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O311 Pathogenesis of non-AIDS morbidities in HIV disease and implications for management

As the ability of highly active antiretroviral therapy (HAART) to suppress virus in a durable and safe manner improves, the inability of HAART to fully restore a normal immune system may emerge as the primary limitation of therapy. Among individuals who initiate HAART at a CD4 cell count <200 and who exhibit a potent and durable virologic response, only 50% are able to achieve normal peripheral CD4+ T cell within the first 10 years of therapy. The inability to restore CD4+ T cell numbers is predicted and perhaps caused by persistent T cell activation on therapy, which in turn may be due to residual HIV replication, persistent microbial translocation, poorly controlled co-infections and/or other mechanisms. Although long-term treated patients with suppressed virus are at low risk for AIDS-related complications, they remain at high risk for significant non-AIDS morbidity, particularly premature cardiovascular disease. Many of these non-AIDS complications are known to be associated with and perhaps caused by chronic inflammation. These data suggest that persistent inflammation during HAART will emerge as primary factor limiting the long-term effectiveness of therapy.

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Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution 2.0 International License (https://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Deeks, S. O311 Pathogenesis of non-AIDS morbidities in HIV disease and implications for management. JIAS 11, O27 (2008). https://doi.org/10.1186/1758-2652-11-S1-O27

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  • DOI: https://doi.org/10.1186/1758-2652-11-S1-O27

Keywords

  • Virologic Response
  • Safe Manner
  • Persistent Inflammation
  • Microbial Translocation
  • Premature Cardiovascular Disease