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A Comparison of Lower Genital Tract Glycogen and Lactic Acid Levels in Women and Macaques: Implications for HIV and SIV Susceptibility

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posted on 30.04.2012 by Paria Mirmonsef, Douglas Gilbert, Ronald S. Veazey, Jing Wang, Sabrina R. Kendrick, Gregory T. Spear
Understanding factors that affect eterosexual transmission of HIV in women is of great importance. Lactobacilli in the lower genital tract of women utilize glycogen in vaginal epithelial cells as an energy source and produce lactic acid. The resultant vaginal acidity is believed to provide protection against HIV infection. Conversely, bacterial vaginosis (BV) is characterized by less lactic acid and a higher pH, and is associated with increased susceptibility to HIV infection. Because vaginal infection of macaques with simian immunodeficiency virus (SIV) or simian-human immunodeficiency virus (SHIV) is used as a model to study HIV sexual transmission, and because previous studies have shown a paucity of lactobacilli in rhesus macaques’ lower genital tract, we compared lactic acid and glycogen levels in the genital fluid of rhesus and pigtail macaques with levels found in humans. The levels of lactic acid were lower in both rhesus (median = 1.2mol lactate/mg protein) and pigtail macaques (median = 0.7mol/mg) compared to women with healthy genital microbiota (median = 4.2mol/mg). Glycogen levels were significantly lower in both rhesus (median = 0.004 lg glycogen/lg protein) and pigtail macaques (median = 0 lg/lg) than in women (median = 0.2 lg/lg). No significant differences in glycogen or lactate levels were observed comparing longitudinally collected samples from cycling pigtail macaques. These data show that the previously reported scarcity of lactobacilli in macaques correlates with low glycogen and lactic acid levels. These findings have important implications for studies of vaginal infection of macaques with SIV or SHIV and further our understanding of how the bacterial microbiota influences HIV infection.

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Funding

This research was funded by NIH Grants U19 AI076981 and P30 AI082151.

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Publisher Statement

This is a copy of an article published in the IDS Research and Human Retroviruses © 2012 copyright Mary Ann Liebert, Inc; IDS Research and Human Retroviruses is available online at: http://www.liebertonline.com. DOI: 10.1089/aid.2011.0071

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Mary Ann Liebert

Language

en_US

issn

0889-2229

Issue date

01/01/2012

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