2016  0,799
2015  0,662
2014  0,740
2013  0,739
2012  0,637
2011  0,658
2010  0,654
2009  0,570
2008  0,849
2007  0,805
2006  0,330
2005  0,435
2004  0,623
2003  0,567
2002  0,641
2001  0,490
2000  0,477
1999  0,762
1998  0,785
1997  0,507
1996  0,518
1995  0,502
Vol 51(2017) N 4 p. 483-495; DOI 10.1134/S0026893317030153 Full Text

D.V. Sosin, N.A. Tchurikov*

Molecular Mechanisms of HIV-1 Genetic Diversity

Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, 119334 Russia

Received - 2016-05-17; Accepted - 2016-09-27

High genetic diversity of HIV-1 is the main factor behind the fact that HIV infection is widespread and difficult to treat. Although a limited number (or only one) of virus particles enters the blood upon infection, the particles are replicated in infected cells and rapidly produce new genetic variants that are resistant to the host immune system and antiretroviral drugs. This circumstance hampers the development of anti-HIV-1 vaccines and requires new antiretroviral drugs to be designed. The cause of the high variation of HIV-1 is related to the properties of its reverse transcriptase, which is error prone and often makes mistakes when transcribing virus RNA. Moreover, host APOBEC3-family proteins deaminate cytosines in the resulting minus strand DNA copy, leading to C/G-T/A transitions. The review considers several mechanisms that generate HIV-1 variants, including multiple recombination events between two different RNA copies colocated within one capsid. To understand the mechanisms of high genetic diversity of HIV-1 is essential for designing basically new approaches to treatment of HIV infection and AIDS.

HIV-1, reverse transcriptase, mutations, recombination, APOBEC