4.4 Article

T-cell dynamics during acute SIV infection

Journal

AIDS
Volume 18, Issue 1, Pages 13-23

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00002030-200401020-00002

Keywords

naive; memory; SIV; acute infection; rhesus macaque; T and B cells; mucosal T cells; coreceptor

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Objectives: To delineate T-cell dynamics during acute SIV infection, particularly of phenotypically defined memory T cell subsets. Design: T cells are a heterogeneous mix of naive and memory subsets delineated by simultaneously measuring CD4, CD8, CD45RA/RO, CD11a, CD28, and CD27. The effects of SIV infection on these subsets was measured to evaluate the impact of changes in functionally distinct cell types during pathogenesis. Methods: Peripheral blood was obtained from six SIV-infected macaques at multiple times before and after SIV infection and analyzed using 12-color flow cytometry. Results: Acute infection was characterized by an initial lymphopenia caused by a decline in B cells. Total T-cell counts remained steady during the early acute phase; however, CD4 cell counts declined while CD8 T cells increased. The decline in CD4 T cells was a result of a decline in both naive and memory cells. CCR5+ or CD103+ subsets of CD4 T cells were depleted but only partially accounted for the decline of CD4 memory T cells, suggesting that acute infection was associated with a rapid redistribution of T cells from the periphery. Naive CD8 cell counts declined while memory CD8 cell counts increased. The increase coincided with declines in plasma viremia and was made up initially of CD27-CD28- (effector) cells; subsequently, the predominant phenotype became CD27+CD28-, akin to central memory cells. Conclusions: A complete understanding of the T-cell dynamics during acute SIV or HIV infection requires the simultaneous evaluation of a broad spectrum of T-cell subsets. Changes in homeostasis and associated immunopathogenesis can no longer be accurately described simply by measuring naive and memory T-cell subsets. (C) 2004 Lippincott Williams Wilkins.

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