Blocking HIV-1 Vif restores a natural mechanism of intracellular antiviral defense.
AIDS has become the greatest pandemic in the human history counting approximately 40 millions people worldwide. To purge HIV-1 infection, new therapeutic approaches need to be searched in alternative and/or in addition to the current pharmacological ones. Recently, several independent laboratories have unveiled a non-immune intracellular anti-HIV-1 defense strategy based on the cytidine deaminase APOBEC3G, which restricts HIV-1 production by directly mutating the proviral DNA in infected cells. To counteract this defense pathway, HIV-1 has developed an evasion strategy by acquiring the accessory protein Vif, which blocks the action of APOBEC3G by inducing its proteasome-mediated degradation.
Bovolenta
Chiara
C
Molmed S.p.A., via Olgettina, 58, 20132 Milano, Italy. chiara.bovolenta@molmed.com
D000818:Animals; D019380:Anti-HIV Agents / Q000494:pharmacology*; D016346:Gene Products, vif / Q000037:antagonists & inhibitors*; D015497:HIV-1 / Q000187:drug effects* / Q000254:growth & development / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000187:drug effects; D007424:Intracellular Fluid / Q000187:drug effects* / Q000276:immunology / Q000821:virology*; D054320:vif Gene Products, Human Immunodeficiency Virus
D019380:Anti-HIV Agents; D016346:Gene Products, vif; D054320:vif Gene Products, Human Immunodeficiency Virus