The hamster polyomavirus--a brief review of recent knowledge

The hamster polyomavirus was first isolated by Graffi et al. in Berlin-Buch from skin epithelioma arising spontaneously in the Buch Syrian hamster colony. Virus particles are assembled in the nuclei of keratinized cell layer. The genome organization is identical to the murine polyomavirus genetic map including, in particular, the existence of a coding capacity for an early gene product analogous to the middle T antigen. The virus and the cloned DNA can immortalize primary cells and transform established cell lines from rodent origin. The HaPV can also induce lymphoma and leukemia after inoculation into newborn animals from a Potsdam Syrian hamster colony geographically separated from the colony affected by the spontaneous epitheliomas. The tumor incidence is high (30-80%), the latency short (4-8 weeks). The lymphomas are virus free but contain large amounts of nonrandomly deleted viral genomes. Transgenic mice produced by microinjection of HaPV DNA into the pronucleus of fertilized eggs of Gat: NMRI mice develop both, epitheliomas and lymphomas. The mice tumors contain extrachromosomal viral DNA. A search for a cellular host fully permissive for HaPV productive cycle in vitro lead to the conclusion that the hamster cells represent the most permissive context for the HaPV genome replication; however, in only one cell line the virus can be propagated by successive productive cycles leading to the establishment of a persistent infection.