Abstract

Residual HIV-1 disease remains in the vast majority of patients treated with even the most intensive highly active antiretroviral therapy (HAART). There are at least two well-described molecular mechanisms for HIV-1 persistence in these patients.These include proviral latency in resting CD4+ T-cells, as well as ‘cryptic’ residual viral replication. As well, potential sanctuary sites, including the brain and testes, may be important areas which will hinder HIV-1 eradication attempts. It is not clear whether other sites of HIV-1 persistence, including tissue-bound infected monocytes/macrophages, may also be involved in residual HIV-1 disease during virally-suppressive HAART.

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