Preferential loss of gut-homing a4β7 CD4＋T cells and their circulating functional subsets in acute HIV-1 infection

Preferential infection and depletion of gut-homing a4β7 CD4＋ T cells in the blood are observed in chronic HIV/SIV infection. The dynamic change in gut-homing a4p7 CD4＋ T cells and their functional subsets during the acute stages of HIV-1 infection are less documented. Therefore, we conducted a cohor...

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Published in:中国免疫学杂志：英文版 2016, Vol.13 (6), p.776-784
Main Author: Xiaofan Lu Zhen Li Qunhui Li Yanmei Jiao Yunxia Ji Hongwei Zhang Zhuoming Liu Wei Li Hao Wu
Format: Article
Language:English
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Summary:Preferential infection and depletion of gut-homing a4β7 CD4＋ T cells in the blood are observed in chronic HIV/SIV infection. The dynamic change in gut-homing a4p7 CD4＋ T cells and their functional subsets during the acute stages of HIV-1 infection are less documented. Therefore, we conducted a cohort study to investigate whether acute HIV-1 infection induced abnormalities in gut-homing a4β7 CD4＋ T cells and their functional subsets. We examined the frequency, absolute number, and functionality of gut-homing a4β7 CD4＋ T cells in 26 acute HIV-l-infected patients compared with 20 healthy individuals. We found that circulating gut-homing a4β7 CD4＋ T cells were preferentially depleted during acute HIV-1 infection and were positively correlated with absolute CD4＋ T-cell count in blood. Notably, Th17 and Thl cell subsets of gut-homing CD4＋ T cells were also decreased, which resulted in an imbalance of T helper cells （Th 1）-regulatory T cells （Treg） and Treg.Th 17 ratios. Gut-homing Th17 and Thl cells were also positively correlated with the absolute number of total CD4＋ T cells and gut-homing CD4＋ T cells. The gut-homing Treg：Th17 ratio was inversely correlated with the CD4＋ T-cell count. Taken together, the analyses of our acute HIV-1 cohort demonstrate that gut-homing a4β7 CD4＋ T cells and their functional subsets were profoundly depleted during acute HIV-1 infection, which may have resulted in the persistent loss of circulating CD4＋ T cells and an imbalance of Thl-Treg and Treg.Th17 ratios and contribute to HIV-1 disease pathogenesis.
ISSN:1672-7681
2042-0226