Pupecka Małgorzata, Pacak Andrzej
Institute of Human Genetics Polish Academy of Sciences, 32 Strzeszyńska St., 60-479 Poznań, Poland.
Postepy Biochem. 2006;52(3):247-52.
The editing process may play an essential role in the antiviral cell defense. The human cytidine deaminase APOBEC3G, that catalyses the deoxycytidine to deoxyuridine deamination reaction in the reverse transcript of the HIV-1 genome, leads to instability of the viral DNA, if only HIV-1 virion is defective and lacks the Vif protein. This mechanism has an affect on G-A hipermutation appearing in the provirus DNA and defective HIV-1 viral RNA, yielded in infected cell. Such hipermutation has previously been discovered in the viral HIV-1 genome, produced in peripheral blood mononuclears that were long-term cultured after collection from infected patient. Probably, the deamination reaction that is inhibited in the wild type HIV-1 by the Vif protein, occurs rarely during infection and thus increases viral diversity and drug's resistance. In this review, we present the results of latest studies concerning the mechanism of viral DNA deamination, specifity of this process and APOBEC3G - HIV-1 Vif interactions, that may be useful in designing the new anti-HIV therapies.
编辑过程可能在抗病毒细胞防御中发挥重要作用。人类胞苷脱氨酶APOBEC3G可催化HIV-1基因组逆转录过程中脱氧胞苷向脱氧尿苷的脱氨反应，若HIV-1病毒体有缺陷且缺乏Vif蛋白，会导致病毒DNA不稳定。这种机制影响前病毒DNA中出现的G-A超突变以及受感染细胞中产生的有缺陷的HIV-1病毒RNA。此前已在从感染患者采集后长期培养的外周血单核细胞中产生的病毒HIV-1基因组中发现这种超突变。野生型HIV-1中的Vif蛋白抑制的脱氨反应可能在感染过程中很少发生，从而增加病毒多样性和耐药性。在本综述中，我们展示了有关病毒DNA脱氨机制、该过程的特异性以及APOBEC3G与HIV-1 Vif相互作用的最新研究结果，这些结果可能有助于设计新的抗HIV疗法。
