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Type I IFN signaling blockade by a PASylated antagonist during chronic SIV infection suppresses specific inflammatory pathways but does not alter T cell activation or virus replication.

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Title: Type I IFN signaling blockade by a PASylated antagonist during chronic SIV infection suppresses specific inflammatory pathways but does not alter T cell activation or virus replication.
Authors: Nganou-Makamdop K; Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Billingsley JM; Division of Microbiology and Immunology, Emory Vaccine Center, Yerkes National Primate Research Center, Atlanta, Georgia, United States of America., Yaffe Z; Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., O'Connor G; Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Tharp GK; Division of Microbiology and Immunology, Emory Vaccine Center, Yerkes National Primate Research Center, Atlanta, Georgia, United States of America., Ransier A; Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Laboune F; Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Matus-Nicodemos R; Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Lerner A; Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Gharu L; Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Robertson JM; Department of Surgery and Emory Transplant Center, Emory University School of Medicine and Emory Healthcare, Atlanta, GA., Ford ML; Department of Surgery and Emory Transplant Center, Emory University School of Medicine and Emory Healthcare, Atlanta, GA., Schlapschy M; Lehrstuhl für Biologische Chemie, Technische Universität München, Freising (Weihenstephan), Germany., Kuhn N; Lehrstuhl für Biologische Chemie, Technische Universität München, Freising (Weihenstephan), Germany., Lensch A; Lehrstuhl für Biologische Chemie, Technische Universität München, Freising (Weihenstephan), Germany., Lifson J; AIDS and Cancer Virus Program, Frederick National Laboratory for Cancer Research, Frederick, Maryland, United States of America., Nason M; Biostatistics Research Branch, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America., Skerra A; Lehrstuhl für Biologische Chemie, Technische Universität München, Freising (Weihenstephan), Germany.; XL-protein GmbH, Freising, Germany., Schreiber G; Department of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, Israel., Bosinger SE; Division of Microbiology and Immunology, Emory Vaccine Center, Yerkes National Primate Research Center, Atlanta, Georgia, United States of America.; Department of Pathology & Laboratory Medicine, Emory University, Atlanta, Georgia, United States of America., Douek DC; Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America.
Source: PLoS pathogens [PLoS Pathog] 2018 Aug 24; Vol. 14 (8), pp. e1007246. Date of Electronic Publication: 2018 Aug 24 (Print Publication: 2018).
Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
Journal Info: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101238921 Publication Model: eCollection Cited Medium: Internet ISSN: 1553-7374 (Electronic) Linking ISSN: 15537366 NLM ISO Abbreviation: PLoS Pathog Subsets: MEDLINE
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  Data: Type I IFN signaling blockade by a PASylated antagonist during chronic SIV infection suppresses specific inflammatory pathways but does not alter T cell activation or virus replication.
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