cytology specimen.
Virus classification OOjs UI icon edit-ltr.svg
(unranked): Virus
Realm: Monodnaviria
Kingdom: Shotokuvirae
Phylum: Cossaviricota
Class: Papovaviricetes
Order: Sepolyvirales
Family:Polyomaviridae
Genera

Polyomaviridae is a family of viruses whose natural hosts are primarily mammals and birds. [1] [2] As of 2024, there are eight recognized genera. [3] Fourteen species are known to infect humans, while others, such as Simian Virus 40, have been identified in humans to a lesser extent. [4] [5] Most of these viruses are very common and typically asymptomatic in most human populations studied. [6] [7] BK virus is associated with nephropathy in renal transplant and non-renal solid organ transplant patients, [8] [9] JC virus with progressive multifocal leukoencephalopathy, [10] and Merkel cell virus with Merkel cell cancer. [11]

Contents

Structure and genome

A rendering of an icosahedral viral capsid comprising 72 pentamers of murine polyomavirus VP1, colored such that areas of the surface closer to the interior center appear blue and areas nearer to the surface appear red. Rendered from PDB: 1SIE . Mpyv colorbydepth.png
A rendering of an icosahedral viral capsid comprising 72 pentamers of murine polyomavirus VP1, colored such that areas of the surface closer to the interior center appear blue and areas nearer to the surface appear red. Rendered from PDB: 1SIE ​.

Polyomaviruses are non-enveloped double-stranded DNA viruses with circular genomes of around 5000 base pairs. With such a small size, they are ranked among the smallest known double stranded DNA viruses. [12] The genome is packaged in a viral capsid of about 40-50 nanometers in diameter, which is icosahedral in shape (T=7 symmetry). [2] [13] The capsid is composed of 72 pentameric capsomeres of a protein called VP1, which is capable of self-assembly into a closed icosahedron; [14] each pentamer of VP1 is associated with one molecule of one of the other two capsid proteins, VP2 or VP3. [5]

Genome structure of the WU virus, a human polyomavirus. The early region is shown on the left and contains the TAg (tumor antigen) proteins; the late region is on the right and contains the capsid proteins. Gaynor plospathogens 2007 WUvirusgenome.png
Genome structure of the WU virus, a human polyomavirus. The early region is shown on the left and contains the TAg (tumor antigen) proteins; the late region is on the right and contains the capsid proteins.

The genome of a typical polyomavirus codes for between five and nine proteins, divided into two transcriptional regions called the early and late regions due to the time during infection in which they are transcribed. Each region is transcribed by the host cell's RNA polymerase II as a single pre-messenger RNA containing multiple genes. The early region usually codes for two proteins, the small and large tumor antigens, produced by alternative splicing. The late region contains the three capsid structural proteins VP1, VP2, and VP3, produced by alternative translational start sites. Additional genes and other variations on this theme are present in some viruses: for example, rodent polyomaviruses have a third protein called middle tumor antigen in the early region, which is extremely efficient at inducing cellular transformation; SV40 has an additional capsid protein VP4; some examples have an additional regulatory protein called agnoprotein expressed from the late region. The genome also contains a non-coding control or regulatory region containing the early and late regions' promoters, transcriptional start sites, and the origin of replication. [2] [13] [5] [16]

Replication and life cycle

Murine polyomavirus VP1 in complex with the GT1a glycan. GT1a is shown in yellow and the VP1 monomer with a white surface and a blue protein backbone. A complex network of hydrogen bonds, many water-mediated, is shown at the binding surface by orange lines, with participating protein residues shown as sticks. Mutations of the two residues shown in cyan at the bottom of the figure can significantly affect pathogenicity. From PDB: 5CPW . Mpyv vp1 gt1a 5cpw.png
Murine polyomavirus VP1 in complex with the GT1a glycan. GT1a is shown in yellow and the VP1 monomer with a white surface and a blue protein backbone. A complex network of hydrogen bonds, many water-mediated, is shown at the binding surface by orange lines, with participating protein residues shown as sticks. Mutations of the two residues shown in cyan at the bottom of the figure can significantly affect pathogenicity. From PDB: 5CPW ​.

