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About the Authors:
Puja Van Epps
* E-mail: [email protected]
Affiliation: Geriatric Research Center Clinical Core (GRECC), Department of Infectious Diseases, Louis Stokes Cleveland VA Medical Center, Case Western Reserve University, Cleveland, Ohio, United States of America
Roy M. Matining
Affiliation: Harvard School of Public Health, Boston, Massachusetts, United States of America
Katherine Tassiopoulos
Affiliation: Harvard School of Public Health, Boston, Massachusetts, United States of America
Donald D. Anthony
Affiliation: Geriatric Research Center Clinical Core (GRECC), Department of Infectious Diseases, Louis Stokes Cleveland VA Medical Center, Case Western Reserve University, Cleveland, Ohio, United States of America
Alan Landay
Affiliation: Department of Immunology and Microbiology, Rush Medical Center, Chicago, Illinois, United States of America
Robert C. Kalayjian
Affiliation: Department of Infectious Diseases, Metrohealth Medical Center, Cleveland, Ohio, United States of America, and Geriatric Research Center Clinical Core (GRECC), Louis Stokes Cleveland VA Medical Center, Cleveland, Ohio, United States of America
David H. Canaday
Affiliation: Geriatric Research Center Clinical Core (GRECC), Department of Infectious Diseases, Louis Stokes Cleveland VA Medical Center, Case Western Reserve University, Cleveland, Ohio, United States of America
Introduction
The effects of HIV infection on B lymphocytes include reduced total B lymphocyte counts, hypergammaglobulinaemia and increased risk of B cell malignancies [1]–[3]. Untreated HIV infection is associated with reduced percentages of naive B cells, increased percentages of immature transitional cells, and expansion of memory B cells in the peripheral blood that exhibit increased turnover and greater susceptibility to apoptosis [3]–[5]. Chronic immune activation during HIV infection may contribute to reduced B cell function, particularly within these memory subsets [3].
ART, especially if initiated early in infection, is associated with recovery of total B cell counts and normalization of most B cell subpopulations, but resting memory cell recovery is incomplete [1], [3], [4]. The aging bone marrow has a reduced ability to generate naive B cells, resulting in a diminished capacity for older individuals to respond to neoantigens [6]. During HIV infection, older individuals have a reduced ability to generate naive T cells, but the effects of aging on B cells in the setting of HIV-infection is not known [7], [8]. Pensieroso et al. have previously reported differences in distributions of B cell subsets in a cross-sectional analysis among HIV-infected (treated and untreated) as well as...