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Research Paper|Volume 9, Issue 4|pp 1307—1325

Paradoxical aging in HIV: immune senescence of B Cells is most prominent in young age

Stefano Rinaldi1, Suresh Pallikkuth1, Varghese K. George1, Lesley R. de Armas1, Rajendra Pahwa1, Celeste M. Sanchez1, Maria Fernanda Pallin1, Li Pan1, Nicola Cotugno4, Gordon Dickinson2, Allan Rodriguez2, Margaret Fischl3, Maria Alcaide2, Louis Gonzalez1, Paolo Palma4, Savita Pahwa1
  • 1Miami Center for AIDS Research, Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL 33136, USA
  • 2Division of Infectious Disease, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL 33136, USA
  • 3AIDS Clinical Research Unit, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL 33136, USA
  • 4Academic Department of Pediatrics (DPUO), Research Unit in Congenital and Perinatal Infections, Bambino Gesù Children's Hospital-University of Rome Tor Vergata, Rome, Italy

* * Equal contribution

Received: January 6, 2017Accepted: April 19, 2017Published: April 27, 2017

Copyright: © 2017 Rinaldi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Combination antiretroviral therapies (cART)can lead to normal life expectancy in HIV-infected persons, and people aged >50 yrs represent the fastest growing HIV group. Although HIV and aging are independently associated with impaired humoral immunity, immune status in people aging with HIV is relatively unexplored. In this study influenza vaccination was used to probe age associated perturbations in the B cell compartment of HIV-negative “healthy controls” (HC) and virologically controlled HIV-infected participants on cART (HIV) (n=124), grouped by age as young (<40 yrs), middle-aged (40-59yrs) or old (>60 yrs). H1N1 antibody response at d21 post-vaccination correlated inversely with age in both HC and HIV. Immunophenotyping of cryopreserved PBMC demonstrated increased frequencies of double negative B cells and decreased plasmablasts in old compared to young HC. Remarkably, young HIV were different from young HC but similar to old HC in B cell phenotype, influenza specific spontaneous (d7) or memory (d21) antibody secreting cells. We conclude that B cell immune senescence is a prominent phenomenon in young HIV in comparison to young HC, but distinctions between old HIV and old HC are less evident though both groups manifest age-associated B cell dysfunction.