Zheng Yong-Hui, Irwin Dan, Kurosu Takeshi, Tokunaga Kenzo, Sata Tetsutaro, Peterlin B Matija
Departments of Medicine, Microbiology, and Immunology, University of California, San Francisco, 3rd and Parnassus Ave., San Francisco, CA 94143-0703, USA.
J Virol. 2004 Jun;78(11):6073-6. doi: 10.1128/JVI.78.11.6073-6076.2004.
Recently, APOBEC3G has been identified as a host factor that blocks retroviral replication. It introduces G to A hypermutations in newly synthesized minus strand viral cDNA at the step of reverse transcription in target cells. Here, we identified the human APOBEC3F protein as another host factor that blocks human immunodeficiency virus type 1 (HIV-1) replication. Similar to APOBEC3G, APOBEC3F also induced G to A hypermutations in HIV genomic DNA, and the viral Vif protein counteracted its activity. Thus, APOBEC family members might have evolved as a general defense mechanism of the body against retroviruses, retrotransposons, and other mobile genetic elements.
最近，载脂蛋白B mRNA编辑酶催化多肽样蛋白3G（APOBEC3G）已被鉴定为一种阻止逆转录病毒复制的宿主因子。在靶细胞的逆转录步骤中，它会在新合成的负链病毒cDNA中引入G到A的超突变。在此，我们鉴定出人类载脂蛋白B mRNA编辑酶催化多肽样蛋白3F（APOBEC3F）蛋白是另一种阻止人类免疫缺陷病毒1型（HIV-1）复制的宿主因子。与APOBEC3G类似，APOBEC3F也会在HIV基因组DNA中诱导G到A的超突变，并且病毒的Vif蛋白会抵消其活性。因此，APOBEC家族成员可能已进化成为机体对抗逆转录病毒、逆转座子和其他可移动遗传元件的一种普遍防御机制。
