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Family: Polyomaviridae
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Definition
The genome is not segmented and contains a single molecule of circular supercoiled double-stranded DNA that forms a covalently closed circle. Used to be a genus in the now obsolete family 47. Papovaviridae

A family of small, non-enveloped DNA viruses, infecting mainly mammals, and containing a single genus: [|POLYOMAVIRUS].

Morphology


Virions have a simple construction (round or elongated or spherical, [|unenveloped] virions); consist(s) of a capsid (including inner and outer capsid). Virus [|capsid]is not enveloped. Capsid/nucleocapsid is round; exhibits [|icosahedral symmetry]; with a triangulation number (T=7). Capsid is or isometric. Rounded capsid (including outer capsid shell) has a diameter of 40 to 55 nm. Capsids with icosahedral symmetry appear round. The surface capsomer arrangement is clearly visible. The capsid consists of 72 [|capsomers]. Surface projections are small (surface appears rough). Isometric capsids can be penetrated by stain and some appear dark in the center; morphologically aberrant forms are observed. These are filamentous or tubular in form as result of aberrant maturation.

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Physical and Physiochemical Properties
Virions have a buoyant density in CsCl of 1.34 g cm-3.

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**Nucleic Acid**
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 * The Mr of the genome constitutes 10 to 13 % of the virion by weight.
 * The genome is not segmented
 * Contains a single molecule of circular supercoiled double-stranded DNA that forms a covalently closed circle.
 * Segment 1 (DNA) is sequenced
 * Complete sequence is 5300 to 8000 nucleotides
 * The genome has a guanine + cytosine content of 40 to 50 %.

**Proteins**
The viral genome encodes structural proteins. There are 3 capsid proteins, VP1-3, which form 72 pentameric capsomers, 60 hexagonally co-ordinated + 12 pentamerically co-ordinated (at the vertices). Each virion contains 360 copies of VP1 (i.e. 72 x 5) + 30-60 copies each of VP2 & VP3, i.e. ~1 copy/pentamer. Each copy of VP1 has a sialic acid binding site on the surface & these form the receptor-binding site for the virus; hence the particles have haemagglutinating properties. VP2/3 have overlapping sequences - VP2 contains the entire sequence of VP3 at its C-terminus, +115 aa at the N-terminus. The precise location of VP2/3 is unknown. VP2 is myristylated at its NH2-terminus, which is believed to be important in holding the particle together (c.f. picornavirus VP4).

The origin of replication is surrounded by non-coding regions which control transcription. VP1 is encoded by a "dedicated" ORF, but the VP2 and 3 genes overlap so that VP3 is contained within VP2. SV40, BKV and JCV encode a small (60-70aa) protein known as the agnoprotein which enhances assembly of virus particles & cell to cell spread. Polyomaviruses also encode "T-antigens" - proteins which can be detected by sera from animals bearing polyomavirus-induced tumours.

These proteins have common N-terminal regions but unique COOH-termini derived from alternative splicing patterns. ([|source])

**Lipids**
Lipids are absent.

**Carbohydrates**
The polyomaviruses use a range of glycans for attachment and cell entry, depending on the virus type. For the simian virus SV40 and murine polyomavirus, the receptors have been identified as gangliosides GM1 and GT1b/GD1a, respectively. The human BK polyomavirus binds to sialylated glycans that include gangliosides GD1b and GT1b. The human JC polyomavirus uses sialylated glycans as well as the serotonin receptor 5HT2aR as attachment receptors. The receptors for other polyomaviruses, such as the recently identified Merkel Cell Polyomavirus, have not been characterized, but at least some of these are likely to also use glycans for cell attachment. Participating investigators (PIs) of the CFG have made major contributions to our understanding of the structural and functional basis of attachment of polyomaviruses to their receptors.

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**Replication Cycle of the Viruses in Host**
Polyomaviruses are first adsorbed and endocytosed by the host cell and transported to the nucleus. In the nucleus, the virus is uncoated and transcription and translation (T proteins) of early region mRNAs takes place. Viral DNA is then replicated and late region mRNAs are transcribe and translated (capsid proteins). The next generation of virions are assembled in the nucleus after which they are transported in vesicles and are released by cell membrane fusion exocytosis. ([|source])


 * Hosts**

During its life cycle, virus infects a single type of vertebrate host. Viral hosts belong to the Domain Eucarya.

Taxonomy

 * Family: Polyomaviridae (1 Genus)
 * Genus: Polyomavirus (13 Species) ([|Wikipedia], [|NCBI taxonomy])
 * Species: African green monkey polyomavirus ([|NCBI taxonomy])
 * Species: Baboon polyomavirus 1 ([|NCBI taxonomy])
 * Species: BK polyomavirus ([|Wikipedia], [|NCBI taxonomy])
 * Species: Bovine polyomavirus ([|NCBI taxonomy])
 * Species: Budgerigar fledgling disease polyomavirus ([|NCBI taxonomy])
 * Species: Hamster polyomavirus ([|NCBI taxonomy])
 * Species: Human polyomavirus ([|Centers for Disease Control and Prevention])
 * Species: JC polyomavirus ([|Wikipedia], [|NCBI taxonomy])
 * Species: Murine pneumotropic virus ([|NCBI taxonomy])
 * Species: Murine polyomavirus ([|NCBI taxonomy])
 * Species: Rabbit kidney vacuolating virus ([|NCBI taxonomy])
 * Species: Simian virus 12 ([|NCBI taxonomy])
 * Species: Simian virus 40 ([|Wikipedia], [|NCBI taxonomy])

The full list of Polyomavirus (Family Polyomaviridae): [|NCBI taxonomy browser], [|ICTV virus taxonomy]

**Pathogenic Polyomavirus**
There are several polyomaviruses causing human diseases.

The 2 human polyoma species, JC and BK, were isolated from patients with the same initials in 1971. BK was isolated from the urine of a person 4 months after renal transplantation. JC was first isolated from the brain from a patient suffering from Hodgkin's disease, and suffering from PML.

BK virus (BKV) and JC virus (JCV) are two of the most common widespread human polyomaviruses, and their pathogenic potential is well known during immunodeficiency.

Clinically significant infections/ disease caused by BK-viruses are primarily seen in the urinary tract, i.e., the bladder and kidneys, whereas JC-viruses mainly cause neurologic disorders, i.e., progressive multifocal leukoencephalopathy.

Approximately 80% of the adult population worldwide is [|seropositive] for JCV and BKV [[|1], [|2]].

The primate polyomavirus SV40 was discovered in 1960 as a passenger virus in cultures of rhesus monkey cells.

Polyomavirus SV40 is significantly associated with some cancers in humans, including malignant mesothelioma, ependymomas, osteosarcoma, and non-Hodgkin lymphoma.

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