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Vaginal concentrations of lactic acid potently inactivate HIV
OBJECTIVES: When Lactobacillus spp. dominate the vaginal microbiota of women of reproductive age they acidify the vagina to pH <4.0 by producing ∼1% lactic acid in a nearly racemic mixture of d- and l-isomers. We determined the HIV virucidal activity of racemic lactic acid, and its d- and l-isome...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3743514/ https://www.ncbi.nlm.nih.gov/pubmed/23657804 http://dx.doi.org/10.1093/jac/dkt156 |
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author | Aldunate, Muriel Tyssen, David Johnson, Adam Zakir, Tasnim Sonza, Secondo Moench, Thomas Cone, Richard Tachedjian, Gilda |
author_facet | Aldunate, Muriel Tyssen, David Johnson, Adam Zakir, Tasnim Sonza, Secondo Moench, Thomas Cone, Richard Tachedjian, Gilda |
author_sort | Aldunate, Muriel |
collection | PubMed |
description | OBJECTIVES: When Lactobacillus spp. dominate the vaginal microbiota of women of reproductive age they acidify the vagina to pH <4.0 by producing ∼1% lactic acid in a nearly racemic mixture of d- and l-isomers. We determined the HIV virucidal activity of racemic lactic acid, and its d- and l-isomers, compared with acetic acid and acidity alone (by the addition of HCl). METHODS: HIV-1 and HIV-2 were transiently treated with acids in the absence or presence of human genital secretions at 37°C for different time intervals, then immediately neutralized and residual infectivity determined in the TZM-bl reporter cell line. RESULTS: l-lactic acid at 0.3% (w/w) was 17-fold more potent than d-lactic acid in inactivating HIV(Ba-L). Complete inactivation of different HIV-1 subtypes and HIV-2 was achieved with ≥0.4% (w/w) l-lactic acid. At a typical vaginal pH of 3.8, l-lactic acid at 1% (w/w) more potently and rapidly inactivated HIV(Ba-L) and HIV-1 transmitter/founder strains compared with 1% (w/w) acetic acid and with acidity alone, all adjusted to pH 3.8. A final concentration of 1% (w/w) l-lactic acid maximally inactivated HIV(Ba-L) in the presence of cervicovaginal secretions and seminal plasma. The anti-HIV activity of l-lactic acid was pH dependent, being abrogated at neutral pH, indicating that its virucidal activity is mediated by protonated lactic acid and not the lactate anion. CONCLUSIONS: l-lactic acid at physiological concentrations demonstrates potent HIV virucidal activity distinct from acidity alone and greater than acetic acid, suggesting a protective role in the sexual transmission of HIV. |
format | Online Article Text |
id | pubmed-3743514 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-37435142013-08-14 Vaginal concentrations of lactic acid potently inactivate HIV Aldunate, Muriel Tyssen, David Johnson, Adam Zakir, Tasnim Sonza, Secondo Moench, Thomas Cone, Richard Tachedjian, Gilda J Antimicrob Chemother Original Research OBJECTIVES: When Lactobacillus spp. dominate the vaginal microbiota of women of reproductive age they acidify the vagina to pH <4.0 by producing ∼1% lactic acid in a nearly racemic mixture of d- and l-isomers. We determined the HIV virucidal activity of racemic lactic acid, and its d- and l-isomers, compared with acetic acid and acidity alone (by the addition of HCl). METHODS: HIV-1 and HIV-2 were transiently treated with acids in the absence or presence of human genital secretions at 37°C for different time intervals, then immediately neutralized and residual infectivity determined in the TZM-bl reporter cell line. RESULTS: l-lactic acid at 0.3% (w/w) was 17-fold more potent than d-lactic acid in inactivating HIV(Ba-L). Complete inactivation of different HIV-1 subtypes and HIV-2 was achieved with ≥0.4% (w/w) l-lactic acid. At a typical vaginal pH of 3.8, l-lactic acid at 1% (w/w) more potently and rapidly inactivated HIV(Ba-L) and HIV-1 transmitter/founder strains compared with 1% (w/w) acetic acid and with acidity alone, all adjusted to pH 3.8. A final concentration of 1% (w/w) l-lactic acid maximally inactivated HIV(Ba-L) in the presence of cervicovaginal secretions and seminal plasma. The anti-HIV activity of l-lactic acid was pH dependent, being abrogated at neutral pH, indicating that its virucidal activity is mediated by protonated lactic acid and not the lactate anion. CONCLUSIONS: l-lactic acid at physiological concentrations demonstrates potent HIV virucidal activity distinct from acidity alone and greater than acetic acid, suggesting a protective role in the sexual transmission of HIV. Oxford University Press 2013-09 2013-05-08 /pmc/articles/PMC3743514/ /pubmed/23657804 http://dx.doi.org/10.1093/jac/dkt156 Text en © The Author 2013. Published by Oxford University Press [on behalf of the British Society for Antimicrobial Chemotherapy]. http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Original Research Aldunate, Muriel Tyssen, David Johnson, Adam Zakir, Tasnim Sonza, Secondo Moench, Thomas Cone, Richard Tachedjian, Gilda Vaginal concentrations of lactic acid potently inactivate HIV |
title | Vaginal concentrations of lactic acid potently inactivate HIV |
title_full | Vaginal concentrations of lactic acid potently inactivate HIV |
title_fullStr | Vaginal concentrations of lactic acid potently inactivate HIV |
title_full_unstemmed | Vaginal concentrations of lactic acid potently inactivate HIV |
title_short | Vaginal concentrations of lactic acid potently inactivate HIV |
title_sort | vaginal concentrations of lactic acid potently inactivate hiv |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3743514/ https://www.ncbi.nlm.nih.gov/pubmed/23657804 http://dx.doi.org/10.1093/jac/dkt156 |
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