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Environmental Pollutants, Mucosal Barriers, and Pathogen Susceptibility; The Case for Aflatoxin B(1) as a Risk Factor for HIV Transmission and Pathogenesis
HIV transmission risk is dependent on the infectivity of the HIV+ partner and personal susceptibility risk factors of the HIV− partner. The mucosal barrier, as the internal gatekeeper between environment and self, concentrates and modulates the internalization of ingested pathogens and pollutants. I...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8537633/ https://www.ncbi.nlm.nih.gov/pubmed/34684180 http://dx.doi.org/10.3390/pathogens10101229 |
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author | Madeen, Erin P. Maldarelli, Frank Groopman, John D. |
author_facet | Madeen, Erin P. Maldarelli, Frank Groopman, John D. |
author_sort | Madeen, Erin P. |
collection | PubMed |
description | HIV transmission risk is dependent on the infectivity of the HIV+ partner and personal susceptibility risk factors of the HIV− partner. The mucosal barrier, as the internal gatekeeper between environment and self, concentrates and modulates the internalization of ingested pathogens and pollutants. In this review, we summarize the localized effects of HIV and dietary toxin aflatoxin B1 (AFB(1)), a common pollutant in high HIV burden regions, e.g., at the mucosal barrier, and evidence for pollutant-viral interactions. We compiled literature on HIV and AFB(1) geographic occurrences, mechanisms of action, related co-exposures, personal risk factors, and HIV key determinants of health. AFB(1) exposure and HIV sexual transmission hotspots geographically co-localize in many low-income countries. AFB(1) distributes to sexual mucosal tissues generating inflammation, microbiome changes and a reduction of mucosal barrier integrity, effects that are risk factors for increasing HIV susceptibility. AFB(1) exposure has a positive correlation to HIV viral load, a risk factor for increasing the infectivity of the HIV+ partner. The AFB(1) exposure and metabolism generates inflammation that recruits HIV susceptible cells and generates chemokine/cytokine activation in tissues exposed to HIV. Although circumstantial, the available evidence makes a compelling case for studies of AFB(1) exposure as a risk factor for HIV transmission, and a modifiable new component for combination HIV prevention efforts. |
format | Online Article Text |
id | pubmed-8537633 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-85376332021-10-24 Environmental Pollutants, Mucosal Barriers, and Pathogen Susceptibility; The Case for Aflatoxin B(1) as a Risk Factor for HIV Transmission and Pathogenesis Madeen, Erin P. Maldarelli, Frank Groopman, John D. Pathogens Review HIV transmission risk is dependent on the infectivity of the HIV+ partner and personal susceptibility risk factors of the HIV− partner. The mucosal barrier, as the internal gatekeeper between environment and self, concentrates and modulates the internalization of ingested pathogens and pollutants. In this review, we summarize the localized effects of HIV and dietary toxin aflatoxin B1 (AFB(1)), a common pollutant in high HIV burden regions, e.g., at the mucosal barrier, and evidence for pollutant-viral interactions. We compiled literature on HIV and AFB(1) geographic occurrences, mechanisms of action, related co-exposures, personal risk factors, and HIV key determinants of health. AFB(1) exposure and HIV sexual transmission hotspots geographically co-localize in many low-income countries. AFB(1) distributes to sexual mucosal tissues generating inflammation, microbiome changes and a reduction of mucosal barrier integrity, effects that are risk factors for increasing HIV susceptibility. AFB(1) exposure has a positive correlation to HIV viral load, a risk factor for increasing the infectivity of the HIV+ partner. The AFB(1) exposure and metabolism generates inflammation that recruits HIV susceptible cells and generates chemokine/cytokine activation in tissues exposed to HIV. Although circumstantial, the available evidence makes a compelling case for studies of AFB(1) exposure as a risk factor for HIV transmission, and a modifiable new component for combination HIV prevention efforts. MDPI 2021-09-23 /pmc/articles/PMC8537633/ /pubmed/34684180 http://dx.doi.org/10.3390/pathogens10101229 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Madeen, Erin P. Maldarelli, Frank Groopman, John D. Environmental Pollutants, Mucosal Barriers, and Pathogen Susceptibility; The Case for Aflatoxin B(1) as a Risk Factor for HIV Transmission and Pathogenesis |
title | Environmental Pollutants, Mucosal Barriers, and Pathogen Susceptibility; The Case for Aflatoxin B(1) as a Risk Factor for HIV Transmission and Pathogenesis |
title_full | Environmental Pollutants, Mucosal Barriers, and Pathogen Susceptibility; The Case for Aflatoxin B(1) as a Risk Factor for HIV Transmission and Pathogenesis |
title_fullStr | Environmental Pollutants, Mucosal Barriers, and Pathogen Susceptibility; The Case for Aflatoxin B(1) as a Risk Factor for HIV Transmission and Pathogenesis |
title_full_unstemmed | Environmental Pollutants, Mucosal Barriers, and Pathogen Susceptibility; The Case for Aflatoxin B(1) as a Risk Factor for HIV Transmission and Pathogenesis |
title_short | Environmental Pollutants, Mucosal Barriers, and Pathogen Susceptibility; The Case for Aflatoxin B(1) as a Risk Factor for HIV Transmission and Pathogenesis |
title_sort | environmental pollutants, mucosal barriers, and pathogen susceptibility; the case for aflatoxin b(1) as a risk factor for hiv transmission and pathogenesis |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8537633/ https://www.ncbi.nlm.nih.gov/pubmed/34684180 http://dx.doi.org/10.3390/pathogens10101229 |
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