The polyomavirus life cycle begins with entry into a host cell. Cellular receptors for polyomaviruses are sialic acid residues of glycans, commonly gangliosides. The attachment of polyomaviruses to host cells is mediated by the binding of VP1 to sialylated glycans on the cell surface. [2] [13] [16] [17] In some particular viruses, additional cell-surface interactions occur; for example, the JC virus is believed to require interaction with the 5HT2A receptor and the Merkel cell virus with heparan sulfate. [16] [18] However, in general virus-cell interactions are mediated by commonly occurring molecules on the cell surface, and therefore are likely not a major contributor to individual viruses' observed cell-type tropism. [16] After binding to molecules on the cell surface, the virion is endocytosed and enters the endoplasmic reticulum - a behavior unique among known non-enveloped viruses [19] - where the viral capsid structure is likely to be disrupted by action of host cell disulfide isomerase enzymes. [2] [13] [20]

The details of transit to the nucleus are not clear and may vary among individual polyomaviruses. It has been frequently reported that an intact, albeit distorted, virion particle is released from the endoplasmic reticulum into the cell cytoplasm, where the genome is released from the capsid, possibly due to the low calcium concentration in the cytoplasm. [19] Both expression of viral genes and replication of the viral genome occur in the nucleus using host cell machinery. The early genes - comprising at minimum the small tumor antigen (ST) and large tumor antigen (LT) - are expressed first, from a single alternatively spliced messenger RNA strand. These proteins serve to manipulate the host's cell cycle - dysregulating the transition from G1 phase to S phase, when the host cell's genome is replicated - because host cell DNA replication machinery is needed for viral genome replication. [2] [13] [16] The precise mechanism of this dysregulation depends on the virus; for example, SV40 LT can directly bind host cell p53, but murine polyomavirus LT does not. [21] LT induces DNA replication from the viral genome's non-coding control region (NCCR), after which expression of the early mRNA is reduced and expression of the late mRNA, which encodes the viral capsid proteins, begins. [20] As these interactions begin, the LTs belonging to several polyomaviruses, including Merkel cell polyomavirus, present oncogenic potential. [22] Several mechanisms have been described for regulating the transition from early to late gene expression, including the involvement of the LT protein in repressing the early promoter, [20] the expression of un-terminated late mRNAs with extensions complementary to early mRNA, [16] and the expression of regulatory microRNA. [16] Expression of the late genes results in accumulation of the viral capsid proteins in the host cell cytoplasm. Capsid components enter the nucleus in order to encapsidate new viral genomic DNA. New virions may be assembled in viral factories. [2] [13] The mechanism of viral release from the host cell varies among polyomaviruses; some express proteins that facilitate cell exit, such as the agnoprotein or VP4. [20] In some cases high levels of encapsidated virus result in cell lysis, releasing the virions. [16]

Viral proteins

Tumor antigens

The large tumor antigen plays a key role in regulating the viral life cycle by binding to the viral origin of DNA replication where it promotes DNA synthesis. Also as the polyomavirus relies on the host cell machinery to replicate the host cell needs to be in s-phase for this to begin. Due to this, large T-antigen also modulates cellular signaling pathways to stimulate progression of the cell cycle by binding to a number of cellular control proteins. [23] This is achieved by a two prong attack of inhibiting tumor suppressing genes p53 and members of the retinoblastoma (pRB) family, [24] and stimulating cell growth pathways by binding cellular DNA, ATPase-helicase, DNA polymerase α association, and binding of transcription preinitiation complex factors. [25] This abnormal stimulation of the cell cycle is a powerful force for oncogenic transformation.[ citation needed ]

