Cater J E, Pintel D J
Department of Molecular Microbiology and Immunology, University of Missouri-Columbia School of Medicine 65212.
J Gen Virol. 1992 Jul;73 ( Pt 7):1839-43. doi: 10.1099/0022-1317-73-7-1839.
Mutants of the autonomous parvovirus minute virus of mice (MVM) strains MVM(p) and MVM(i) that either fail to produce or produce a truncated NS2 protein, were deficient in the production of infectious virus and attained lower levels of viral DNA synthesis than wild-type virus following infection of a series of normal and transformed murine cell lines. Mutant virus growth and the levels of DNA replication were similar to those of wild-type virus in the rat, hamster and human lines tested. These results suggest that the requirement of NS2 for the growth of MVM is murine species-specific.
小鼠自主细小病毒(MVM)的MVM(p)和MVM(i)毒株的突变体,要么无法产生NS2蛋白,要么产生截短的NS2蛋白,在感染一系列正常和转化的鼠细胞系后,其感染性病毒的产生存在缺陷,并且病毒DNA合成水平低于野生型病毒。在测试的大鼠、仓鼠和人类细胞系中,突变病毒的生长和DNA复制水平与野生型病毒相似。这些结果表明,NS2对MVM生长的需求具有鼠类物种特异性。