Start Date
2021
Description
It is generally understood that HIV-1 does not effectively infect resting CD4+ T cells, and latent infection in those cells may arise when activated infected CD4+ T Cells return to a resting state. However, we found that stimulation by intestinal endothelial cells (IEC) can render resting CD4+ T cells permissible for direct HIV infection. Upon infection, these stimulated T cells remain largely phenotypically inactivated. This study was centered around HIV-1 infection in the context of intestinal tissues, as HIV has extensive gut pathology. Endothelial cells are abundant in mucosal tissues and would have direct, constant interactions with CD4+ T Cells in vivo. We also sought to compare intestinal, small intestinal, lymphatic and umbilical cord endothelial cells to compare the levels of direct HIV infection. Our study proposes that next to umbilical cord endothelial cells, sIECs induce the highest levels of HIV infection in resting CD4+ T Cells. We found that microvascular IEC sand LECs are clinically relevant and offer a new mechanism for infection of resting CD4+ T cells in vivo.
Recommended Citation
Eddy, Jessica; Chee, Rachel; Park, Esther; and Shen, Anding, "Intestinal Endothelial Cells Promote HIV-1 Infection in Resting CD4+ T-Cells Without Causing T-Cell Activation" (2021). Summer Research. 30.
https://digitalcommons.calvin.edu/summer_research/2021/Posters/30
Included in
Intestinal Endothelial Cells Promote HIV-1 Infection in Resting CD4+ T-Cells Without Causing T-Cell Activation
It is generally understood that HIV-1 does not effectively infect resting CD4+ T cells, and latent infection in those cells may arise when activated infected CD4+ T Cells return to a resting state. However, we found that stimulation by intestinal endothelial cells (IEC) can render resting CD4+ T cells permissible for direct HIV infection. Upon infection, these stimulated T cells remain largely phenotypically inactivated. This study was centered around HIV-1 infection in the context of intestinal tissues, as HIV has extensive gut pathology. Endothelial cells are abundant in mucosal tissues and would have direct, constant interactions with CD4+ T Cells in vivo. We also sought to compare intestinal, small intestinal, lymphatic and umbilical cord endothelial cells to compare the levels of direct HIV infection. Our study proposes that next to umbilical cord endothelial cells, sIECs induce the highest levels of HIV infection in resting CD4+ T Cells. We found that microvascular IEC sand LECs are clinically relevant and offer a new mechanism for infection of resting CD4+ T cells in vivo.