The small tumor antigen protein is also able to activate several cellular pathways that stimulate cell proliferation. Polyomavirus small T antigens commonly target protein phosphatase 2A (PP2A), [26] a key multisubunit regulator of multiple pathways including Akt, the mitogen-activated protein kinase (MAPK) pathway, and the stress-activated protein kinase (SAPK) pathway. [27] [28] Merkel cell polyomavirus small T antigen encodes a unique domain, called the LT-stabilization domain (LSD), that binds to and inhibits the FBXW7 E3 ligase regulating both cellular and viral oncoproteins. [29] Unlike for SV40, the MCV small T antigen directly transforms rodent cells in vitro. [30]

The middle tumor antigen is used in model organisms developed to study cancer, such as the MMTV-PyMT system where middle T is coupled to the MMTV promoter. There it functions as an oncogene, while the tissue where the tumor develops is determined by the MMTV promoter.[ citation needed ]

Capsid proteins

The polyomavirus capsid consists of one major component, major capsid protein VP1, and one or two minor components, minor capsid proteins VP2 and VP3. VP1 pentamers form the closed icosahedral viral capsid, and in the interior of the capsid each pentamer is associated with one molecule of either VP2 or VP3. [5] [31] Some polyomaviruses, such as Merkel cell polyomavirus, do not encode or express VP3. [32] The capsid proteins are expressed from the late region of the genome. [5]

Agnoprotein

The agnoprotein is a small multifunctional phospho-protein found in the late coding part of the genome of some polyomaviruses, most notably BK virus, JC virus, and SV40. It is essential for proliferation in the viruses that express it and is thought to be involved in regulating the viral life cycle, particularly replication and viral exit from the host cell, but the exact mechanisms are unclear. [33] [34]

Taxonomy

The polyomaviruses are members of group I (dsDNA viruses). The classification of polyomaviruses has been the subject of several proposed revisions as new members of the group are discovered. Formerly, polyomaviruses and papillomaviruses, which share many structural features but have very different genomic organizations, were classified together in the now-obsolete family Papovaviridae . [35] (The name Papovaviridae derived from three abbreviations: Pa for Papillomavirus, Po for Polyomavirus, and Va for "vacuolating.") [36] The polyomaviruses were divided into three major clades (that is, genetically related groups): the SV40 clade, the avian clade, and the murine polyomavirus clade. [37] A subsequent proposed reclassification by the International Committee on Taxonomy of Viruses (ICTV) recommended dividing the family of Polyomaviridae into three genera: [38]

The current ICTV classification system recognises six genera and 117 species, of which five could not be assigned a genus. This system retains the distinction between avian and mammalian viruses, grouping the avian subset into the genus Gammapolyomavirus. The six genera are: [39]

The following species are unassigned to a genus: [39]

Description of additional viruses is ongoing. These include the sea otter polyomavirus 1 [40] and Alpaca polyomavirus [41] Another virus is the giant panda polyomavirus 1. [42] Another virus has been described from sigmodontine rodents. [43] Another - tree shrew polyomavirus 1 - has been described in the tree shrew. [44]

Human polyomaviruses

Most polyomaviruses do not infect humans. Of the polyomaviruses cataloged as of 2017, a total of 14 were known with human hosts. [4] However, some polyomaviruses are associated with human disease, particularly in immunocompromised individuals. MCV is highly divergent from the other human polyomaviruses and is most closely related to murine polyomavirus. Trichodysplasia spinulosa-associated polyomavirus (TSV) is distantly related to MCV. Two viruses—HPyV6 and HPyV7—are most closely related to KI and WU viruses, while HPyV9 is most closely related to the African green monkey-derived lymphotropic polyomavirus (LPV).[ citation needed ]

A fourteenth virus has been described. [45] Lyon IARC polyomavirus is related to raccoon polyomavirus.[ citation needed ]

List of human polyomaviruses

The following 14 polyomaviruses with human hosts had been identified and had their genomes sequenced as of 2017: [4]

