SUMMARYHIV infection is associated with cytokine production by monocytes and expansion of a monocyte subset that expresses high levels of CD16. Our study was designed to investigate the effects of anti-retroviral therapies on these immune parameters. Four groups of HIV 1 patients were included in the study. The first group comprised drug-naive patients (n 20); the second included patients who received two inhibitors of HIV reverse transcriptase (n 45); the third group received a therapy combining these two inhibitors and one inhibitor of HIV protease (HAART) (n 35); the fourth consisted of patients who had stopped their treatment (n 20). The release of inflammatory cytokines (tumour necrosis factor, IL-1b , IL-6) and immunoregulatory cytokines such as IL-10 by monocytes was determined by ELISA. The monocyte subsets expressing low or high levels of CD16 were studied by flow cytometry. Monocytes from patients naive of treatment released higher amounts of inflammatory cytokines and IL-10 than HIV 2 individuals. Each anti-retroviral therapy restored a normal pattern of cytokine secretion. Nevertheless, the release of cytokines increased again after the arrest of the treatment. The expansion of the monocyte subset that expresses high levels of CD16 was significantly decreased by HAART but not by the treatment including two inhibitors of reverse transcriptase. These results suggest that only HAART controls monocyte activation in the treatment of HIV infection.

The circulating levels of immune activation markers, including neopterin, tumor necrosis factor receptor type II, and interleukin-2 receptors, are increased in human immunodeficiency virus-infected patients. We show here that highly active antiretroviral therapy significantly decreased neopterin levels. This effect is reversible, since neopterin levels increased after the arrest of treatment. Their determination may be useful in the evaluation of the efficacy of antiretroviral therapy.

Chronic asymptomatic bacteremia caused by Bartonella quintana occurs in homeless people, but its pathophysiology is unknown. We investigated homeless people with bacteremia to determine whether the persistence of B. quintana is associated with a specific immune profile. Homeless people without B. quintana infection exhibited an inflammatory profile--levels of circulating markers of leukocyte activation (soluble interleukin [IL]-2 receptor and neopterin) and cytokines released by mononuclear cells (tumor necrosis factor, IL-1beta, IL-6, and IL-10) were significantly higher than levels in healthy control subjects. In contrast, homeless people with B. quintana bacteremia exhibited specific increases in IL-10 secretion by mononuclear cells. This overproduction of IL-10 was associated with an attenuated inflammatory profile. The depressed inflammatory response was specific of bacteremia, because patients with specific antibodies and without bacteremia had responses similar to those of homeless people. The overproduction of IL-10 and attenuated inflammatory response may account for the persistence of B. quintana in homeless people.