Maxwell I H, Spitzer A L, Maxwell F, Pintel D J
University of Colorado Cancer Center, Denver 80262, USA.
J Virol. 1995 Sep;69(9):5829-32. doi: 10.1128/JVI.69.9.5829-5832.1995.
The minute virus of mice, prototype strain MVMp, productively infects cultured murine fibroblasts but not T cells. The immunosuppressive strain, MVMi, shows the converse tropism. These reciprocal tropisms are mediated by the viral capsids, in which their determinants have been mapped to a few specific amino acids in the primary sequence shared by VP1 and VP2. Which of these proteins is relevant in presenting these determinants during infection is not known. We have approached this question using a recombinant parvovirus system in which a LuIII-derived transducing genome, containing the luciferase reporter in place of viral coding sequences, can be packaged by capsid proteins from separate helper sources. We generated transducing virions by using helper constructs expressing either VP1 or VP2, containing the MVMp or MVMi tropic determinant region, in various combinations. The virions were used to infect human NB324K cells and murine A9 fibroblasts. Transduction of the human cells (permissive for both MVMp and MVMi) required both VP1 and VP2 and was successful with all combinations of these proteins. In contrast, significant transducing activity for A9 cells was detected only with recombinant virions containing VP2 of MVMp, while the use of either source of VP1 had little effect. We conclude that VP2 from MVMp is necessary to enable infection of murine A9 fibroblasts.
小鼠微小病毒的原型株MVMp能有效感染培养的鼠源成纤维细胞，但不能感染T细胞。免疫抑制株MVMi则表现出相反的嗜性。这些相互的嗜性由病毒衣壳介导，其决定因素已定位到VP1和VP2共有的一级序列中的几个特定氨基酸上。在感染过程中，这些蛋白质中哪一种与呈现这些决定因素相关尚不清楚。我们使用重组细小病毒系统来解决这个问题，在该系统中，一个源自LuIII的转导基因组，用荧光素酶报告基因代替病毒编码序列，可以由来自不同辅助来源的衣壳蛋白包装。我们通过使用表达VP1或VP2的辅助构建体，以各种组合包含MVMp或MVMi嗜性决定因素区域，产生转导病毒粒子。这些病毒粒子用于感染人NB324K细胞和鼠源A9成纤维细胞。人细胞（对MVMp和MVMi均允许感染）的转导需要VP1和VP2两者，并且这些蛋白质的所有组合都成功实现了转导。相比之下，仅用含有MVMp的VP2的重组病毒粒子检测到对A9细胞有显著的转导活性，而使用任何一种VP1来源的效果都很小。我们得出结论，MVMp的VP2是使鼠源A9成纤维细胞感染所必需的。