SpeciesProposed genusVirus nameAbbreviation NCBI RefSeqYear of discoveryClinical correlate (if any)References
Human polyomavirus 5Alpha Merkel cell polyomavirus MCPyV NC_010277 2008 Merkel cell cancer [5] [46] [11] [47]
Human polyomavirus 8Alpha Trichodysplasia spinulosa polyomavirus TSPyV NC_014361 2010 Trichodysplasia spinulosa [5] [48] [49]
Human polyomavirus 9Alpha Human polyomavirus 9 HPyV9 NC_015150 2011None known [50]
Human polyomavirus 12Alpha Human polyomavirus 12 HPyV12 NC_020890 2013None known [51]
Human polyomavirus 13Alpha New Jersey polyomavirus NJPyV NC_024118 2014None known [52]
Human polyomavirus 1Beta BK polyomavirus BKPyV NC_001538 1971Polyomavirus-associated nephropathy; haemorrhagic cystitis [5] [53]
Human polyomavirus 2Beta JC polyomavirus JCPyV NC_001699 1971 Progressive multifocal leukoencephalopathy [5] [54]
Human polyomavirus 3Beta KI polyomavirus KIPyV NC_009238 2007None known [55]
Human polyomavirus 4Beta WU polyomavirus WUPyV NC_009539 2007None known [15]
Human polyomavirus 6Delta Human polyomavirus 6 HPyV6 NC_014406 2010HPyV6 associated pruritic and dyskeratotic dermatosis (H6PD) [56] [32]
Human polyomavirus 7Delta Human polyomavirus 7 HPyV7 NC_014407 2010HPyV7-related epithelial hyperplasia [56] [57] [58] [32]
Human polyomavirus 10Delta MW polyomavirus MWPyV NC_018102 2012None known [59] [60] [61]
Human polyomavirus 11Delta STL polyomavirus STLPyV NC_020106 2013None known [62]
Human polyomavirus 14AlphaLyon IARC polyomavirusLIPyV NC_034253.1 2017None known [63] [64]

Deltapolyomavirus contains only the four human viruses shown in the above table. The Alpha and Beta groups contain viruses that infect a variety of mammals. The Gamma group contains the avian viruses. [4] Clinically significant disease associations are shown only where causality is expected. [5] [65]

Antibodies to the monkey lymphotropic polyomavirus have been detected in humans suggesting that this virus - or a closely related virus - can infect humans. [66]

Clinical relevance

All the polyomaviruses are highly common childhood and young adult infections. [67] Most of these infections appear to cause little or no symptoms. These viruses are probably lifelong persistent among almost all adults. Diseases caused by human polyomavirus infections are most common among immunocompromised people; disease associations include BK virus with nephropathy in renal transplant and non-renal solid organ transplant patients, [8] [9] JC virus with progressive multifocal leukoencephalopathy, [10] and Merkel cell virus (MCV) with Merkel cell cancer. [11]

SV40

SV40 replicates in the kidneys of monkeys without causing disease, but can cause cancer in rodents under laboratory conditions. In the 1950s and early 1960s, well over 100 million people may have been exposed to SV40 due to previously undetected SV40 contamination of polio vaccine, prompting concern about the possibility that the virus might cause disease in humans. [68] [69] Although it has been reported as present in some human cancers, including brain tumors, bone tumors, mesotheliomas, and non-Hodgkin's lymphomas, [70] accurate detection is often confounded by high levels of cross-reactivity for SV40 with widespread human polyomaviruses. [69] Most virologists dismiss SV40 as a cause for human cancers. [68] [71] [72]

Diagnosis

The diagnosis of polyomavirus almost always occurs after the primary infection as it is either asymptomatic or sub-clinical. Antibody assays are commonly used to detect presence of antibodies against individual viruses. [73] Competition assays are frequently needed to distinguish among highly similar polyomaviruses. [74]

In cases of progressive multifocal leucoencephalopathy (PML), a cross-reactive antibody to SV40 T antigen (commonly Pab419) is used to stain tissues directly for the presence of JC virus T antigen. PCR can be used on a biopsy of the tissue or cerebrospinal fluid to amplify the polyomavirus DNA. This allows not only the detection of polyomavirus but also which sub type it is. [75]

