scholarly journals Attenuation of Respiratory Syncytial Virus–Induced and RIG-I–Dependent Type I IFN Responses in Human Neonates and Very Young Children

2014 ◽  
Vol 192 (3) ◽  
pp. 948-957 ◽  
Author(s):  
Nico Marr ◽  
Ting-I Wang ◽  
Sarah H. Y. Kam ◽  
Yuan Shen Hu ◽  
Ashish A. Sharma ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Young Children ◽  
Type I ◽  
Type I Ifn ◽  
Very Young Children ◽  
Syncytial Virus ◽  
Human Neonates ◽  
Dependent Type

scholarly journals Replication of Bovine respiratory syncytial virus in murine cells depends on type I interferon-receptor functionality

2006 ◽  
Vol 87 (8) ◽  
pp. 2145-2148 ◽  
Author(s):  
Sabine Riffault ◽  
Catherine Dubuquoy ◽  
Nathalie Castagné ◽  
Eric Baranowski ◽  
Bernard Charley ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Cellular Level ◽  
Bovine Respiratory Syncytial Virus ◽  
Type I ◽  
Type I Ifn ◽  
Efficient Replication ◽  
Control Virus ◽  
Syncytial Virus ◽  
Virus Strains

Bovine respiratory syncytial virus (BRSV) is able to counteract the alpha/beta interferon (IFN-α/β)-mediated antiviral response for efficient replication in a host-specific manner. Mice models have been developed for experimental infection with human, but not bovine, respiratory syncytial virus strains. Here, it is shown that BRSV can replicate efficiently on primary cell cultures derived from type I IFN receptor-deficient, but not from wild-type IFN-competent, mice. However, BRSV infection was not enhanced in mice devoid of the type I IFN receptor. These results show that type I IFN is a major host-range determinant for infection at the cellular level, but that other factors control virus replication and pathology in vivo.

scholarly journals Induction of type I interferons and interferon-inducible Mx genes during respiratory syncytial virus infection and reinfection in cotton rats

2008 ◽  
Vol 89 (1) ◽  
pp. 261-270 ◽  
Author(s):  
Lioubov M. Pletneva ◽  
Otto Haller ◽  
David D. Porter ◽  
Gregory A. Prince ◽  
Jorge C. G. Blanco
Keyword(s):  
Gene Expression ◽  
Respiratory Syncytial Virus ◽  
Virus Replication ◽  
Surrogate Marker ◽  
Type I Interferons ◽  
Type I ◽  
Dependent Manner ◽  
Type I Ifn ◽  
Syncytial Virus

Respiratory syncytial virus (RSV) is the primary cause of bronchiolitis in young children. In general, RSV is considered to be a poor inducer of type I (alpha/beta) interferons (IFNs). Measurement of active type I IFN production during infection in vivo is demanding, as multiple IFN subtypes with overlapping activities are produced. In contrast, Mx gene expression, which is tightly regulated by type I IFN expression, is easily determined. This study therefore measured Mx expression as a reliable surrogate marker of type I IFN activity during RSV infection in vivo in a cotton rat model. It was shown that expression of Mx genes was dramatically augmented in the lungs of infected animals in a dose- and virus strain-dependent manner. The expression of Mx genes in the lungs was paralleled by their induction in the nose and spleen, although in spleen no simultaneous virus gene expression was detected. Reinfection of RSV-immune animals leads to abortive virus replication in the lungs. Thus, type I IFN and Mx gene expression was triggered in reinfected animals, even though virus could not be isolated from their lungs. Furthermore, it was demonstrated that immunity to RSV wanes with time. Virus replication and Mx gene expression became more prominent with increasing intervals between primary infection and reinfection. These results highlight the role of type I IFN in modulation of the immune response to RSV.

scholarly journals Lack of Type I Interferon Signaling Ameliorates Respiratory Syncytial Virus-Induced Lung Inflammation and Restores Antioxidant Defenses

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 67
Author(s):  
Maria Ansar ◽  
Yue Qu ◽  
Teodora Ivanciuc ◽  
Roberto P. Garofalo ◽  
Antonella Casola
Keyword(s):  
Respiratory Syncytial Virus ◽  
Airway Inflammation ◽  
Type I Interferon ◽  
Cell Model ◽  
Antioxidant Defenses ◽  
Related Factor ◽  
Type I ◽  
Type I Ifn ◽  
Rsv Infection ◽  
Syncytial Virus

