Our data suggest that persistent Kaposi’s sarcoma despite apparently effective antiretroviral therapy is not a rare, isolated, or recent phenomenon, as suggested by Maurer and colleagues in their letter to the editor (Sept. 27 issue). 1 On the contrary, our findings indicate that since the introduction of effective antiretroviral therapy, many patients with AIDS-associated Kaposi’s sarcoma have CD4 counts above the level typically associated with susceptibility to opportunistic diseases. Furthermore, although effective HIV suppression has been correlated with regression of Kaposi’s sarcoma after antiretroviral therapy, 2 a substantial proportion of our patients had undetectable HIV viral loads.

These findings raise important questions about the mechanisms that control the progression of human herpesvirus 8 and Kaposi’s sarcoma. They also suggest a need for studies to identify clinically relevant correlates that can distinguish between patients whose Kaposi’s sarcoma responds to antiretroviral therapy and those who do not have such a response. These factors may include age, duration of HIV infection, human herpesvirus 8 viral load, and patterns of viral gene expression within tumors.