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Review

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

by
Carsten Münk
1,
Björn-Erik O. Jensen
1,
Jörg Zielonka
1,2,
Dieter Häussinger
1 and
Christel Kamp
3,*
1
Clinic for Gastroenterology, Hepatology and Infectiology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany
2
Roche Glycart AG, Schlieren 8952, Switzerland
3
Paul-Ehrlich-Institut, Federal Institute for Vaccines and Biomedicines, Paul-Ehrlich-Straße 51-59, 63225 Langen, Germany
*
Author to whom correspondence should be addressed.
Viruses 2012, 4(11), 3132-3161; https://doi.org/10.3390/v4113132
Submission received: 25 September 2012 / Revised: 29 October 2012 / Accepted: 5 November 2012 / Published: 14 November 2012
(This article belongs to the Special Issue HIV Dynamics and Evolution)
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Abstract

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

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MDPI and ACS Style

Münk, C.; Jensen, B.-E.O.; Zielonka, J.; Häussinger, D.; Kamp, C. Running Loose or Getting Lost: How HIV-1 Counters and Capitalizes on APOBEC3-Induced Mutagenesis through Its Vif Protein. Viruses 2012, 4, 3132-3161. https://doi.org/10.3390/v4113132

AMA Style

Münk C, Jensen B-EO, Zielonka J, Häussinger D, Kamp C. Running Loose or Getting Lost: How HIV-1 Counters and Capitalizes on APOBEC3-Induced Mutagenesis through Its Vif Protein. Viruses. 2012; 4(11):3132-3161. https://doi.org/10.3390/v4113132

Chicago/Turabian Style

Münk, Carsten, Björn-Erik O. Jensen, Jörg Zielonka, Dieter Häussinger, and Christel Kamp. 2012. "Running Loose or Getting Lost: How HIV-1 Counters and Capitalizes on APOBEC3-Induced Mutagenesis through Its Vif Protein" Viruses 4, no. 11: 3132-3161. https://doi.org/10.3390/v4113132

APA Style

Münk, C., Jensen, B.-E. O., Zielonka, J., Häussinger, D., & Kamp, C. (2012). Running Loose or Getting Lost: How HIV-1 Counters and Capitalizes on APOBEC3-Induced Mutagenesis through Its Vif Protein. Viruses, 4(11), 3132-3161. https://doi.org/10.3390/v4113132

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