梅迪-维斯纳病毒的vif基因对于体内和体外感染至关重要。
The vif gene of maedi-visna virus is essential for infectivity in vivo and in vitro.
作者信息
Kristbjörnsdóttir Helga Bryndís, Andrésdóttir Valgerdur, Svansson Vilhjálmur, Torsteinsdóttir Sigurbjörg, Matthíasdóttir Sigrídur, Andrésson Olafur S
机构信息
Institute for Experimental Pathology, University of Iceland, Keldur, IS-112 Reykjavík, Iceland.
出版信息
Virology. 2004 Jan 5;318(1):350-9. doi: 10.1016/j.virol.2003.09.044.
We have investigated the role of vif in maedi-visna virus (MVV), a lentivirus of sheep, by studying in vitro replication of vif-deleted MVV in several cell types, and the effects of vif deletion on in vivo infection. By measuring RT activity, we found that in comparison to wild-type MVV, growth of vif-deleted MVV was similar in fetal ovine synovial (FOS) cells, highly attenuated in sheep choroid plexus (SCP) cells, and not detectable in macrophages, natural target cells of MVV. Productive infection by vif-deleted MVV could not be demonstrated in sheep. An increased mutation frequency was observed in DNA produced by endogenous reverse transcription of viral RNA in vif-deleted virions, indicating the existence of a factor comparable in action to human APOBEC3G. These results suggest that the vif gene of MVV is essential for infectivity and that the Vif protein protects the viral genome from enpackaged mutagenic activities.
我们通过研究缺失vif的梅迪-维斯纳病毒（MVV，一种绵羊慢病毒）在几种细胞类型中的体外复制以及vif缺失对体内感染的影响，来探究vif在MVV中的作用。通过测量逆转录酶（RT）活性，我们发现，与野生型MVV相比，缺失vif的MVV在胎羊滑膜（FOS）细胞中的生长情况相似，在绵羊脉络丛（SCP）细胞中高度衰减，而在MVV的天然靶细胞巨噬细胞中则无法检测到。在绵羊中未证实缺失vif的MVV能产生有效感染。在缺失vif的病毒粒子中，由病毒RNA的内源性逆转录产生的DNA中观察到突变频率增加，这表明存在一种在作用上与人类载脂蛋白B编辑酶催化多肽样蛋白3G（APOBEC3G）相当的因子。这些结果表明，MVV的vif基因对于感染性至关重要，并且Vif蛋白可保护病毒基因组免受包装过程中的诱变活性影响。
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