Running Loose or Getting Lost: How HIV-1 Counters and Capitalizes on APOBEC3-Induced Mutagenesis through Its Vif Protein

Viruses

Carsten Münk¹  Björn-Erik O. Jensen¹  Jörg Zielonka¹  Dieter Häussinger¹ 

[1] Clinic for Gastroenterology, Hepatology and Infectiology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany;

关键词: HIV-1;    APOBEC3;    Vif;    coevolution;    quasispecies;    population genetics;    modeling;    drug resistance;    escape mutant;   

DOI  :  10.3390/v4113132

来源: mdpi

【 摘 要 】

Human immunodeficiency virus-1 (HIV-1) dynamics reflect an intricate balance within the viruses’ host. The virus relies on host replication factors, but must escape or counter its host’s antiviral restriction factors. The interaction between the HIV-1 protein Vif and many cellular restriction factors from the APOBEC3 protein family is a prominent example of this evolutionary arms race. The viral infectivity factor (Vif) protein largely neutralizes APOBEC3 proteins, which can induce in vivo hypermutations in HIV-1 to the extent of lethal mutagenesis, and ensures the production of viable virus particles. HIV-1 also uses the APOBEC3-Vif interaction to modulate its own mutation rate in harsh or variable environments, and it is a model of adaptation in a coevolutionary setting. Both experimental evidence and the substantiation of the underlying dynamics through coevolutionary models are presented as complementary views of a coevolutionary arms race.

【 授权许可】

CC BY   
© 2012 by the authors; licensee MDPI, Basel, Switzerland.