Towers Greg J, Goff Stephen P
Wohl Virion Center, Department of Immunology and Molecular Pathology, Windeyer Institute, University College London, 46 Cleveland St., London W1T 4JF, UK.
AIDS Rev. 2003 Jul-Sep;5(3):156-64.
Pathogenic retroviruses have driven the evolution of several dominant-acting mechanisms able to block infection and protect the host. These are exemplified by the mouse gene Fv1, which encodes a Gag-like protein able to protect against murine leukemia virus (MLV) infection. The block is saturable, occurs after reverse transcription and is directed against the viral capsid gene. Several other mammalian species are also able to block MLV infection with the same capsid specificity. A human gene with this activity has been named Ref1. Recently, primates have been shown to restrict a variety of retroviruses only very distantly related to MLVs through a gene named Lv1. Restricted viruses include MLV as well as lentiviruses such as human immunodeficiency viruses 1 and 2, simian immunodeficiency virus and equine infectious anemia virus. In each case the block to one retrovirus can be saturated by co-infection with a second restricted virus. The possible mechanisms of action, and evolutionary consequences of restriction, are reviewed.
致病性逆转录病毒推动了几种主要作用机制的进化，这些机制能够阻止感染并保护宿主。小鼠基因Fv1就是一个例子，它编码一种类似Gag的蛋白质，能够抵御鼠白血病病毒（MLV）感染。这种阻断作用是可饱和的，发生在逆转录之后，并且针对病毒衣壳基因。其他几种哺乳动物也能够以相同的衣壳特异性阻断MLV感染。具有这种活性的人类基因被命名为Ref1。最近发现，灵长类动物通过一种名为Lv1的基因，能够限制多种与MLV亲缘关系非常远的逆转录病毒。被限制的病毒包括MLV以及慢病毒，如人类免疫缺陷病毒1型和2型、猴免疫缺陷病毒和马传染性贫血病毒。在每种情况下，一种逆转录病毒的阻断作用都可以通过与第二种受限制病毒共同感染而饱和。本文综述了可能的作用机制以及限制作用的进化后果。
