Open AccessHost Transcription Profiles upon Primary Respiratory Syncytial Virus Infection
Author(s) -
Riny Janssen,
Jeroen L. A. Pennings,
Hennie M. Hodemaekers,
AnneMarie Buisman,
Marijke van Oosten,
Lia de Rond,
Kemal Öztürk,
J. A. M. A. Dormans,
Tjeerd G. Kimman,
Barbara Hoebee
Publication year - 2007
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.02220-06
Subject(s) - biology , immunology , virus , immune system , viral replication , interferon , chemokine , respiratory tract , innate immune system , gene , proinflammatory cytokine , lung , virology , viral pathogenesis , inflammation , respiratory system , genetics , medicine , anatomy
Respiratory syncytial virus (RSV) is a common cause of severe lower respiratory tract infection in children. Severe RSV disease is related to an inappropriate immune response to RSV resulting in enhanced lung pathology which is influenced by host genetic factors. To gain insight into the early pathways of the pathogenesis of and immune response to RSV infection, we determined the transcription profiles of lungs and lymph nodes on days 1 and 3 after infection of mice. Primary RSV infection resulted in a rapid but transient innate, proinflammatory response, as exemplified by the induction of a large number of type I interferon-regulated genes and chemokine genes, genes involved in inflammation, and genes involved in antigen processing. Interestingly, this response is much stronger on day 1 than on day 3 after infection, indicating that the strong transcriptional response in the lung precedes the peak of viral replication. Surprisingly, the set of down-regulated genes was small and none of these genes displayed strong down-regulation. Responses in the lung-draining lymph nodes were much less prominent than lung responses and are suggestive of NK cell activation. Our data indicate that at time points prior to the peak of viral replication and influx of inflammatory cells, the local lung response, measured at the transcriptional level, has already dampened down. The processes and pathways induced shortly after RSV infection can now be used for the selection of candidate genes for human genetic studies of children with severe RSV infection.