Respiratory syncytial virus (RSV) infection in mouse and human lung is associated with pathogenic inflammation and oxidative injury. RSV impairs antioxidant responses by increasing the degradation of transcription factor NF-E2-related factor 2 (NRF2), which controls the expression of several antioxidant enzymes (AOEs). In addition to its protective effects, type I IFNs have been increasingly recognized as important mediators of host pathogenic responses during acute respiratory viral infections. We used a mouse model of RSV infection to investigate the effect of lack of type I interferon (IFN) receptor on viral-mediated clinical disease, airway inflammation, NRF2 expression, and antioxidant defenses. In the absence of type I IFN signaling, RSV-infected mice showed significantly less body weight loss and airway obstruction, as well as a significant reduction in cytokine and chemokine secretion and airway inflammation. Lack of type I IFN receptor was associated with greatly reduced virus-induced promyelocytic leukemia lung protein expression, which we showed to be necessary for virus-induced NRF2 degradation in a cell model of infection, resulting in restoration of NRF2 levels, AOE expression, and airway antioxidant capacity. Our data support the concept that modulation of type I IFN production and/or signaling could represent an important therapeutic strategy to ameliorate severity of RSV-induced lung disease.

scholarly journals Respiratory Syncytial Virus Induced Type I IFN Production by pDC Is Regulated by RSV-Infected Airway Epithelial Cells, RSV-Exposed Monocytes and Virus Specific Antibodies

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e81695 ◽  
Author(s):  
Marcel A. Schijf ◽  
Michael V. Lukens ◽  
Debby Kruijsen ◽  
Nathalie O. P. van Uden ◽  
Johan Garssen ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Type I ◽  
Airway Epithelial ◽  
Type I Ifn ◽  
Specific Antibodies ◽  
Syncytial Virus

scholarly journals Differential Type I Interferon Induction by Respiratory Syncytial Virus and Influenza A Virus In Vivo

2007 ◽  
Vol 81 (18) ◽  
pp. 9790-9800 ◽  
Author(s):  
Nancy A. Jewell ◽  
Negin Vaghefi ◽  
Sara E. Mertz ◽  
Parvis Akter ◽  
R. Stokes Peebles ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Respiratory Syncytial Virus ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Influenza A ◽  
Type I Interferon ◽  
Type I ◽  
Type I Ifn ◽  
Syncytial Virus

ABSTRACTType I interferon (IFN) induction is an immediate response to virus infection, and very high levels of these cytokines are produced when the Toll-like receptors (TLRs) expressed at high levels by plasmacytoid dendritic cells (pDCs) are triggered by viral nucleic acids. Unlike many RNA viruses, respiratory syncytial virus (RSV) does not appear to activate pDCs through their TLRs and it is not clear how this difference affects IFN-α/β induction in vivo. In this study, we investigated type I IFN production triggered by RSV or influenza A virus infection of BALB/c mice and found that while both viruses induced IFN-α/β production by pDCs in vitro, only influenza virus infection could stimulate type I IFN synthesis by pDCs in vivo. In situ hybridization studies demonstrated that the infected respiratory epithelium was a major source of IFN-α/β in response to either infection, but in pDC-depleted animals only type I IFN induction by influenza virus was impaired.

scholarly journals The NS2 Protein of Human Respiratory Syncytial Virus Suppresses the Cytotoxic T-Cell Response as a Consequence of Suppressing the Type I Interferon Response

2006 ◽  
Vol 80 (12) ◽  
pp. 5958-5967 ◽  
Author(s):  
Alexander Kotelkin ◽  
Igor M. Belyakov ◽  
Lijuan Yang ◽  
Jay A. Berzofsky ◽  
Peter L. Collins ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Type I Interferon ◽  
Human Respiratory Syncytial Virus ◽  
Interferon Response ◽  
Cytotoxic T Cell ◽  
Type I ◽  
Type I Ifn ◽  
Ifn Γ ◽  
Syncytial Virus

ABSTRACT The NS1 and NS2 proteins of human respiratory syncytial virus (HRSV) have been shown to antagonize the type I interferon (IFN) response, an effect subject to host range constraints. We have now found that the HRSV NS2 protein strongly controls IFN induction in mouse cells in vitro, validating the use of the mouse model to study the consequences of these gene deletions on host immunity. We evaluated the effects of deleting the NS1 and/or NS2 gene on the induction of HRSV-specific pulmonary cytotoxic T lymphocytes (CTL) in BALB/c and 129S6 mice in response to intranasal infection with HRSV lacking the NS1 and/or NS2 gene and subsequent challenge with wild-type (wt) HRSV. In mice infected with HRSV lacking the NS2 gene (ΔNS2) or lacking the NS2 gene in combination with the NS1 gene (ΔNS1/2 HRSV), the magnitude of the pulmonary CTL response was substantially elevated compared to that of mice infected with wt HRSV or the ΔNS1 mutant, whether measured by binding of CD8+ cells to an HRSV-specific major histocompatibility complex class I tetramer, by measurement of CD8+ cells secreting gamma interferon (IFN-γ) in response to specific in vitro stimulation, or by a standard chromium release cell-killing assay. In contrast, in STAT1 knockout mice, which lack responsiveness to type I IFN, the level of IFN-γ-secreting CD8+ cells was not significantly different for HRSV lacking the NS2 gene, suggesting that the increase in CTL observed in IFN-responsive mice is type I IFN dependent. Thus, the NS2 protein of HRSV suppresses the CTL component of the adaptive immune response, and this appears to be a consequence of its suppression of type I IFN.

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