SUMMARY
Thymic function can become severely compromised with HIV infection. The virus directly infects a variety of thymocyte subsets, including DP cells, SP CD4 cells, and thymic stromal cells, resulting in thymocyte depletion and suppression of thymic output.
HIV directly kills many of the thymocytes it infects by altering intracellular signal transduction pathways; however, the virus can indirectly kill thymocytes by disrupting the thymic microenvironment. Consequently, HIV inhibits thymopoie- sis by direct and indirect mechanisms. In addition, the virus indirectly inhibits hematopoiesis on a more global scale. As a result, the host’s ability to replenish the peripheral T cell pool after depletion by HIV becomes compromised. With the advent of more effective antiretroviral therapies to eliminate viremia, the next immediate challenge will be to develop new strategies to promote thymic output and, thus, restore a diverse T cell repertoire to the host.references
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