Defect of NK regulation in HIV-infected patients.

In Buenos Aires Argentina health workers obtained peripheral blood samples from 22 HIV-infected people with either no symptoms or persistent lymphadenopathy to examine natural killer cytotoxicity (NKC) of asymptomatic HIV-infected (HIV+AS) cases and the effect of factors that regulate normal NKC. Researchers compared these results with those of 10 healthy heterosexual controls. Even though NK cells of the HIV+AS cases were present in the same numbers and functioned as well as those in the controls an inducer of interferon (Concanavalin A or ConA) could not force the cell system in vitro which demonstrated NK defectiveness. NK response to ConA of HIV+AS cases was lower than that of the healthy controls (p<.05). On the other hand the NK response to a prostaglandin antagonist (Indomethacin or IM) matched that of the healthy controls. Cell supernatants from normal peripheral blood mononuclear cells increased normal NK cell function (p<.001) but those from HIV+AS cases did not do so. Thus it appeared that the HIV+AS cases were unable to produce sufficient NK enhancer factors. Cell supernatants from HIV+AS reduced normal NKC below baseline (p<.05) indicating the presence of NK suppressor factors. The researchers believed products of the arachidonic acid metabolism by the cyclooexgenase pathway maybe PGE2 may have contributed to NK suppression since IM negated suppressor activity of cell supernatants from HIV+AS subjects on normal NK function. They concluded that reduced production of enhancing factors additional release of inhibitory factors and deficiency at the NK effector system are likely to be the underlying causes for NK deficient function in AIDS. They noted that these effects function synergistically.