We analyzed same-gender couples discordant in their HIV status. The HIV+ partner was homozygous for CCR5 while his receptive HIV- partner was a CCR5Δ32 heterozygote with a C20S missense mutation in his CCR5 allele. The cells from the HIV- partner showed significant resistance to R5 fusion/infection and had no chemotactic response to CCL4 (MIP-1β). We demonstrated abundant CCR5-specific RNA in the HIV- partner’s cells but no detectable CCR5 protein. CCR5 promoter region cloned from each partner’s DNA indicated no significant impact on RNA transcription. The compound effect of CCR5Δ32 and C20S mutation impaired CCR5 coreceptor function and conferred resistance to HIV-1.

Cardiovascular disease affects 1 to 4% of the nearly 4 million pregnancies in the U.S. each year and is the primary cause of pregnancy-related mortality. Adverse pregnancy outcomes (APOs) are associated with cardiovascular complications during pregnancy persisting into the postpartum period. Recently, investigations have identified an altered sex hormone milieu, such as in the case of hyperandrogenism, as a causative factor in the development of gestational cardiovascular dysfunction. The mechanisms involved in the development of cardiovascular disease in postpartum women are largely unknown. Animal studies have attempted to recapitulate adverse pregnancy outcomes to investigate causal relationships and molecular underpinnings of adverse gestational cardiac events and progression to the development of cardiovascular disease postpartum. This review will focus on summarizing clinical and animal studies detailing the impact of adverse pregnancy outcomes, including preeclampsia, gestational diabetes mellitus, and maternal obesity, on gestational cardiometabolic dysfunction and postpartum cardiovascular disease. Specifically, we will highlight the adverse impact of gestational hyperandrogenism and its potential to serve as a biomarker for maternal gestational and postpartum cardiovascular dysfunctions.