Background Natural Killer (NK) cells are the most potent effectors of natural immunity. Their ability to lyse virus infected cells as well as produce cytokines and chemokines without prior activation may be important in supporting adaptive immune response in HIV infection. Cellular immune response by NK cells may play a major role in slowing disease progression in HIV-2 infection. Methods Peripheral blood mononuclear cells (PBMC) were obtained from 81 HIV-1, 76 HIV-2 infected and 50 HIV uninfected individuals. Cytotoxic activity and IFNgamma secretion by NK cells in HIV-1 and HIV-2 infections were compared by chromium release and ELISPOT assays respectively, using K562 cells as targets. The HIV infected subjects were of 3 categories: high (CD4>28%), medium (CD4=14-28%) and low (CD4<14%). The high CD4% were 26 HIV-1 and 30 HIV-2; medium categories were 30 HIV-1 and 24 HIV-2, whereas low CD4 were 25 and 22 subjects respectively. The frequency of NK cell population was also measured by flow cytometry. Results Cytolytic activity by NK cells was similar in both HIV-1 and HIV-2 infections at all CD4% categories but showed a significant lower lysis at CD4<14% than in the healthy control (p<0.05). There was significant correlation between frequency of NK population and cytolytic activity in HIV-2 individuals (r=0.52). Level of interferongamma secretion by NK cells was also similar in HIV-1 and HIV-2 infections at CD4<28% and significantly lower than healthy controls (p<0.05). There was however, higher IFNgamma levels in HIV-1 than in HIV-2 infection at CD4>28% but similar to healthy controls. Conclusion Similar cytolytic activity and IFNgamma levels by NK cells in HIV-1 and HIV-2 subjects suggest that effector function may not be influencing slow disease progression in HIV-2 infection. Chemokines levels comparison between the two infections needs to be assessed.
Keywords: AEGIS, HIV-1, Killer Cells, Natural, HIV-2, Interferon Type II, HIV Infections, Antigens, CD4, Acquired Immunodeficiency Syndrome, secretion, Exocytosis, immunology
