Human parainfluenza virus type 1 but not Sendai virus replicates in human respiratory cells despite IFN treatment

Bousse, Tatiana; Chambers, Raychel; Scroggs, Ruth Ann; Portner, Allen; Takimoto, Toru

doi:10.1016/j.virusres.2006.03.012

Cited by 46 publications

(70 citation statements)

References 41 publications

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“…al. [45] provides at least one explanation for this finding. These researchers compared the growth of human (hPIV-1) and mouse (SV) parainfluenza viruses on human respiratory cells in vitro and found that unlike hPIV-1, SV was naturally attenuated in the context of human interferon-mediated protective mechanisms.…”

Section: Discussionmentioning

confidence: 88%

Respiratory syncytial virus (RSV) fusion protein expressed by recombinant Sendai virus elicits B-cell and T-cell responses in cotton rats and confers protection against RSV subtypes A and B

Zhan

Hurwitz

Krishnamurthy

et al. 2007

Vaccine

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The respiratory syncytial virus (RSV) is a serious pediatric pathogen for which there is currently no clinically-approved vaccine. This report describes the design and testing of a new RSV vaccine construct (rSV-RSV-F), created by the recombination of an RSV F sequence with the murine parainfluenza virus type 1 (Sendai virus, SV) genome. SV was selected as the vaccine backbone for this study, because it has previously been shown to elicit high-magnitude, durable immune activities in animal studies and has advanced to human safety trials as a xenogenic vaccine for human parainfluenza virus-type 1 (hPIV-1). Cells infected with the recombinant SV expressed RSV F protein, but F was not incorporated into progeny SV virions. When cotton rats were inoculated with the vaccine, high-titer RSV-binding and neutralizing antibodies were induced as well as interferon-γ-producing T-cells. Most striking was the protection against intra-nasal RSV challenge conferred by the vaccine. The rSV-RSV-F construct was also tested as a mixture with a second SV construct expressing the RSV G protein, but no clear advantage was demonstrated by combining the two vaccines. As a final analysis, the efficacy of the rSV-RSV-F vaccine was tested against an array of RSV isolates. Results showed that neutralizing and protective responses were effective against RSV isolates of both A and B subtypes. Together, experimental results encourage promotion of this recombinant SV construct as a vaccine candidate for the prevention of RSV in humans.

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Section: Discussionmentioning

confidence: 88%

Respiratory syncytial virus (RSV) fusion protein expressed by recombinant Sendai virus elicits B-cell and T-cell responses in cotton rats and confers protection against RSV subtypes A and B

Zhan

Hurwitz

Krishnamurthy

et al. 2007

Vaccine

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“…The HPIV-1 P/C gene expresses C but not V protein; however, the C protein blocks the Jak/STAT pathway in normal human lung fibroblast MRC-5 cells (Bousse et al, 2006) and inhibits IRF-3 activation and subsequent IFN production in human respiratory epithelial A549 cells and primary human airway epithelial (HAE) cells (Bartlett et al, 2008b;Van Cleve et al, 2006). The specificity of the anti-IFN activities of HPIV-1 C protein has not been characterized in detail.…”

Section: Resultsmentioning

confidence: 99%

“…5(b), all of the viruses blocked nuclear translocation of STAT1 induced by exogenously added IFN-b. These data indicated that, although the HPIV-1 P/C gene products were unable to block NF-kB and IRF-3 activation, they were capable of blocking the Jak/STAT pathway in murine cells, as in human MRC-5 cells (Bousse et al, 2006).…”

Section: Both Sev and Rsevhp Prevent Ifn-induced Nuclear Translocatiomentioning

confidence: 91%

“…We reported previously that SeV is able to replicate in murine cells pre-treated with IFN-b, but not in human cells that are in an IFN-induced antiviral state (Bousse et al, 2006). We next determined the ability of the recombinant viruses to replicate in murine cells in an antiviral state induced by IFN-b pre-treatment.…”

Section: Sev But Not Rsevhp Replicates In Murine Cells Pre-treated mentioning

confidence: 99%

“…SeV and HPIV-3 C proteins inhibit IFN signalling by precluding the appropriate phosphorylation of STAT1 (Komatsu et al, 2002;Young et al, 2000). HPIV-1 C protein also prevents the nuclear translocation of STAT1 and STAT2 in human cells (Bousse et al, 2006). factor (NF)-kB, interferon regulatory transcription factor (IRF)-3 and ATF-2/c-Jun (Andrejeva et al, 2004;Kato et al, 2006;Strahle et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

Chambers

Takimoto

2009

Journal of General Virology

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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 antiinterferon (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-kB, resulting in an increased level of IFN-b 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-b 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.

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Respirovirus C protein inhibits activation of type I interferon receptor‐associated kinases to block JAK‐STAT signaling

et al. 2019

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Respirovirus C protein blocks the type I interferon (IFN)‐stimulated activation of the JAK‐STAT pathway. It has been reported that C protein inhibits IFN‐α‐stimulated tyrosine phosphorylation of STATs, but the underlying mechanism is poorly understood. Here, we show that the C protein of Sendai virus (SeV), a member of the Respirovirus genus, binds to the IFN receptor subunit IFN‐α/β receptor subunit (IFNAR)2 and inhibits IFN‐α‐stimulated tyrosine phosphorylation of the upstream receptor‐associated kinases, JAK1 and TYK2. Analysis of various SeV C mutant (Cm) proteins demonstrates the importance of the inhibitory effect on receptor‐associated kinase phosphorylation for blockade of JAK‐STAT signaling. Furthermore, this inhibitory effect and the IFNAR2 binding capacity are observed for all the respirovirus C proteins examined. Our results suggest that respirovirus C protein inhibits activation of the receptor‐associated kinases JAK1 and TYK2 possibly through interaction with IFNAR2.

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Human parainfluenza virus type 1 but not Sendai virus replicates in human respiratory cells despite IFN treatment

Cited by 46 publications

References 41 publications

Respiratory syncytial virus (RSV) fusion protein expressed by recombinant Sendai virus elicits B-cell and T-cell responses in cotton rats and confers protection against RSV subtypes A and B

Respiratory syncytial virus (RSV) fusion protein expressed by recombinant Sendai virus elicits B-cell and T-cell responses in cotton rats and confers protection against RSV subtypes A and B

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

Respirovirus C protein inhibits activation of type I interferon receptor‐associated kinases to block JAK‐STAT signaling

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