Species tropism of HIV-1 modulated by viral accessory proteins

Human immunodeficiency virus type 1 (HIV-1) is tropic and pathogenic only for humans, and does not replicate in macaque monkeys routinely used for experimental infections. This specially narrow host range (species tropism) has impeded much the progress of HIV-1/acquired immunodeficiency syndrome (AI...

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Published inFrontiers in microbiology Vol. 3; p. 267
Main Authors Nomaguchi, Masako, Doi, Naoya, Matsumoto, Yui, Sakai, Yosuke, Fujiwara, Sachi, Adachi, Akio
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 01.01.2012
Frontiers Media S.A
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Summary:Human immunodeficiency virus type 1 (HIV-1) is tropic and pathogenic only for humans, and does not replicate in macaque monkeys routinely used for experimental infections. This specially narrow host range (species tropism) has impeded much the progress of HIV-1/acquired immunodeficiency syndrome (AIDS) basic research. Extensive studies on the underlying mechanism have revealed that Vif, one of viral accessory proteins, is critical for the HIV-1 species tropism in addition to Gag-capsid protein. Another auxiliary protein Vpu also has been demonstrated to affect this HIV-1 property. In this review, we focus on functional interactions of these HIV-1 proteins and species specific-restriction factors. In addition, we describe an evolutional viewpoint that is relevant to the species tropism of HIV-1 controlled by the accessory proteins.
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Edited by: Mikako Fujita, Kumamoto University, Japan Yasuyuki Miyazaki, The University of Tokushima Graduate School, Japan
This article was submitted to Frontiers in Virology, a specialty of Frontiers in Microbiology.
Edited by: Mikako Fujita, Kumamoto University, Japan
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2012.00267