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CONCLUDING REMARKS

As evidenced by the reduced thymic cellularity, increase in apoptosis, and altered T cell develop­ment, HIV infection strongly affects thymic function. The viability of many thymocyte subsets is impaired either as a direct consequence of HIV infection or through indirect mechanisms.

Variation in cytokine levels or the simple presence of HIV proteins can alter thymocyte susceptibility to apoptosis. Furthermore, HIV affects thymic stromal cell functions, modifying the thymic microen­vironment and leading to a decrease in thymocyte survival. Controlling the viral load after HAART eliminates many of these detrimental effects. However, better comprehension of the mechanisms involved in thymopoiesis will be essential to enhance the immune reconstitution after HAART and may help toward the stimulation of a protective immunity.

acknowledgments

The work from our laboratory supporting this review was funded by the CIHR, the NIH, CANVAC, and Genome Canada. MLD is a recipient of a doctoral research award from the CIHR. RPS holds the Canada Research Chair in Human Immunology and is a senior scientist of the CIHR.

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Source: Badley A.D. (ed.). Cell Death During HIV Infection. Taylor & Francis,2006. — 511 p.. 2006
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