Iwatani Yasumasa
National Hospital Organization Nagoya Medical Center, 4-1-1 San-no-Maru, Naka-ku, Nagoya, Aichi 460-0001, Japan.
Uirusu. 2011 Jun;61(1):67-72. doi: 10.2222/jsv.61.67.
Human cells developed the defense systems against retrovirus infections during the evolutions. These systems include retroviral restrictions by DNA cytidine deaminases of APOBEC3 family (A, B, C, DE, F, G, and H), which are potent factors to block the viral replication by blocking reverse transcription and/or integration and by hypermutating viral cDNA. In case of HIV-1, the viral protein, Vif abrogates the APOBEC3F/G function through specific machinery of ubiquitination and proteasomal degradation. Without Vif, APOBEC3F/G are incorporated into virus particles and block reverse transcription and/or integration in a newly infected cell. Recent advances in our understanding about biochemical and structure-biological characteristics of the enzymes provide new insights to reveal more detailed molecular mechanisms for anti-retroviral activity by APOBEC3 family. Here I briefly review how APOBEC3 proteins block retrovirus replications, focusing on APOBEC3G.
在进化过程中，人类细胞形成了针对逆转录病毒感染的防御系统。这些系统包括APOBEC3家族（A、B、C、DE、F、G和H）的DNA胞嘧啶脱氨酶对逆转录病毒的限制，它们是通过阻断逆转录和/或整合以及使病毒cDNA发生超突变来阻断病毒复制的有效因子。就HIV-1而言，病毒蛋白Vif通过泛素化和蛋白酶体降解的特定机制废除APOBEC3F/G的功能。没有Vif，APOBEC3F/G会被整合到病毒颗粒中，并在新感染的细胞中阻断逆转录和/或整合。我们对这些酶的生化和结构生物学特性的最新认识进展为揭示APOBEC3家族抗逆转录病毒活性的更详细分子机制提供了新的见解。在此，我简要回顾APOBEC3蛋白如何阻断逆转录病毒复制，重点是APOBEC3G。
