Not all retrovirus infections require active viral replication to accelerate the disease course. A good case in point is Adult T-cell Leukemia associated with the human Leukemia Virus, HTLV-1. Once the patient is diagnosed with ATL, there is no sign of virus expression of any kind in the tumor cells. In contrast, clinical progression in AIDS does correlate with elevated level of virus expression and continuous recruitment of new infected cells. There are several important implications from this observation: (1) Regulation of HIV expression by viral and cellular factors play a key role in AIDS pathogenesis. (2) Exogenous factors may contribute to clinical progression. (3) Agents that inhibit the virus replication cycle would be appropriate therapeutic agents. In this paper, I would focus on two regulatory genes of HIV relating to their function and their potential use as targets in antiviral therapy.
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