Journal
MBIO
Volume 5, Issue 3, Pages -Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/mBio.01396-14
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Funding
- NHLBI NIH HHS [R01 HL101274, R01 HL093818] Funding Source: Medline
- NIAID NIH HHS [R37 AI030861, P30 AI087714, P30 AI051519] Funding Source: Medline
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A small percentage of HIV-infected subjects (2 to 15%) are able to control disease progression for many years without antiretroviral therapy. Years of intense studies of virologic and immunologic mechanisms of disease control in such individuals yielded a number of possible host genes that could be responsible for the preservation of immune functions, from immune surveillance genes, chemokines, or their receptors to anti-HIV restriction factors. A recent mBio paper by Rappocciolo et al. (G. Rappocciolo, M. Jais, P. Piazza, T. A. Reinhart, S. J. Berendam, L. Garcia-Exposito, P. Gupta, and C. R. Rinaldo, mBio 5:e01031-13, 2014) describes another potential factor controlling disease progression: cholesterol levels in antigen-presenting cells. In this commentary, we provide a brief background of the role of cholesterol in HIV infection, discuss the results of the study by Rappocciolo et al., and present the implications of their findings.
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