Downregulation of Robust Acute Type I Interferon Responses Distinguishes Nonpathogenic Simian Immunodeficiency Virus (SIV) Infection of Natural Hosts from Pathogenic SIV Infection of Rhesus Macaques
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Published:2010-08
Issue:15
Volume:84
Page:7886-7891
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ISSN:0022-538X
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Container-title:Journal of Virology
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language:en
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Short-container-title:J Virol
Author:
Harris Levelle D.1, Tabb Brian2, Sodora Donald L.3, Paiardini Mirko4, Klatt Nichole R.1, Douek Daniel C.5, Silvestri Guido4, Müller-Trutwin Michaela6, Vasile-Pandrea Ivona7, Apetrei Cristian7, Hirsch Vanessa1, Lifson Jeffrey8, Brenchley Jason M.1, Estes Jacob D.8
Affiliation:
1. Laboratory of Molecular Microbiology, NIAID, NIH, Bethesda, Maryland 2. Laboratory Animal Science Program, SAIC-Frederick, Inc., NCI-Frederick, Frederick, Maryland 3. Seattle BioMed, Seattle, Washington 4. Department of Pathology and Laboratory of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 5. Human Immunology Section, Vaccine Research Center, NIAID, NIH, Bethesda, Maryland 6. Institut Pasteur, Régulation des Infections Rétrovirales, Paris, France 7. Center for Vaccine Research, University of Pittsburgh, Pittsburgh, Pennsylvania 8. AIDS and Cancer Virus Program, SAIC-Frederick, Inc., NCI-Frederick, Frederick, Maryland
Abstract
ABSTRACT
The mechanisms underlying the AIDS resistance of natural hosts for simian immunodeficiency virus (SIV) remain unknown. Recently, it was proposed that natural SIV hosts avoid disease because their plasmacytoid dendritic cells (pDCs) are intrinsically unable to produce alpha interferon (IFN-α) in response to SIV RNA stimulation. However, here we show that (i) acute SIV infections of natural hosts are associated with a rapid and robust type I IFN response
in vivo
, (ii) pDCs are the principal
in vivo
producers of IFN-α/β at peak acute infection in lymphatic tissues, and (iii) natural SIV hosts downregulate these responses in early chronic infection. In contrast, persistently high type I IFN responses are observed during pathogenic SIV infection of rhesus macaques.
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
Reference29 articles.
1. Bosinger, S. E., Q. Li, S. N. Gordon, N. R. Klatt, L. Duan, L. Xu, N. Francella, A. Sidahmed, A. J. Smith, E. M. Cramer, M. Zeng, D. Masopust, J. V. Carlis, L. Ran, T. H. Vanderford, M. Paiardini, R. B. Isett, D. A. Baldwin, J. G. Else, S. I. Staprans, G. Silvestri, A. T. Haase, and D. J. Kelvin. 2009. Global genomic analysis reveals rapid control of a robust innate response in SIV-infected sooty mangabeys. J. Clin. Invest.119:3556-3572. 2. Brenchley, J. M., M. Paiardini, K. S. Knox, A. I. Asher, B. Cervasi, T. E. Asher, P. Scheinberg, D. A. Price, C. A. Hage, L. M. Kholi, A. Khoruts, I. Frank, J. Else, T. Schacker, G. Silvestri, and D. C. Douek. 2008. Differential Th17 CD4 T-cell depletion in pathogenic and nonpathogenic lentiviral infections. Blood112:2826-2835. 3. Cella, M., D. Jarrossay, F. Facchetti, O. Alebardi, H. Nakajima, A. Lanzavecchia, and M. Colonna. 1999. Plasmacytoid monocytes migrate to inflamed lymph nodes and produce large amounts of type I interferon. Nat. Med.5:919-923. 4. Der, S. D., A. Zhou, B. R. Williams, and R. H. Silverman. 1998. Identification of genes differentially regulated by interferon alpha, beta, or gamma using oligonucleotide arrays. Proc. Natl. Acad. Sci. U. S. A.95:15623-15628. 5. Estes, J. D., S. N. Gordon, M. Zeng, A. M. Chahroudi, R. M. Dunham, S. I. Staprans, C. S. Reilly, G. Silvestri, and A. T. Haase. 2008. Early resolution of acute immune activation and induction of PD-1 in SIV-infected sooty mangabeys distinguishes nonpathogenic from pathogenic infection in rhesus macaques. J. Immunol.180:6798-6807.
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