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Immunosenescence of CD4+ T cells in male homosexual patients with HIV-1 infection
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  • Li Li,
  • Linghang Wang,
  • Fengting Yu,
  • Siyuan Yang,
  • Shujing Song,
  • Yunxia Tang,
  • Chengjie Ma,
  • Xingwang Li
Li Li
Capital Medical University Affiliated Beijing Ditan Hospital
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Linghang Wang
Capital Medical University Affiliated Beijing Ditan Hospital
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Fengting Yu
Capital Medical University Affiliated Beijing Ditan Hospital
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Siyuan Yang
Capital Medical University Affiliated Beijing Ditan Hospital
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Shujing Song
Capital Medical University Affiliated Beijing Ditan Hospital
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Yunxia Tang
Capital Medical University Affiliated Beijing Ditan Hospital
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Chengjie Ma
Capital Medical University Affiliated Beijing Ditan Hospital
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Xingwang Li
Capital Medical University Affiliated Beijing Ditan Hospital
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Abstract

The average lifespan of HIV-infected subjects remains shorter compared to uninfected individuals. Immunosenescence may be responsible for this difference despite effective antiretroviral therapy (ART) with successful viral suppression. Here, we evaluated the effects of HIV and ART exposure on T cell aging in male homosexual HIV subjects. CD4+ T cell activation (HLA-DR+) and senescence (CD57+) markers were analyzed by flow cytometry, and telomere length was quantified by real-time PCR. Specifically, we observed an increase in activation and senescence markers on total CD4+ T cell populations in HIV-infected subjects. We also observed a reduction in senescence markers on terminally differentiated memory T(TemRA) cells and activation markers on central memory T(TCM), effector memory T(TEM), and TemRA cells in ART-treated HIV subjects. Furthermore, we also observed an extension of telomere length in memory CD4+ T cells, rather than naive CD4+ T cells, after viral control by ART. Our results indicate that HIV-infected patients exhibit a premature T cell aging phenotype with accelerated immune senescence. Partial recovery of immune senescence and differentiation aberrances is achieved in CD4+ T cells in HIV patients on ART. Overall, these results suggest that HIV infection, rather than ART exposure, influences the T cell aging process.