Parvovirus B19 infection increases proliferative activity of non-permissive cells

Parvovirus B19 (B19) is associated with a wide spectrum of diseases in humans, including autoimmune disorders and is possibly involved in the pathogenesis of some carcinomas. The appearance of B19 infection in non-permissive cells is poorly explored. Our study demonstrates that B19 virus is able to infect epithelial-like HOS TE85 cells. Although the virus particles were not found, the virus genomic DNA was detected in HOS cells during 3-11 passages. More-over, the expression of B19 VP1 and NS1 mRNAs and the presence VP1/VP2 proteins were revealed in infected cells. The manifestation of B19 infection was dependent on virus dose. At the high dose (5000-8000 virus genomes/cell) massive apoptosis developed on the 6th day after infection and the cells were lost. Morphological and electron microscopy studies showed that the cytopathic effect was associated with apoptotic alteration in HOS cells. At the lower virus dose (100-1000 virus genomes/cell) the B19 infection in HOS cells was accompanied by a 1.5-1.8 times elevated IL-6 level and by 1.5-1.9 times increased proliferative activity of the infected cells. An intact VP1 unique region and a VP1u with a point mutation in the sPLA₂ catalytic site were expressed in E. coli. The intact VP1u protein increased the cells proliferative activity by up to 2-3.5 times in a dose-dependent manner while mutated sPLA₂ deficient VP1u had no effect on the cell proliferation. We suggest that the stimulation of the cells’ proliferation is associated with phospholipase A₂activity of B19 capside protein VP1.