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This Article Full Text (Papers in Press[PDF]) All Versions of this Article: vir.0.011700-0v1 90/8/1906    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Chambers, R. Articles by Takimoto, T. Search for Related Content PubMed PubMed Citation Articles by Chambers, R. Articles by Takimoto, T. Agricola Articles by Chambers, R. Articles by Takimoto, T.

Host specificity of the anti-interferon and anti-apoptosis activities of parainfluenza virus P/C gene products

University of Rochester Medical Center

¹ E-mail: toru_takimoto{at}urmc.rochester.edu

Human parainfluenza virus type 1 (hPIV1) and Sendai virus (SeV) are highly homologous in structure and sequence, while maintaining distinct host ranges. These viruses express accessory proteins from their P/C gene, which are known to have anti-innate activities. The accessory proteins expressed from the P/C genes are different between these viruses. In addition to the nested set of C proteins, SeV expresses V protein from edited P mRNA, which is not expressed by hPIV1. In this study, we evaluated the host specificity and role of P/C gene products in anti-IFN and anti-apoptosis activity by characterizing a recombinant SeV, rSeVhP, in which the SeV P/C gene was replaced with that of hPIV1. Unlike SeV, rSeVhP infection strongly activated IRF-3 and NF-B, resulting in an increased level in IFN-β induction compared to SeV in murine cells. In contrast, activation of IRF-3 was not observed in rSeVhP-infected human A549 cells. rSeVhPSV, which expresses SeV V protein from an inserted gene in rSeVhP induced less IFN-β than rSeVhP, suggesting V contributes to suppression of IFN production in murine cells. Furthermore, rSeVhP induced apoptotic cell death in murine but not in A549 cells. These data indicate the functional difference of P/C gene products from SeV and hPIV1 in antagonizing IFN induction and apoptosis, which is likely to be one of the major factors for pathogenicity to specific hosts.

Received 9 March 2009; accepted 23 April 2009.