Start Date
2022
Description
A major barrier to eradicating HIV is latent reservoirs in resting CD4+ T cells. Antiretroviral therapy is effective in bringing the viral load down to undetectable levels but is unable to eradicate the latent reservoir. Previous data from our lab revealed that when stimulated by intestinal endothelial cells (IEC), resting CD4+ T cells can be directly infected while remaining in a resting state, allowing formation of latent reservoirs. An additional study found that integrins, which are cell surface molecules, play a role in the interactions between endothelial cells (EC) and T cells. Our research further examines the role of integrins (rhICAM & rhVCAM) in the context of HIV infection. Resting CD4+ T cells were stimulated with integrins, and increased levels of HIV infection were observed. A pro-inflammatory cytokine, IL-6, was previously found to increase productive infection rates in resting CD4+ T cells, and when combined with integrins, infection rates of resting CD4+ T Cells reached those of IEC, indicating that these may be two of the main mechanisms by which HIV-1 infects resting CD4+ T cells. Our studies show that IEC allow HIV infection of resting CD4+ T cells through an integrin dependent manner in conjunction with IL-6
Recommended Citation
Eddy, Jessica; Pham, Fisher; Dapprich, Nathan; and Shen, Anding, "The Role of Integrins in HIV-1 Infection of Intestinal Endothelial Cell Stimulated Resting CD4+ T Cells" (2022). Summer Research. 26.
https://digitalcommons.calvin.edu/summer_research/2022/Posters/26
Included in
The Role of Integrins in HIV-1 Infection of Intestinal Endothelial Cell Stimulated Resting CD4+ T Cells
A major barrier to eradicating HIV is latent reservoirs in resting CD4+ T cells. Antiretroviral therapy is effective in bringing the viral load down to undetectable levels but is unable to eradicate the latent reservoir. Previous data from our lab revealed that when stimulated by intestinal endothelial cells (IEC), resting CD4+ T cells can be directly infected while remaining in a resting state, allowing formation of latent reservoirs. An additional study found that integrins, which are cell surface molecules, play a role in the interactions between endothelial cells (EC) and T cells. Our research further examines the role of integrins (rhICAM & rhVCAM) in the context of HIV infection. Resting CD4+ T cells were stimulated with integrins, and increased levels of HIV infection were observed. A pro-inflammatory cytokine, IL-6, was previously found to increase productive infection rates in resting CD4+ T cells, and when combined with integrins, infection rates of resting CD4+ T Cells reached those of IEC, indicating that these may be two of the main mechanisms by which HIV-1 infects resting CD4+ T cells. Our studies show that IEC allow HIV infection of resting CD4+ T cells through an integrin dependent manner in conjunction with IL-6