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 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.

Subgrouping of bovine respiratory syncytial virus strains detected in lung tissue

1996 ◽  
Vol 53 (3-4) ◽  
pp. 253-260 ◽  
Author(s):  
R.S. Schrijver ◽  
F. Daus ◽  
J.A. Kramps ◽  
J.P.M. Langedijk ◽  
R. Buijs ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Lung Tissue ◽  
Bovine Respiratory Syncytial Virus ◽  
Syncytial Virus ◽  
Virus Strains

scholarly journals Genetic and antigenic analysis of the G attachment protein of bovine respiratory syncytial virus strains.

1998 ◽  
Vol 79 (12) ◽  
pp. 2939-2946 ◽  
Author(s):  
M Elvander ◽  
A Uttenthal ◽  
S Vilcek ◽  
A Ballagi-Pord√°ny ◽  
C Baule ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Bovine Respiratory Syncytial Virus ◽  
Antigenic Analysis ◽  
Attachment Protein ◽  
Syncytial Virus ◽  
Virus Strains

scholarly journals ORF7-encoded accessory protein 7a of feline infectious peritonitis virus as a counteragent against IFN-α-induced antiviral response

2014 ◽  
Vol 95 (2) ◽  
pp. 393-402 ◽  
Author(s):  
Annelike Dedeurwaerder ◽  
Dominique A. J. Olyslaegers ◽  
Lowiese M. B. Desmarets ◽  
Inge D. M. Roukaerts ◽  
Sebastiaan Theuns ◽  
...  
Keyword(s):  
Antiviral Response ◽  
Replication Capacity ◽  
Type I ◽  
Type I Ifn ◽  
Feline Infectious Peritonitis Virus ◽  
Feline Infectious Peritonitis ◽  
Efficient Replication ◽  
In Trans

The type I IFN-mediated immune response is the first line of antiviral defence. Coronaviruses, like many other viruses, have evolved mechanisms to evade this innate response, ensuring their survival. Several coronavirus accessory genes play a central role in these pathways, but for feline coronaviruses this has never to our knowledge been studied. As it has been demonstrated previously that ORF7 is essential for efficient replication in vitro and virulence in vivo of feline infectious peritonitis virus (FIPV), the role of this ORF in the evasion of the IFN-α antiviral response was investigated. Deletion of ORF7 from FIPV strain 79-1146 (FIPV-Δ7) rendered the virus more susceptible to IFN-α treatment. Given that ORF7 encodes two proteins, 7a and 7b, it was further explored which of these proteins is active in this mechanism. Providing 7a protein in trans rescued the mutant FIPV-Δ7 from IFN sensitivity, which was not achieved by addition of 7b protein. Nevertheless, addition of protein 7a to FIPV-Δ3Δ7, a FIPV mutant deleted in both ORF3 and ORF7, could no longer increase the replication capacity of this mutant in the presence of IFN. These results indicate that FIPV 7a protein is a type I IFN antagonist and protects the virus from the antiviral state induced by IFN, but it needs the presence of ORF3-encoded proteins to exert its antagonistic function.

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 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

CASE REPORT: A DISEASE OUTBREAK OF BOVINE RESPIRATORY SYNCYTIAL VIRUS IN TAIWAN

2014 ◽  
Vol 40 (03) ◽  
pp. 123-130
Author(s):  
Shyh-Shyan Liu ◽  
Hsiu-Yen Shen ◽  
Jai-Wei Lee ◽  
Show-Win Lin ◽  
Hunter Chen ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Respiratory Disease ◽  
Clinical Symptoms ◽  
Early Stage ◽  
Bovine Respiratory Syncytial Virus ◽  
Type I ◽  
Herpesvirus Type ◽  
Diarrhea Virus ◽  
Disease Case ◽  
Syncytial Virus

A dairy farm with 300 Holstein cattle in Hsin-Chu County, Taiwan, had an outbreak of a respiratory disease from the end of September to November, 2013. Adult animals (1–5-year-old) showed clinical symptoms of anorexia, depression, fever, and dropped milk production during the early stage of infection. In severe cases, animals suffered from dyspnea with frothy saliva at the edge of opened mouth. Samples were collected from eight sick animals, amplified in the baby hamster kidney cell-21 (BHK-21), and the cytopathic effect (CPE) was confirmed. Primers specific to Bovine respiratory syncytial virus (BRSV), Bovine viral diarrhea virus (BVDV), Bovine herpesvirus type I (BHV-I), Bovine ephemeral fever virus (BEFV) and Mannheimia haemolytica were used to identify the pathogen responsible for this respiratory disease by polymerase chain reaction (PCR). Results of sequence analysis confirmed that BRSV is the causative pathogen for the respiratory infection. This is, to the best of our knowledge, the first disease case of BRSV reported in Taiwan.

scholarly journals Recombinant bovine respiratory syncytial virus with deletion of the SH gene induces increased apoptosis and pro-inflammatory cytokines in vitro, and is attenuated and induces protective immunity in calves

2014 ◽  
Vol 95 (6) ◽  
pp. 1244-1254 ◽  
Author(s):  
Geraldine Taylor ◽  
Sara Wyld ◽  
Jean-Francois Valarcher ◽  
Efrain Guzman ◽  
Michelle Thom ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Inflammatory Cytokines ◽  
Bovine Respiratory Syncytial Virus ◽  
Small Airways ◽  
Upper Respiratory Tract ◽  
Virus Challenge ◽  
Syncytial Virus ◽  
Pro Inflammatory Cytokines

Bovine respiratory syncytial virus (BRSV) causes inflammation and obstruction of the small airways, leading to severe respiratory disease in young calves. The virus is closely related to human (H)RSV, a major cause of bronchiolitis and pneumonia in young children. The ability to manipulate the genome of RSV has provided opportunities for the development of stable, live attenuated RSV vaccines. The role of the SH protein in the pathogenesis of BRSV was evaluated in vitro and in vivo using a recombinant (r)BRSV in which the SH gene had been deleted. Infection of bovine epithelial cells and monocytes with rBRSVΔSH, in vitro, resulted in an increase in apoptosis, and higher levels of TNF-α and IL-1β compared with cells infected with parental, wild-type (WT) rBRSV. Although replication of rBRSVΔSH and WT rBRSV, in vitro, were similar, the replication of rBRSVΔSH was moderately reduced in the lower, but not the upper, respiratory tract of experimentally infected calves. Despite the greater ability of rBRSVΔSH to induce pro-inflammatory cytokines, in vitro, the pulmonary inflammatory response in rBRSVΔSH-infected calves was significantly reduced compared with that in calves inoculated with WT rBRSV, 6 days previously. Virus lacking SH appeared to be as immunogenic and effective in inducing resistance to virulent virus challenge, 6 months later, as the parental rBRSV. These findings suggest that rBRSVΔSH may be an ideal live attenuated virus vaccine candidate, combining safety with a high level of immunogenicity.

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