Over the years, industrial accidents and military actions have led to unintentional, large-scale, high-dose human exposure to environmental contaminants with endocrine-disrupting action. These historical events, in addition to laboratory studies, suggest that exposure to toxicants such as dioxins and polychlorinated biphenyls negatively impact the reproductive system and likely influence the development of gynecologic diseases. Although high-level exposure to a single toxicant is rare, humans living in industrialized countries are continuously exposed to a complex mixture of manmade and naturally produced endocrine disruptors, including persistent organic pollutants and heavy metals. Since minorities are more likely to live in areas with known environmental contamination; herein, we conducted a literature review to identify potential associations between toxicant exposure and racial disparities in women’s health. Evidence within the literature suggests that the body burden of environmental contaminants, especially in combination with inherent genetic variations, likely contributes to previously observed racial disparities in women’s health conditions such as breast cancer, endometriosis, polycystic ovarian syndrome, uterine fibroids, and premature birth.

APOBEC3G (A3G) restricts HIV-1 replication primarily by reducing viral cDNA and inducing G-to-A hypermutations in viral cDNA. HIV-1 encodes virion infectivity factor (Vif) to counteract A3G primarily by excluding A3G viral encapsidation. Even though the Vif-induced exclusion is robust, studies suggest that A3G is still detectable in the virion. The impact of encapsidated A3G in the HIV-1 replication is unclear. Using a highly sensitive next-generation sequencing (NGS)-based G-to-A hypermutation detecting assay, we found that wild-type HIV-1 produced from A3G-expressing T-cells induced higher G-to-A hypermutation frequency in viral cDNA than HIV-1 from non-A3G-expressing T-cells. Interestingly, although the virus produced from A3G-expressing T-cells induced higher hypermutation frequency, there was no significant difference in viral infectivity, revealing a disassociation of cDNA G-to-A hypermutation to viral infectivity. We also measured G-to-A hypermutation in the viral RNA genome. Surprisingly, our data showed that hypermutation frequency in the viral RNA genome was significantly lower than in the integrated DNA, suggesting a mechanism exists to preferentially select intact genomic RNA for viral packing. This study revealed a new insight into the mechanism of HIV-1 counteracting A3G antiviral function and might lay a foundation for new antiviral strategies.