Cell Biology of HIV: From Immune Cells Dysregulation to HIV-Related Cardiovascular Diseases

Dear Colleagues,

Human immunodeficiency virus (HIV) remains a worldwide burden despite available treatments, such as antiretroviral therapy (ART). ART can durably suppress HIV replication; however, it is not curative as integrated HIV genome persists within CD4+ T cells and perhaps other immune cells. The virus induces dysregulations in major immune cells (T follicular helper (Tfh), CD8+ T cells, macrophages, dendritic cells (DC) from myeloid to plasmacytoid (pDC)) and uses cell-to-cell contact for transmission and dissemination. Thus, HIV infection is accompanied by persistent immune activation despite effective ART and maintained viral suppression. This constant activation of both the innate and adaptive immune systems results in low grade inflammation, leading to circulating proinflammatory and profibrotic cytokines, which may contribute to cardiac and endothelial dysfunction, hypercoagulation, and fibrotic remodeling and increase the risk of cardiovascular disease (CVD) onset in people living with HIV. In fact, HIV+ patients with access to modern ART face a two-fold increased risk of heart failure as compared to non-HIV-infected individuals.

This Special Issue will examine how HIV interferes with immune cell subsets (Tfh, CD8+ T Cells, B cells and myeloid cells) activity in vitro and in vivo after traditional ART or early onset of ART during acute HIV infection. Finally, the special issue will emphasize how HIV interferes with cardiomyocytes function in vitro and how HIV-impaired immune cells activity may lead to higher risk of CVD. 

Dr. Virginie Tardif
Guest Editor

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