Start Date
2023
Description
Eradicating HIV remains a formidable challenge due to the persistence of latent reservoirs within resting CD4+ T cells. Intestinal endothelial cells (IECs) have been shown to promote HIV infection and latent reservoir formation in resting CD4+ T cells. Our research investigates the role of integrins and their ligands, specifically ICAM, VCAM, and MAdCAM, in resting T cells and their impact on productive and latent HIV infection. Findings reveal that VCAM stimulation was the most effective in promoting productive HIV infection. MAdCAM and ICAM had minimal effect. Cytokine IL-6 consistently displayed synergy with all CAMs, amplifying effects on productive HIV infection. VCAM combined with IL-6 surpassed the effect of IEC stimulation in inducing HIV infection in resting T cells. Blocking integrins CD11a (aL), CD49d (a4), or antibody-mediated blocking of MAdCAM in IEC and T cell co-culture did not affect HIV infection. ICAM and VCAM co-stimulation increased latent infection in resting T cells. Addition of IL-6, however, reduced latent infection. This study underscores the role of integrins, particularly VCAM and ICAM, in HIV infection within resting CD4+ T cells and highlights the influence of IL-6 in potentiating these interactions
Recommended Citation
Shen, Anding; Logan, Sarah; Kim, Tim; and Zhang, Zihan, "Role of Integrins in HIV infection of Resting CD4+ T Cells Stimulated by Intestinal Endothelial Cells" (2023). Summer Research. 26.
https://digitalcommons.calvin.edu/summer_research/2023/Posters/26
Included in
Role of Integrins in HIV infection of Resting CD4+ T Cells Stimulated by Intestinal Endothelial Cells
Eradicating HIV remains a formidable challenge due to the persistence of latent reservoirs within resting CD4+ T cells. Intestinal endothelial cells (IECs) have been shown to promote HIV infection and latent reservoir formation in resting CD4+ T cells. Our research investigates the role of integrins and their ligands, specifically ICAM, VCAM, and MAdCAM, in resting T cells and their impact on productive and latent HIV infection. Findings reveal that VCAM stimulation was the most effective in promoting productive HIV infection. MAdCAM and ICAM had minimal effect. Cytokine IL-6 consistently displayed synergy with all CAMs, amplifying effects on productive HIV infection. VCAM combined with IL-6 surpassed the effect of IEC stimulation in inducing HIV infection in resting T cells. Blocking integrins CD11a (aL), CD49d (a4), or antibody-mediated blocking of MAdCAM in IEC and T cell co-culture did not affect HIV infection. ICAM and VCAM co-stimulation increased latent infection in resting T cells. Addition of IL-6, however, reduced latent infection. This study underscores the role of integrins, particularly VCAM and ICAM, in HIV infection within resting CD4+ T cells and highlights the influence of IL-6 in potentiating these interactions