<p>In many patients with HIV-1 infection, highly active antiretroviral therapy (HAART) successfully suppresses viral loads and restores the immune system. However, a major latent reservoir identified in resting T helper cells (a type of white blood cells) poses a great barrier to viral eradication and ensures viral persistence in patients. A more complete understanding of the mechanisms contributing to the establishment of the reservoir will influence the strategies in battling viral persistence. Some recent studies demonstrated that endothelial cells increased the level of HIV infection in resting T helper cells and might play a significant role in latency formation in these cells. In this study, a replication incompetent pseudotyped virus system is used to investigate how endothelial cells interact with resting T helper cells to promote HIV infection and latency formation.</p>