| Hamster polyomavirus | |
|---|---|
Virus classification | |
| (unranked): | Virus |
| Realm: | Monodnaviria |
| Kingdom: | Shotokuvirae |
| Phylum: | Cossaviricota |
| Class: | Papovaviricetes |
| Order: | Sepolyvirales |
| Family: | Polyomaviridae |
| Genus: | Alphapolyomavirus |
| Species: | Alphapolyomavirus mauratus |
| Synonyms[1] | |
| |
Hamster polyomavirus (abbreviatedHaPyV orHaPV,[note 1][2] scientific nameAlphapolyomavirus mauratus[1][3]) is anunenvelopeddouble-strandedDNA virus of thepolyomavirus family whose naturalhost is thehamster. It was originally described in 1967 byArnold Graffi as a cause ofepithelioma inSyrian hamsters (Mesocricetus auratus).[4][5]
The organization of the HaPyVgenome is typical of polyomaviruses. At around 5.3kilobase pairs in length, it containsgenes for thesmall,middle, andlarge tumor antigens and threeviral coat proteins,VP1, VP2, and VP3.[4] In the 2015 taxonomic update to the polyomavirus group, theInternational Committee on Taxonomy of Viruses classified HaPyV in thegenusAlphapolyomavirus, whosetype species ismouse polyomavirus (MPyV).[3]
HaPyV and MPyV are closely genetically related; until recently, they were the only two members of the polyomavirus family known to express themiddle tumor antigen protein, which is uniquely efficient at inducingneoplastic transformation in infectedcells, resulting intransformation inin vitrocell culture and in the formation oftumorsin vivo.[6] In 2015 thegenome sequence of a rat polyomavirus was reported to contain middle tumor antigen as well,[7] consistent with expectations that it evolved uniquely in the rodent lineage of the polyomavirus family.[8] However, middle tumor antigen has also recently been reported in at least one virus of unrelated lineage, thetrichodysplasia spinulosa polyomavirus, which is a normally asymptomatic infection in humans that sometimes causestrichodysplasia spinulosa inimmunocompromised individuals.[9]
Following the typical pattern for polyomaviruses, the HaPyVviral capsid contains three proteins: VP1, VP2, and VP3, of which VP1 is the primary component. VP1 monomers assemble into a closedicosahedral structure. However, the HaPyV capsid differs from its close relative MPyV and from another well-studied polyomavirus,SV40, in having aT=7levo rather thandextro symmetry.[10]
Hamster polyomavirus was originally identified in hamsterepithelial tumors, where virus particles can be readily detected. When the virus is injected into juvenile hamsters from naive populations, it inducesleukemias andlymphomas which are free of virus particles but whose cells contain extra-chromosomal viral DNA.[4][11] This observation is in contrast to the skin tumors, which carry substantial viral loads.[4] The capacity to inducehematopoietic tumors is unusual for polyomaviruses[2][4] and may be associated with the properties of the HaPyV middle tumor antigen.[12]
HaPyV has primarily been reported in research colonies; it appeared apparently spontaneously in the colony from which it was first described and in which it becameenzootic.[4] It was also identified in a 2001 case report as naturally occurring in a pet Syrian hamster.[13] It is shed inurine and this is believed to be the mechanism for transmission, similar to what is observed in mouse polyomavirus. While many known hamster viruses are clinically inapparent, HaPyV (along withhamster parvovirus) is unusual in causing clinically significant disease.[2] Thevirulence of HaPyV in Syrian hamsters may be due to cross-species transmission from theEuropean hamster, most likely the naturalhost.[11]