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

Levelle D. Harris, Brian Tabb, Donald L. Sodora, Mirko Paiardini, Nichole R. Klatt, Daniel C. Douek, Guido Silvestri, Michaela Müller-Trutwin, Ivona Vasile-Pandrea, Cristian Apetrei, Vanessa Hirsch, Jeffrey Lifson, Jason M. Brenchley, Jacob Estes

Research output: Contribution to journalArticle

110 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)7886-7891
Number of pages6
JournalJournal of Virology
Volume84
Issue number15
DOIs
StatePublished - Aug 1 2010
Externally publishedYes

Fingerprint

Simian immunodeficiency virus
Simian Immunodeficiency Virus
Interferon Type I
Virus Diseases
interferons
Macaca mulatta
Down-Regulation
infection
dendritic cells
Dendritic Cells
interferon-alpha
Lymphoid Tissue
Infection
Innate Immunity
Interferon-alpha
Interferons
Acquired Immunodeficiency Syndrome
RNA

ASJC Scopus subject areas

  • Immunology
  • Virology

Cite this

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. / Harris, Levelle D.; Tabb, Brian; Sodora, Donald L.; Paiardini, Mirko; Klatt, Nichole R.; Douek, Daniel C.; Silvestri, Guido; Müller-Trutwin, Michaela; Vasile-Pandrea, Ivona; Apetrei, Cristian; Hirsch, Vanessa; Lifson, Jeffrey; Brenchley, Jason M.; Estes, Jacob.

In: Journal of Virology, Vol. 84, No. 15, 01.08.2010, p. 7886-7891.

Research output: Contribution to journalArticle

Harris, LD, Tabb, B, Sodora, DL, Paiardini, M, Klatt, NR, Douek, DC, Silvestri, G, Müller-Trutwin, M, Vasile-Pandrea, I, Apetrei, C, Hirsch, V, Lifson, J, Brenchley, JM & Estes, J 2010, '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', Journal of Virology, vol. 84, no. 15, pp. 7886-7891. https://doi.org/10.1128/JVI.02612-09
Harris, Levelle D. ; Tabb, Brian ; Sodora, Donald L. ; Paiardini, Mirko ; Klatt, Nichole R. ; Douek, Daniel C. ; Silvestri, Guido ; Müller-Trutwin, Michaela ; Vasile-Pandrea, Ivona ; Apetrei, Cristian ; Hirsch, Vanessa ; Lifson, Jeffrey ; Brenchley, Jason M. ; Estes, Jacob. / 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. In: Journal of Virology. 2010 ; Vol. 84, No. 15. pp. 7886-7891.
@article{8919cc1a64c24dfa8bb1e981d357e03d,
title = "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",
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.",
author = "Harris, {Levelle D.} and Brian Tabb and Sodora, {Donald L.} and Mirko Paiardini and Klatt, {Nichole R.} and Douek, {Daniel C.} and Guido Silvestri and Michaela M{\"u}ller-Trutwin and Ivona Vasile-Pandrea and Cristian Apetrei and Vanessa Hirsch and Jeffrey Lifson and Brenchley, {Jason M.} and Jacob Estes",
year = "2010",
month = "8",
day = "1",
doi = "10.1128/JVI.02612-09",
language = "English (US)",
volume = "84",
pages = "7886--7891",
journal = "Journal of Virology",
issn = "0022-538X",
publisher = "American Society for Microbiology",
number = "15",

}

TY - JOUR

T1 - 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

AU - Harris, Levelle D.

AU - Tabb, Brian

AU - Sodora, Donald L.

AU - Paiardini, Mirko

AU - Klatt, Nichole R.

AU - Douek, Daniel C.

AU - Silvestri, Guido

AU - Müller-Trutwin, Michaela

AU - Vasile-Pandrea, Ivona

AU - Apetrei, Cristian

AU - Hirsch, Vanessa

AU - Lifson, Jeffrey

AU - Brenchley, Jason M.

AU - Estes, Jacob

PY - 2010/8/1

Y1 - 2010/8/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=77954498359&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77954498359&partnerID=8YFLogxK

U2 - 10.1128/JVI.02612-09

DO - 10.1128/JVI.02612-09

M3 - Article

C2 - 20484518

AN - SCOPUS:77954498359

VL - 84

SP - 7886

EP - 7891

JO - Journal of Virology

JF - Journal of Virology

SN - 0022-538X

IS - 15

ER -