Originally published as JGV in Press, 10.1099/vir.0.011700-0 on May 7, 2009
J Gen Virol 90 (2009), 1906-1915; DOI 10.1099/vir.0.011700-0
Host specificity of the anti-interferon and anti-apoptosis activities of parainfluenza virus P/C gene products
Raychel Chambers and
Toru Takimoto
Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA
Correspondence
Toru Takimoto
toru_takimoto{at}urmc.rochester.edu
Human parainfluenza virus type 1 (HPIV-1) and Sendai virus (SeV) are highly homologous in structure and sequence, whilst maintaining distinct host ranges. These viruses express accessory proteins from their P/C gene that are known to have activities against innate immunity. The accessory proteins expressed from the P/C gene of these viruses are different. In addition to the nested set of C proteins, SeV expresses V protein from edited P mRNA, which is not expressed by HPIV-1. This study evaluated the host specificity and role of the P/C gene products in anti-interferon (IFN) and anti-apoptosis activity by characterizing a recombinant SeV, rSeVhP, in which the SeV P/C gene was replaced with that of HPIV-1. Unlike SeV, rSeVhP infection strongly activated IFN regulatory transcription factor (IRF)-3 and nuclear factor-
B, resulting in an increased level of IFN-β induction compared with SeV in murine cells. In contrast, activation of IRF-3 was not observed in rSeVhP-infected human A549 cells. rSeVhPSV, which expressed SeV V protein from an inserted gene in rSeVhP, induced less IFN-β than rSeVhP, suggesting that V contributes to the 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 in P/C gene products from SeV and HPIV-1 in antagonizing IFN induction and apoptosis, which is likely to be one of the major factors for pathogenicity in specific hosts.
Copyright © 2009 by the Society for General Microbiology.
