Abstract
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 (AFB1), 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 AFB1 geographic occurrences, mechanisms of action, related co-exposures, personal risk factors, and HIV key determinants of health. AFB1 exposure and HIV sexual transmission hotspots geographically co-localize in many low-income countries. AFB1 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. AFB1 exposure has a positive correlation to HIV viral load, a risk factor for increasing the infectivity of the HIV+ partner. The AFB1 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 AFB1 exposure as a risk factor for HIV transmission, and a modifiable new component for combination HIV prevention efforts.
Highlights
The mucosal surface acts as the initial barrier to HIV acquisition, preventing interactions with underlying epithelial tissues and immunological cells
The most vulnerable sites for sexual transmission of HIV, in order of highest to lowest susceptibility, are colorectal/anal tissues, vaginal tissues, foreskin, and penile/urethra tissues. Factors such as the physical anatomy of the barrier, cellular immunity, soluble factors, and interactions between the epithelial barrier and the local microenvironment, such as mucus and host microbiota can block viral entry [3,4]. Defects to this barrier are a risk factor for microbial infections and HIV acquisition is elevated in individuals with mucosal inflammation, such as those with sexually transmitted infections (STIs) Environmental agents, such as aflatoxin B1, are immunotoxicants have been described in veterinary and toxologic studies, but their potential role as inflammatory agents acting at mucosal sites and contributing to HIV transmission and pathogenesis remains largely unexplored
To shed light on the potential role of immunotoxicants as cofactors in HIV transmission and pathogenesis, we review the mucosal immunotoxic characteristics of environmental pollutants, such as aflatoxin B1, in the context of the local settings where
Summary
The mucosal surface acts as the initial barrier to HIV acquisition, preventing interactions with underlying epithelial tissues and immunological cells. The most vulnerable sites for sexual transmission (mucosal barrier translocation) of HIV, in order of highest to lowest susceptibility, are colorectal/anal tissues, vaginal tissues, foreskin, and penile/urethra tissues (reviewed in [1,2]) Factors such as the physical anatomy of the barrier, cellular immunity, soluble factors, and interactions between the epithelial barrier and the local microenvironment, such as mucus and host microbiota can block viral entry [3,4]. The dietary environmental pollutant and International Agency for Research on Cancer (IARC) class-1 carcinogen, aflatoxin B1 (AFB1 ), is prevalent in many regions with high HIV instances, including China and low and middle income countries in Sub-Saharan Africa and South East Asia [9,10]. Rodent AFB1 exposure models have altered intestinal morphology, including an increase in villus length, width and crypt depth and a decrease in mucus-producing goblet cell number, and a decrease in microflora genera and phyla representation [30,31]
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