There are three main diagnostic techniques used for the diagnosis of the reactivation of polyomavirus in polyomavirus nephropathy (PVN): urine cytology, quantification of the viral load in both urine and blood, and a renal biopsy. [73] The reactivation of polyomavirus in the kidneys and urinary tract causes the shedding of infected cells, virions, and/or viral proteins in the urine. This allows urine cytology to examine these cells, which if there is polyomavirus inclusion of the nucleus, is diagnostic of infection. [76] Also as the urine of an infected individual will contain virions and/or viral DNA, quantitation of the viral load can be done through PCR. [77] This is also true for the blood.

Renal biopsy can also be used if the two methods just described are inconclusive or if the specific viral load for the renal tissue is desired. Similarly to the urine cytology, the renal cells are examined under light microscopy for polyomavirus inclusion of the nucleus, as well as cell lysis and viral partials in the extra cellular fluid. The viral load as before is also measure by PCR.[ citation needed ]

Tissue staining using a monoclonal antibody against MCV T antigen shows utility in differentiating Merkel cell carcinoma from other small, round cell tumors. [78] Blood tests to detect MCV antibodies have been developed and show that infection with the virus is widespread although Merkel cell carcinoma patients have exceptionally higher antibody responses than asymptomatically infected persons. [7] [79] [80] [81]

Use in tracing human migration

The JC virus offers a promising genetic marker for human evolution and migration. [82] [83] It is carried by 70–90 percent of humans and is usually transmitted from parents to offspring. This method does not appear to be reliable for tracing the recent African origin of modern humans.[ citation needed ]

History

Murine polyomavirus was the first polyomavirus discovered, having been reported by Ludwik Gross in 1953 as an extract of mouse leukemias capable of inducing parotid gland tumors. [84] The causative agent was identified as a virus by Sarah Stewart and Bernice Eddy, after whom it was once called "SE polyoma". [85] [86] [87] The term "polyoma" refers to the viruses' ability to produce multiple (poly-) tumors (-oma) under certain conditions. The name has been criticized as a "meatless linguistic sandwich" ("meatless" because both morphemes in "polyoma" are affixes) giving little insight into the viruses' biology; in fact, subsequent research has found that most polyomaviruses rarely cause clinically significant disease in their host organisms under natural conditions. [88]

Dozens of polyomaviruses have been identified and sequenced as of 2017, infecting mainly birds and mammals. Two polyomaviruses are known to infect fish, the black sea bass [89] and gilthead seabream. [90] A total of fourteen polyomaviruses are known to infect humans. [4]

Related Research Articles

<span class="mw-page-title-main">SV40</span> Species of virus

SV40 is an abbreviation for simian vacuolating virus 40 or simian virus 40, a polyomavirus that is found in both monkeys and humans. Like other polyomaviruses, SV40 is a DNA virus that is found to cause tumors in animals, but most often persists as a latent infection. SV40 has been widely studied as a model eukaryotic virus, leading to many early discoveries in eukaryotic DNA replication and transcription.

<span class="mw-page-title-main">Oncovirus</span> Viruses that can cause cancer

An oncovirus or oncogenic virus is a virus that can cause cancer. This term originated from studies of acutely transforming retroviruses in the 1950–60s, when the term oncornaviruses was used to denote their RNA virus origin. With the letters RNA removed, it now refers to any virus with a DNA or RNA genome causing cancer and is synonymous with tumor virus or cancer virus. The vast majority of human and animal viruses do not cause cancer, probably because of longstanding co-evolution between the virus and its host. Oncoviruses have been important not only in epidemiology, but also in investigations of cell cycle control mechanisms such as the retinoblastoma protein.

<span class="mw-page-title-main">BK virus</span> Member of the polyomavirus family

The BK virus, also known as Human polyomavirus 1, is a member of the polyomavirus family. Past infection with the BK virus is widespread, but significant consequences of infection are uncommon, with the exception of the immunocompromised and the immunosuppressed. BK virus is an abbreviation of the name of the first patient, from whom the virus was isolated in 1971. This patient - a male - was then 39 years old, who had developed constriction of the ureter after a renal transplant.

