Human immunodeficiency virus type 1 infection of human monocytes and macrophages does not alter their ability to generate an oxidative burst.
Human immunodeficiency virus type 1 (HIV-1) infects mononuclear phagocytes, cells that may serve as a reservoir for viral persistence. Infection with HIV-1 leads to progressive compromise of the immune system, resulting in infections with opportunistic pathogens and eventual death. Experiments were designed to determine if in vitro HIV-1 infection of mononuclear phagocytes would diminish their oxidative capabilities, thus decreasing their antimicrobial effectiveness. Blood monocytes and peritoneal macrophages were obtained from uninfected donors and inoculated with a monocytotropic strain of HIV-1. Hydrogen peroxide production and reduction of nitroblue tetrazolium were measured after acute stimulation of cells with PMA or a phagocytic stimulus. Despite vigorous virus production, no difference was seen in oxidative burst between uninfected cells and infected cells or between monocyte-derived and peritoneal macrophages. In conclusion, reduced antimicrobial activity of HIV-infected mononuclear phagocytes is probably not secondary to decreased ability to generate reactive oxygen species.
Dukes
C S
CS
Department of Medicine, Duke University Medical Center, Durham, North Carolina.
Matthews
T J
TJ
Weinberg
J B
JB
D002478:Cells, Cultured; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism / Q000382:microbiology*; D009000:Monocytes / Q000382:microbiology*; D016897:Respiratory Burst; D014779:Virus Replication
D006861:Hydrogen Peroxide