biostudies-literatureFunderburg NTNCATS NIH HHSNIAID NIH HHSNHLBI NIH HHS4599-608https://www.ebi.ac.uk/biostudies/studies/S-EPMC3512236biostudies-literatureUnknown120(23)The mechanisms responsible for increased cardiovascular risk associated with HIV-1 infection are incompletely defined. Using flow cytometry, in the present study, we examined activation phenotypes of monocyte subpopulations in patients with HIV-1 infection or acute coronary syndrome to find common cellular profiles. Nonclassic (CD14(+)CD16(++)) and intermediate (CD14(++)CD16(+)) monocytes are proportionally increased and express high levels of tissue factor and CD62P in HIV-1 infection. These proportions are related to viremia, T-cell activation, and plasma levels of IL-6. In vitro exposure of whole blood samples from uninfected control donors to lipopolysaccharide increased surface tissue factor expression on all monocyte subsets, but exposure to HIV-1 resulted in activation only of nonclassic monocytes. Remarkably, the profile of monocyte activation in uncontrolled HIV-1 disease mirrors that of acute coronary syndrome in uninfected persons. Therefore, drivers of immune activation and inflammation in HIV-1 disease may alter monocyte subpopulations and activation phenotype, contributing to a pro-atherothrombotic state that may drive cardiovascular risk in HIV-1 infection.BloodShared monocyte subset phenotypes in HIV-1 infection and in uninfected subjects with acute coronary syndrome.PMC3512236R24 AI067039R37 HL057506AI-670391K99HL108743-01A1U01 AI068636AI-68636KL2 TR000440UM1 AI068636P30 AI036219AI-07164T32 AI089474K99 HL108743Zidar DASimon DIFunderburg NTLioi AMudd JMusselwhite LWSieg SFShive CCosta MALederman MMRodriguez BfalseShared monocyte subset phenotypes in HIV-1 infection and in uninfected subjects with acute coronary syndrome.The mechanisms responsible for increased cardiovascular risk associated with HIV-1 infection are incompletely defined. Using flow cytometry, in the present study, we examined activation phenotypes of monocyte subpopulations in patients with HIV-1 infection or acute coronary syndrome to find common cellular profiles. Nonclassic (CD14(+)CD16(++)) and intermediate (CD14(++)CD16(+)) monocytes are proportionally increased and express high levels of tissue factor and CD62P in HIV-1 infection. These proportions are related to viremia, T-cell activation, and plasma levels of IL-6. In vitro exposure of whole blood samples from uninfected control donors to lipopolysaccharide increased surface tissue factor expression on all monocyte subsets, but exposure to HIV-1 resulted in activation only of nonclassic monocytes. Remarkably, the profile of monocyte activation in uncontrolled HIV-1 disease mirrors that of acute coronary syndrome in uninfected persons. Therefore, drivers of immune activation and inflammation in HIV-1 disease may alter monocyte subpopulations and activation phenotype, contributing to a pro-atherothrombotic state that may drive cardiovascular risk in HIV-1 infection.2012-01-01T00:00:00Z2012 Nov2024-12-03T18:49:02.162Z2019-03-27T01:01:20ZS-EPMC35122362306515110.1182/blood-2012-05-433946