Merkel cell polyomavirus was first described in January 2008 in Pittsburgh, Pennsylvania. It was the first example of a human viral pathogen discovered using unbiased metagenomic next-generation sequencing with a technique called digital transcriptome subtraction. MCV is one of seven currently known human oncoviruses. It is suspected to cause the majority of cases of Merkel cell carcinoma, a rare but aggressive form of skin cancer. Approximately 80% of Merkel cell carcinoma (MCC) tumors have been found to be infected with MCV. MCV appears to be a common—if not universal—infection of older children and adults. It is found in respiratory secretions, suggesting that it might be transmitted via a respiratory route. However, it has also been found elsewhere, such as in shedded healthy skin and gastrointestinal tract tissues, thus its precise mode of transmission remains unknown. In addition, recent studies suggest that this virus may latently infect the human sera and peripheral blood mononuclear cells.

Trichodysplasia spinulosa polyomavirus is a member virus of Human polyomavirus 8 that infects human hosts. First discovered in 2010, TSPyV is associated with Trichodysplasia spinulosa, a rare skin disease only seen in immunocompromised patients. The virus causes hyperproliferation and enlargement of hair follicles by modulating PP2A protein phosphatase signaling pathways. TSPyV was the eighth human polyomavirus to be discovered, and one of four associated with human disease, out of 13 human polyomaviruses known as of the 2015 update to polyomavirus taxonomy released by the International Committee on Taxonomy of Viruses.

<span class="mw-page-title-main">Murine polyomavirus</span> Species of virus

Murine polyomavirus is an unenveloped double-stranded DNA virus of the polyomavirus family. The first member of the family discovered, it was originally identified by accident in the 1950s. A component of mouse leukemia extract capable of causing tumors, particularly in the parotid gland, in newborn mice was reported by Ludwik Gross in 1953 and identified as a virus by Sarah Stewart and Bernice Eddy at the National Cancer Institute, after whom it was once called "SE polyoma". Stewart and Eddy would go on to study related polyomaviruses such as SV40 that infect primates, including humans. These discoveries were widely reported at the time and formed the early stages of understanding of oncoviruses.

<span class="mw-page-title-main">Major capsid protein VP1</span> Protein family

Major capsid protein VP1 is a viral protein that is the main component of the polyomavirus capsid. VP1 monomers are generally around 350 amino acids long and are capable of self-assembly into an icosahedral structure consisting of 360 VP1 molecules organized into 72 pentamers. VP1 molecules possess a surface binding site that interacts with sialic acids attached to glycans, including some gangliosides, on the surfaces of cells to initiate the process of viral infection. The VP1 protein, along with capsid components VP2 and VP3, is expressed from the "late region" of the circular viral genome.

Hamster polyomavirus is an unenveloped double-stranded DNA virus of the polyomavirus family whose natural host is the hamster. It was originally described in 1967 by Arnold Graffi as a cause of epithelioma in Syrian hamsters.

WU polyomavirus is a virus of the family Polyomaviridae. It was discovered in 2007 in samples of human respiratory secretions, originally from a child patient in Australia who presented with clinical signs of pneumonia and in whom other common respiratory viruses were not detected. Follow-up studies identified the presence of WU virus in respiratory secretion samples from patients in Australia and the United States, suggesting that, like other human polyomaviruses, WU virus is widely distributed.

KI polyomavirus is a virus of the family Polyomaviridae. It was discovered in 2007 in stored samples of human respiratory secretions collected by the Karolinska Institute, after which the virus is named.

<span class="mw-page-title-main">Agnoprotein</span> Viral protein found in some polyomaviruses

Agnoprotein is a protein expressed by some members of the polyomavirus family from a gene called the agnogene. Polyomaviruses in which it occurs include two human polyomaviruses associated with disease, BK virus and JC virus, as well as the simian polyomavirus SV40.

