[The innate antiretroviral defense of human cells, based on the DNA editing]

Abstract

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.