HIV-1 evolution under pressure of protease inhibitors: climbing the stairs of viral fitness.
The human immunodeficiency virus (HIV-1) has evolved into a viral quasispecies with a high replication capacity or fitness. Antiretroviral drugs potently inhibit replication of the wild-type virus, but HIV-1 responds by selection of drug-resistant variants. Here we review, in brief, the evolution of resistance to protease inhibitors that is characterized by severe fitness losses and an abundance of subsequent repair strategies. The possibility to restrict HIV-1 fitness is discussed in relation to the control of HIV-1 pathogenesis.
Berkhout
B
B
Department of Human Retrovirology, Academic Medical Center, Amsterdam, The Netherlands. b.berkhout@amc.uva.nl
D019380:Anti-HIV Agents / Q000494:pharmacology*; D004352:Drug Resistance, Microbial / Q000235:genetics; D019143:Evolution, Molecular; D016333:HIV Protease / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D017320:HIV Protease Inhibitors / Q000494:pharmacology*; D015497:HIV-1 / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics* / Q000502:physiology; D006801:Humans; D009154:Mutation / Q000235:genetics; D011499:Protein Processing, Post-Translational / Q000235:genetics; D012641:Selection, Genetic; D014779:Virus Replication / Q000187:drug effects
D019380:Anti-HIV Agents; D017320:HIV Protease Inhibitors; D016333:HIV Protease