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n p 12 n p 10 IL-2-related serious adverse events and no significant differences in plasma human immu- nodeficiency virus (HIV) RNA level were observed in the 2 groups. A higher incidence of HIV-related clinical events was observed among patients receiving HAART alone (3/10) than among subjects receiving HAART plus IL-2 (0/12). Significant increases in CD4 + , naive, and CD4 + CD7 + cells and plasma levels of IL-7 were observed in patients receiving IL-2 versus patients receiving HAART alone. A significant increase in cell turnover did not lead to a decrease in the frequency of T cell receptor excision circles, which remained stable. Rather, increased numbers of T cell receptor excision circles per microliter of blood were observed (not statistically significant). Thus, adjuvant IL-2 therapy in immunologic nonresponders resulted in a clinical benefit, suggesting that the quantitative cell recovery involves functionally competent immune cells. Although highly active antiretroviral therapy (HAART) can provide sustained control of human immunodeficiency virus (HIV) replication, it allows for only a partial immune reconsti- tution (1-3). Moreover, up to 27% of HIV-positive patients un- dergoing HAART fail to restore the circulating CD4 T cell compartment, despite good control of HIV plasma viremia ("im- munologic nonresponders" (INRs)) (4-7). Even if several varia- bles have been identified that correlate with the degree of CD4 T cell restoration during HAART (6, 8-10), the actual underlying factors responsible for the inappropriate immune recovery ob- served in INRs have not been completely understood thus far.

Kaposi sarcoma–associated herpesvirus (KSHV)–related multicentric Castleman disease (MCD) is potentially lethal. Growing evidence indicates that, as in Epstein-Barr virus–driven lymphoproliferative disorders after transplantation, KSHV DNA burden in peripheral blood mononuclear cells (PBMCs) may represent the most accurate marker of disease activity. This report describes a patient with human immunodeficiency virus who was followed up clinically and by quantitative polymerase chain reaction for KSHV DNA sequences in PBMCs for more than 3 years following the diagnosis of KSHV-related MCD. Therapy with the antiherpesvirus agent cidofovir, antihuman interleukin-6 antibody BE-8, antiblastic chemotherapy, and combination antiretroviral agents did not achieve durable clinical or virologic remission of the disease. By contrast, administration of the anti-CD20 monoclonal antibody rituximab was well tolerated and allowed a 14-month remission of clinical symptoms and KSHV viremia. Rituximab should be added to the therapeutic armamentarium for KSHV-related MCD.