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Increased HLA-DR Expression on Peripheral Blood Monocytes in Subsets of Subjects With Primary HIV Infection Is Associated With Elevated CD4 T-Cell Apoptosis and CD4 T-Cell Depletion.

Gascon, Ronnie L.; Narváez, Amy B.; Zhang, Rongzhen; Kahn, James O.; Hecht, Frederick M.; Herndier, Brian G.; McGrath, Michael S.
JAIDS Journal of Acquired Immune Deficiency Syndromes: June 1, 2002
doi: 10.1097/01.QAI.0000017720.31903.6E
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: Whereas T-cell activation parameters of HIV disease have been extensively studied, the activation status of circulating monocytes has received less attention. Sixty-one subjects with primary HIV infection were evaluated by fluorescentactivated cell sorter (FACS) analysis at baseline (pretreatment) for CD4 T-cell count, CD4 T-cell apoptosis, and immune activation. A subset of 15 subjects with marked elevated (3 standard deviations above normal) monocyte DR expression had significantly reduced CD4 T-cell counts at baseline (p < .01) when compared with 46 subjects without monocyte activation. Ten subjects who presented with elevated levels of both CD14/DR, and CD4/CD38, had higher CD4 T-cell apoptosis (p < .001), and lower CD4 T-cell counts (p < .001) and higher baseline plasma HIV RNA (p < .01) than 21 subjects without elevated CD14/DR and CD4/CD38 coexpression. Fifty subjects were subsequently evaluated for immune cell activation over 24 weeks postinitiation of highly active antiretroviral therapy (HAART). A subgroup of 5 subjects who had persistent CD14/DR activation showed continuous depression of CD4 T-cell counts persisting for up to 2 years. The CD4 T-cell counts of this subgroup were significantly lower, at all time points, in comparison to 35 subjects who lacked any persistent expression of monocyte or CD4 T-cell activation (at 24 weeks, p < .002). We conclude that monocyte activation as defined by elevation of CDI4/DR expression correlates to CD4 T-cell depletion in primary HIV infection, and is predictive of a poor CD4 T-cell response to HAART in a subset of patients.

(C) 2002 Lippincott Williams & Wilkins, Inc.