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About the Authors:
Jack T. Stapleton
* E-mail: [email protected]
Affiliations Research and Medical Services, Iowa City VA Medical Center, Iowa City, Iowa, United States of America, Departments of Internal Medicine, Microbiology and Immunology, The University of Iowa, Iowa City, Iowa, United States of America
Kathryn Chaloner
Affiliations Department of Biostatistics, College of Public Health, The University of Iowa, Iowa City, Iowa, United States of America, Department of Statistics & Actuarial Science, College of Public Health, The University of Iowa, Iowa City, Iowa, United States of America
Jeffrey A. Martenson
Affiliation: Department of Microbiology, Rush University, Chicago, Illinois, United States of America
Jingyang Zhang
Affiliation: Department of Biostatistics, College of Public Health, The University of Iowa, Iowa City, Iowa, United States of America
Donna Klinzman
Affiliation: Research and Medical Services, Iowa City VA Medical Center, Iowa City, Iowa, United States of America
Jinhua Xiang
Affiliations Research and Medical Services, Iowa City VA Medical Center, Iowa City, Iowa, United States of America, Departments of Internal Medicine, Microbiology and Immunology, The University of Iowa, Iowa City, Iowa, United States of America
Wendy Sauter
Affiliation: Departments of Internal Medicine, Microbiology and Immunology, The University of Iowa, Iowa City, Iowa, United States of America
Seema N. Desai
Affiliation: Department of Microbiology, Rush University, Chicago, Illinois, United States of America
Alan Landay
Affiliation: Department of Microbiology, Rush University, Chicago, Illinois, United States of America
Introduction
Chronic T cell activation accompanies HIV infection and contributes to HIV-related pathogenesis, and CD4+ T cell activation is required for efficient HIV replication [1]–[4]. The extent of activation, measured by CD38 and HLA-DR co-expression on CD4+ and CD8+ T cells, correlates with HIV disease progression [3]; [5]; [6]. Persistent activation leads to activation induced cell death, which contributes to the depletion of CD4+ T cells during chronic HIV infection [2]; [3]; [7]; [8]. Although combination antiretroviral therapy (cART) lowers HIV viral load (VL) below the limit of detection in most recipients, and reduces activation markers on CD4+ and CD8+ T cells, the level of activation does not return to levels found in healthy, uninfected subjects [9]; [10]. The increase in T cell activation appears to contribute to an increased risk for cardiovascular, malignant and hepatic disease among treated HIV-infected people [11]; [12].
GB Virus C (GBV-C)...