Infectious Causes of Cancer Codexery

Hamster polyomavirus

A hamster virus causing tumors and expressing middle tumor antigen.

Hamster polyomavirus

Hamster polyomavirus, or HaPyV (formally *Alphapolyomavirus mauratus*), is a non-enveloped virus with a double-stranded DNA genome. Its natural host is the hamster, and it was first identified in 1967 by Arnold Graffi as the agent behind epithelioma in Syrian hamsters. The virus stands out because it can trigger both epithelial tumors and hematopoietic tumors, and it produces a middle tumor antigen that is particularly effective at causing neoplastic transformation.

The HaPyV genome is about 5.3 kilobase pairs long and follows the standard polyomavirus layout, coding for small, middle, and large tumor antigens, plus three capsid proteins: VP1, VP2, and VP3. In the 2015 taxonomic update, the International Committee on Taxonomy of Viruses placed it in the genus *Alphapolyomavirus*, whose type species is mouse polyomavirus (MPyV). HaPyV and MPyV are close genetic relatives; until recently, they were the only polyomaviruses known to express the middle tumor antigen, which efficiently drives neoplastic transformation in cell culture and in living animals. A 2015 report found a rat polyomavirus with this antigen too, suggesting it evolved specifically in rodent lineages. However, the middle tumor antigen has also turned up in a human virus, trichodysplasia spinulosa polyomavirus, which usually causes no symptoms but can lead to disease in immunocompromised people.

The viral capsid is built from VP1, VP2, and VP3, with VP1 forming the main structural component. VP1 monomers assemble into a closed icosahedral shell, but HaPyV’s capsid has a T=7 levo symmetry, differing from the dextro symmetry seen in MPyV and SV40.

HaPyV was first found in hamster epithelial tumors, where virus particles are abundant. When injected into young hamsters from unexposed populations, it causes leukemias and lymphomas that lack virus particles but contain extra-chromosomal viral DNA. This contrasts with skin tumors, which carry high viral loads. The ability to induce blood cancers is unusual for polyomaviruses and may relate to the middle tumor antigen’s properties. The virus has mainly been reported in research colonies, where it appeared spontaneously and became enzootic. A 2001 case report also identified it in a pet Syrian hamster. It is shed in urine, likely the main transmission route, similar to mouse polyomavirus.

Type
Virus
Family
Polyomaviridae
Genus
Alphapolyomavirus
Natural host
Hamster
Genome length
~5.3 kilobase pairs
First described
1967
Discoverer
Arnold Graffi

Lore & Background

Hamster polyomavirus was originally identified in hamster epithelial tumors, where virus particles can be readily detected. When the virus is injected into juvenile hamsters from naive populations, it induces leukemias and lymphomas which are free of virus particles but whose cells contain extra-chromosomal viral DNA. This observation is in contrast to the skin tumors, which carry substantial viral loads. The capacity to induce hematopoietic tumors is unusual for polyomaviruses and may be associated with the properties of the HaPyV middle tumor antigen.

Reader's Guide

Hamster polyomavirus is significant as a model for understanding viral oncogenesis, particularly due to its expression of the middle tumor antigen, which is uniquely efficient at inducing neoplastic transformation in infected cells. Until recently, HaPyV and mouse polyomavirus were the only two polyomaviruses known to express this protein, though a rat polyomavirus and the trichodysplasia spinulosa polyomavirus have since been reported to also contain it. The virus's ability to cause both epithelial tumors and hematopoietic tumors is unusual among polyomaviruses. HaPyV has primarily been reported in research colonies, though it was also identified in a pet Syrian hamster in 2001. It is shed in urine, believed to be the transmission mechanism, and its virulence in Syrian hamsters may be due to cross-species transmission from the European hamster. The virus's capsid differs from close relatives in having T=7 levo symmetry rather than dextro.

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