4th Conference on Retroviruses and Opportunistic Infections Washington, DC - January 22-26, 1997

Conf Retroviruses Opportunistic Infect 1997 Jan 22-26; 4th:65 (abstract no. 1)

Bush CE, Donovan RM, Markowitz NP, Sluchak-Carlsen J, Kvale P, Saravolatz LD
Henry Ford Hospital, Detroit, MI.

Immune activation during opportunistic infection may increase HIV replication, thereby facilitating HIV pathogenesis and also confound the interpretation of HIV RNA viral load measurements. This retrospective study examined the serum HIV RNA level, neopterin level, and CD4 count in 10 subjects prior to the development of PCP, at the time of diagnosis of PCP, and after the resolution of PCP. Patients were either not on antiretroviral therapy (7 patients), or were maintained on antiretroviral monotherapy during the course of PCR (3 patients). The median serum HIV RNA prior to diagnosis of PCP (median time before disease = 81 days) was 113,850 copies per mL. At the time of diagnosis of PCP, the median serum HIV RNA was 231,450 copies per mL (P=.03). Nine of 10 patients had increased HIV RNA levels upon developing PCP, and 5 of these were 3x baseline or more. The median serum HIV RNA after resolution of PCP (median assay time after diagnosis = 108 days) was 198,500 copies per mL, and 7 of 10 patients had decreased RNA levels compared with levels at time of diagnosis. The median CD4 count prior to PCP was 103/µL, at diagnosis of PCP was 52/µL (P=.04), and after resolution of disease was 36/µL (P=.03). Overall, 9 of the 10 patients lost CD4+ cells over the illness (median loss of 43 CD4+ cells). The median neopterin level prior to PCP was 10 ng/mL and did not change during disease or recovery. In conclusion, PCP was associated with a significant and usually transient increase in HIV RNA, and an overall decline in CD4+ cells.

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