The use of highly active antiretroviral therapy to control infection with human immunodeficiency virus type 1 (HIV-1) is in many ways a success story. Under optimal circumstances, combinations of drugs that inhibit the viral protease and reverse transcriptase suppress replication to below the limits of detection in the circulation. The production of the virus is stifled at its source in lymphatic tissues, and the large pools of virus stored in that reservoir are reduced to undetectable levels.1,2 The control of viral replication benefits the ravaged immune system, even in the late stages of infection. The numbers of CD4+ T . . .
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Haase et al. (1998) studied this question.
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