Skip to content Skip to navigation
University of Warwick
  • Study
  • |
  • Research
  • |
  • Business
  • |
  • Alumni
  • |
  • News
  • |
  • About

University of Warwick
Publications service & WRAP

Highlight your research

  • WRAP
    • Home
    • Search WRAP
    • Browse by Warwick Author
    • Browse WRAP by Year
    • Browse WRAP by Subject
    • Browse WRAP by Department
    • Browse WRAP by Funder
    • Browse Theses by Department
  • Publications Service
    • Home
    • Search Publications Service
    • Browse by Warwick Author
    • Browse Publications service by Year
    • Browse Publications service by Subject
    • Browse Publications service by Department
    • Browse Publications service by Funder
  • Statistics
  • Help & Advice
University of Warwick

The Library

  • Login

Differential expression of proinflammatory cytokine genes in vivo in response to pathogenic and nonpathogenic pneumovirus infections

Tools
- Tools
+ Tools

UNSPECIFIED (2002) Differential expression of proinflammatory cytokine genes in vivo in response to pathogenic and nonpathogenic pneumovirus infections. JOURNAL OF INFECTIOUS DISEASES, 186 (1). pp. 8-14. ISSN 0022-1899

Full text not available from this repository.

Abstract

Pneumonia virus of mice (PVM; Paramyxoviridae, subfamily Pneumovirinae) is an important pathogen for the study of physiologically relevant acute inflammatory responses in rodent hosts. In contrast to the severe symptomatology observed in response to infection with PVM strain J3666, infection with strain 15 resulted in few clinical symptoms, limited cellular inflammatory response, and no production of macrophage inflammatory protein-1alpha or monocyte chemoattractant peptide (MCP)-1. Microarray analysis of transcripts from lung tissue indicates that PVM J3666 infection promotes up-regulation of specific proinflammatory genes, most notably interferon (IFN)-1beta, IFN response genes, and chemokines MCP-1, MCP-3, RANTES (regulated on activation, normally T cell-expressed and secreted), and eotaxin. Of these, only RANTES expression increased in response to infection with strain 15, with no increased expression of IFN or IFN response genes, despite ongoing viral replication. These results suggest that pneumovirus replication alone is insufficient to promote antiviral inflammation and that evaluation of the more divergent strain-specific pneumovirus proteins may provide some intriguing leads toward the molecular basis of this differential response.

Item Type: Journal Article
Subjects: Q Science > QR Microbiology > QR180 Immunology
Q Science > QR Microbiology > QR355 Virology
Q Science > QR Microbiology
Journal or Publication Title: JOURNAL OF INFECTIOUS DISEASES
Publisher: UNIV CHICAGO PRESS
ISSN: 0022-1899
Date: 1 July 2002
Volume: 186
Number: 1
Number of Pages: 7
Page Range: pp. 8-14
Publication Status: Published
URI: http://wrap.warwick.ac.uk/id/eprint/10836

Data sourced from Thomson Reuters' Web of Knowledge

Request changes to a record

Actions (login required)

View Item View Item
twitter

Email us: publications@warwick.ac.uk
Contact Details
About Us