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About the Authors:
Julia L. Drewes
Affiliation: Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
Gregory L. Szeto
Current address: Departments of Materials Science and Engineering, Biological Engineering, and the David H. Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology, and the Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge, Massachusetts, United States of America
Affiliation: Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
Elizabeth L. Engle
Affiliation: Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
Zhaohao Liao
Affiliation: Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
Gene M. Shearer
Affiliation: Experimental Immunology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
M. Christine Zink
* E-mail: [email protected] (DRG); [email protected] (MCZ)
Affiliation: Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
David R. Graham
* E-mail: [email protected] (DRG); [email protected] (MCZ)
Affiliations Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America, Johns Hopkins Bayview Proteomics Center, Department of Medicine, Division of Cardiology, Johns Hopkins School of Medicine Bayview Campus, Baltimore, Maryland, United States of America
Introduction
In the absence of antiretroviral therapy, the majority of HIV-infected patients develop chronic immune activation, immunosuppression and eventually AIDS in a disease process representative of HIV/SIV infection in non-natural hosts (NNH). In contrast, most natural hosts (NH) of SIV such as African green monkeys, gorillas, and sooty mangabeys avert immune pathogenesis despite high viral loads [1]–[4]. One hypothesis for the different outcomes in NH versus NNH focuses on host immune responses to the virus. Documented immune differences include differential induction of type I IFN and IFN-stimulated genes (ISGs) such as TNF-related apoptosis inducing ligand (TRAIL), as well as the immune regulators cytotoxic T-lymphocyte antigen-4 (CTLA-4) and indoleamine 2,3-dioxygenase (IDO), all of which contribute to T cell dysfunction and potentially the development of AIDS [5]–[12]. IDO activity and TRAIL (both soluble and membrane-associated) remain elevated...