Human polyomavirus 6 (HPyV6) is a virus of the polyomavirus family that infects human hosts. It was discovered in 2010 and is a component of the skin flora in healthy adults.

Sorex araneus polyomavirus 1, formerly known as Human polyomavirus 12 (HPyV12), is a virus of the polyomavirus family that was first identified in human hosts and also infects shrews. It was discovered and reported in 2013 after isolation from the organs of the gastrointestinal tract, particularly the liver. The virus was renamed to Sorex araneus polyomavirus 1 in 2018, after discovery of the same virus in shrews. Infecting multiple hosts is rare among mammalian polyomaviruses.

MW polyomavirus is a virus of the polyomavirus family that infects human hosts. It was discovered in 2012 and reported independently by several research groups. It has been identified mostly in stool samples from children and has been detected in a variety of geographic locations.

STL polyomavirus is a virus of the polyomavirus family that infects human hosts. It was first reported in 2013 and is most closely related to MW polyomavirus. It has been identified mostly in stool samples from children and has been detected in a variety of geographic locations.

New Jersey polyomavirus is a virus of the polyomavirus family that infects human hosts. It was first identified in 2014 in a pancreatic transplant patient in New Jersey. It is the 13th and most recent human polyomavirus to be described.

<span class="mw-page-title-main">Large tumor antigen</span>

The large tumor antigen is a protein encoded in the genomes of polyomaviruses, which are small double-stranded DNA viruses. LTag is expressed early in the infectious cycle and is essential for viral proliferation. Containing four well-conserved protein domains as well as several intrinsically disordered regions, LTag is a fairly large multifunctional protein; in most polyomaviruses, it ranges from around 600-800 amino acids in length. LTag has two primary functions, both related to replication of the viral genome: it unwinds the virus's DNA to prepare it for replication, and it interacts with proteins in the host cell to dysregulate the cell cycle so that the host's DNA replication machinery can be used to replicate the virus's genome. Some polyomavirus LTag proteins - most notably the well-studied SV40 large tumor antigen from the SV40 virus - are oncoproteins that can induce neoplastic transformation in the host cell.

<span class="mw-page-title-main">Small tumor antigen</span>

The small tumor antigen is a protein encoded in the genomes of polyomaviruses, which are small double-stranded DNA viruses. STag is expressed early in the infectious cycle and is usually not essential for viral proliferation, though in most polyomaviruses it does improve replication efficiency. The STag protein is expressed from a gene that overlaps the large tumor antigen (LTag) such that the two proteins share an N-terminal DnaJ-like domain but have distinct C-terminal regions. STag is known to interact with host cell proteins, most notably protein phosphatase 2A (PP2A), and may activate the expression of cellular proteins associated with the cell cycle transition to S phase. In some polyomaviruses - such as the well-studied SV40, which natively infects monkeys - STag is unable to induce neoplastic transformation in the host cell on its own, but its presence may increase the transforming efficiency of LTag. In other polyomaviruses, such as Merkel cell polyomavirus, which causes Merkel cell carcinoma in humans, STag appears to be important for replication and to be an oncoprotein in its own right.

The middle tumor antigen is a protein encoded in the genomes of some polyomaviruses, which are small double-stranded DNA viruses. MTag is expressed early in the infectious cycle along with two other related proteins, the small tumor antigen and large tumor antigen. MTag occurs only in a few known polyomaviruses, while STag and LTag are universal - it was first identified in mouse polyomavirus (MPyV), the first polyomavirus discovered, and also occurs in hamster polyomavirus. In MPyV, MTag is an efficient oncoprotein that can be sufficient to induce neoplastic transformation in some cells.

Minor capsid protein VP2 and minor capsid protein VP3 are viral proteins that are components of the polyomavirus capsid. Polyomavirus capsids are composed of three proteins; the major component is major capsid protein VP1, which self-assembles into pentamers that in turn self-assemble into enclosed icosahedral structures. The minor components are VP2 and VP3, which bind in the interior of the capsid.

References

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