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Front Med. 2017 Dec;11(4):536-547. doi: 10.1007/s11684-017-0592-x. Epub 2017 Nov 27.

Irreversible phenotypic perturbation and functional impairment of B cells during HIV-1 infection.

Author information

1
Shanghai Public Health Clinical Center & Institutes of Biomedical Sciences, Fudan University, Shanghai, 201508, China.
2
Shanghai Public Health Clinical Center & Institutes of Biomedical Sciences, Fudan University, Shanghai, 201508, China. xujianqing@shphc.org.cn.
3
Shanghai Public Health Clinical Center & Institutes of Biomedical Sciences, Fudan University, Shanghai, 201508, China. zhangxiaoyan@shphc.org.cn.

Abstract

Human immunodeficiency virus type 1 (HIV-1) infection can damage humoral immunity. The knowledge of B cell perturbations during chronic HIV-1 infection and their recovery after combined antiretroviral therapy (cART) is not complete yet, and thus attempts to further improve humoral immunity are impeded. In this study, an HIV-1 chronically infected cohort with similar demographics, infection history, genetic background, and HIV-1 genotype was established to probe B cell perturbations. Results showed that the B cells from this cohort were highly activated and prone to cell death, and B cell compartments were altered significantly. Notably, although cART partially reversed the hyperactivation and reduced tissue-like memory B cells, other B cell perturbations, including impaired expression of survival factor Bcl-2, costimulatory molecules, and shrunken resting memory B cells, were irreversible. Further functional characterization revealed that the influenza HAspecific antibody-secreting cells were significantly lower during HIV-1 infection, whereas the recalled antibody response to HIV-1-specific antigens was decreased after cART. Finally, CpG plus R848 treatment increased the survival of B cells and memory B cells in vitro from HIV-1-infected patients. In conclusion, this study identified irreversible B cell immune perturbations in chronic HIV-1 infections regardless of cART and proposed the potential strategy to enhance B cell functions through the improvement of cell survival.

KEYWORDS:

B cell; HIV-1; antiretroviral therapy; functionality; phenotype

PMID:
29181691
DOI:
10.1007/s11684-017-0592-x
[Indexed for MEDLINE]

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