HIV infection persists during antiretroviral therapy (ART) due to a reservoir of latently infected cells that harbor replication-competent virus and evade immunity. Previous ex vivo studies suggested that CD8 T cells from people with HIV may suppress HIV expression via non-cytolytic mechanisms, but the mechanisms responsible for this effect remain unclear. Here, we used a primary cell-based in vitro latency model and demonstrated that co-culture of autologous activated CD8 T cells with HIV-infected memory CD4 T cells promoted specific changes in metabolic and/or signaling pathways resulting in increased CD4 T cell survival, quiescence, and stemness.
View Article and Find Full Text PDFMethods Mol Biol
March 2022
During antiretroviral therapy (ART), HIV-1 persists as a latent reservoir in CD4+ T cell subsets in central (T), transitional (T) and effector memory (T) CD4+ T cells. Understanding the mechanisms that support HIV-1 latency in each of these subsets is essential to the identification of cure strategies to eliminate them. Due to the very low frequency of latently infected cells in vivo, model systems that can accurately reflect the heterogenous population of HIV-1 infected cells are a critical component in HIV cure discoveries.
View Article and Find Full Text PDFBackground: Historically, groups that are most susceptible to health and healthcare disparities have been underrepresented in medical research. It is imperative to explore approaches that can facilitate the recruitment of underrepresented individuals into research studies.
Methods: Two approaches, hospital and community-based recruitment (CBR), were developed and implemented over 36 months to study the genetics of hereditary breast cancer and associated cancers in Alabama, a medically underserved state with double the national percentage of self-identifying African Americans, establishing the Alabama Hereditary Cancer Cohort.