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Viral Immunol. 2017 Nov;30(9):642-648. doi: 10.1089/vim.2017.0017. Epub 2017 Oct 16.

CD4+ T Memory Stem Cells Correlate with Disease Progression in Chronically HIV-1-Infected Patients.

Lu X1,2, Song B2, Weng W2, Xia H1, Su B1,2, Wu H2, Zhang T2, Li W3, Gao Y2.

Author information

1
1 Beijing Key Laboratory for HIV/AIDS Research , Beijing, People's Republic of China .
2
2 Center for Infectious Disease, Capital Medical University , Beijing, People's Republic of China .
3
3 Center for Interventional Oncology, Beijing You'an Hospital, Capital Medical University , Beijing, People's Republic of China .

Abstract

Recently identified T memory stem (Tscm) cells have stem-cell-like properties, including long lifespan, self-renewal capacity, and multipotency to differentiate into other memory T cell types. In the study of simian immunodeficiency virus (SIV) infection, selective depletion of CCR5+CD4+ Tscm cells and the high proliferation rate of these cells are believed to be responsible for the pathogenesis of SIV-infected rhesus macaques. Here, we conducted a cohort study to investigate the influence of chronic human immunodeficiency virus (HIV)-1 infection on CD4+ Tscm cell homeostasis, and the effect of antiretroviral therapy (ART) on CD4+ Tscm cells. Chronic HIV-1 infection resulted in a decrease of the CD4+ Tscm cell proportion in HIV-1 patients. The decreased number of CD4+ Tscm cells in HIV-1 patients correlated positively with that of circulating CD4+ T cells. Further, the depletion of CD4+ Tscm cells was inversely correlated with an increased level of T cell immune activation during chronic HIV-1 infection. Prolonged ART recovered the CD4+ Tscm cells, and the dynamic change of CD4+ Tscm cells was in parallel with CD4+ T cell restoration and a decrease in the level of T cell immune activation. We propose that the abnormity of CD4+ Tscm cells may contribute to the pathogenesis and disease progression in HIV-1-infected individuals.

KEYWORDS:

HIV-1 pathogenesis; Tscm; disease progression; immune reconstitution

PMID:
29035156
DOI:
10.1089/vim.2017.0017
[Indexed for MEDLINE]

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