Special Issue "HIV Dynamics and Evolution"

Guest Editor
Dr. Viktor Müller
Institute of Biology, Eötvös Loránd University, Pázmány P. s. 1/C, 1117 Budapest, Hungary
Website: http://ramet.elte.hu/~viktor/
E-Mail: mueller.viktor@gmail.com
Phone: +36 1 372 2500/8798
Fax: +36 1 381 2188
Interests: virus dynamics; HIV evolution and epidemiology

Dear Colleagues,

HIV is the youngest of the major human pathogens, yet it has become the leading infectious cause of death worldwide. Thirty years of intensive research have revealed a highly complex disease dynamics, calling for quantitative approaches to interpret the experimental data and to aid the understanding of the underlying processes that govern the dynamics and progression of the disease. This Special Issue of Viruses is open to both empirical and mathematical/modelling papers addressing HIV/SIV dynamics in a broad sense (including within-host, cellular and population level dynamics).

The second focus topic is the evolution of HIV: its origins and historical evolution, its current evolution within the host and at the population level, co-evolution of virus and host, molecular evolution and the evolution of phenotypic traits (e.g. virulence, replication capacity or drug resistance). The Special Issue is open to both phylogenetic and bioinformatics analyses, and to theoretical/modelling approaches to the evolution of HIV and SIV viruses.

Dr. Viktor Müller
Guest Editor

Submission

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Type of Paper: Review
Title: Running Loose or Getting Lost: How HIV-1 Vif Counters and Capitalises APOBEC3
Authors: Carsten Münk ¹ and Christel Kamp ^2,*
Affiliations: ¹ Clinic for Gastroenterology, Hepatology and Infectiology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany; ² Paul-Ehrlich-Institut, Federal Institute for Vaccines and Biomedicines, Langen, Germany; *Corresponding author
Abstract: HIV-1 dynamics in its host is determined through an intricate balance: for replication HI viruses have to rely on host factors while at the same time there is a need to either escape or counter anti-viral restriction factors in host cells. The interaction between the cellular restriction factor APOBEC3 and the HIV-1 protein Vif is a prominent example for this evolutionary arms race: APOBEC3 proteins can induce in vivo hypermutations in HIV-1 to the extent of lethal mutagenesis. The viral Vif protein neutralizes APOBEC3s to a large extent and ensures the production of viable virus particles. HIV-1 also capitalises the APOBEC3-Vif interaction to modulate its mutation rate in harsh or variable environments and therefore represents a model case for adaptation in a co-evolutionary setting. Both experimental evidence and the substantiation of the underlying dynamics through co-evolutionary models are presented as complementary views at a co-evolutionary arms race of clinical relevance.