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Respiratory syncytial virus (RSV) attachment and nonstructural proteins modify the type I interferon response associated with suppressor of cytokine signaling (SOCS) proteins and IFN-stimulated gene-15 (ISG15).

Moore EC, Barber J, Tripp RA - Virol. J. (2008)

Bottom Line: Respiratory syncytial virus (RSV) is a major cause of severe lower airway disease in infants and young children, but no safe and effective RSV vaccine is yet available.In the present study, we investigate suppressor of cytokine signaling (SOCS)-1 and SOCS3 expression associated with the type I IFN and IFN-stimulated gene (ISG)-15 response following infection of mouse lung epithelial (MLE-15) cells with RSV or RSV mutant viruses lacking the G gene, or NS1 and NS2 gene deletions.These results show an important role for SOCS1 regulation of the antiviral host response to RSV infection, and demonstrate a novel role for RSV G protein manipulation of SOCS3 and modulation of ISG15 and IFNbeta mRNA expression.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Infectious Diseases, Center for Disease Intervention, University of Georgia, Athens, GA 30602, USA. ecmoore@uga.edu

ABSTRACT
Respiratory syncytial virus (RSV) is a major cause of severe lower airway disease in infants and young children, but no safe and effective RSV vaccine is yet available. Factors attributing to this problem are associated with an incomplete understanding of the mechanisms by which RSV modulates the host cell response to infection. In the present study, we investigate suppressor of cytokine signaling (SOCS)-1 and SOCS3 expression associated with the type I IFN and IFN-stimulated gene (ISG)-15 response following infection of mouse lung epithelial (MLE-15) cells with RSV or RSV mutant viruses lacking the G gene, or NS1 and NS2 gene deletions. Studies in MLE-15 cells are important as this cell line represents the distal bronchiolar and alveolar epithelium of mice, the most common animal model used to evaluate the host cell response to RSV infection, and exhibit morphologic characteristics of alveolar type II cells, a primary cell type targeted during RSV infection. These results show an important role for SOCS1 regulation of the antiviral host response to RSV infection, and demonstrate a novel role for RSV G protein manipulation of SOCS3 and modulation of ISG15 and IFNbeta mRNA expression.

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RSVΔG virus infection mediates enhanced IFNβ secretion. The levels of IFNβ in MLE-15 cell culture supernatant were determined following infection with WT, ΔG, or ΔNS1/2 virus at a multiplicity of infection (MOI) of 1 for 24 h (A) or 48 h (B) as indicated. Data are shown as means ± standard errors (SE) of the means.
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Figure 3: RSVΔG virus infection mediates enhanced IFNβ secretion. The levels of IFNβ in MLE-15 cell culture supernatant were determined following infection with WT, ΔG, or ΔNS1/2 virus at a multiplicity of infection (MOI) of 1 for 24 h (A) or 48 h (B) as indicated. Data are shown as means ± standard errors (SE) of the means.

Mentions: Commercially available mouse IFNα ELISA kits were evaluated but found to have a poor threshold of detection as expected given the limited specificity of the detection antibody used in the kits for detection of the numerous IFNα isoforms [57]. However, IFNβ was detected in all RSV and RSV mutant virus infected MLE-15 cell culture supernatants (Figure 3).


Respiratory syncytial virus (RSV) attachment and nonstructural proteins modify the type I interferon response associated with suppressor of cytokine signaling (SOCS) proteins and IFN-stimulated gene-15 (ISG15).

Moore EC, Barber J, Tripp RA - Virol. J. (2008)

RSVΔG virus infection mediates enhanced IFNβ secretion. The levels of IFNβ in MLE-15 cell culture supernatant were determined following infection with WT, ΔG, or ΔNS1/2 virus at a multiplicity of infection (MOI) of 1 for 24 h (A) or 48 h (B) as indicated. Data are shown as means ± standard errors (SE) of the means.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2577635&req=5

Figure 3: RSVΔG virus infection mediates enhanced IFNβ secretion. The levels of IFNβ in MLE-15 cell culture supernatant were determined following infection with WT, ΔG, or ΔNS1/2 virus at a multiplicity of infection (MOI) of 1 for 24 h (A) or 48 h (B) as indicated. Data are shown as means ± standard errors (SE) of the means.
Mentions: Commercially available mouse IFNα ELISA kits were evaluated but found to have a poor threshold of detection as expected given the limited specificity of the detection antibody used in the kits for detection of the numerous IFNα isoforms [57]. However, IFNβ was detected in all RSV and RSV mutant virus infected MLE-15 cell culture supernatants (Figure 3).

Bottom Line: Respiratory syncytial virus (RSV) is a major cause of severe lower airway disease in infants and young children, but no safe and effective RSV vaccine is yet available.In the present study, we investigate suppressor of cytokine signaling (SOCS)-1 and SOCS3 expression associated with the type I IFN and IFN-stimulated gene (ISG)-15 response following infection of mouse lung epithelial (MLE-15) cells with RSV or RSV mutant viruses lacking the G gene, or NS1 and NS2 gene deletions.These results show an important role for SOCS1 regulation of the antiviral host response to RSV infection, and demonstrate a novel role for RSV G protein manipulation of SOCS3 and modulation of ISG15 and IFNbeta mRNA expression.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Infectious Diseases, Center for Disease Intervention, University of Georgia, Athens, GA 30602, USA. ecmoore@uga.edu

ABSTRACT
Respiratory syncytial virus (RSV) is a major cause of severe lower airway disease in infants and young children, but no safe and effective RSV vaccine is yet available. Factors attributing to this problem are associated with an incomplete understanding of the mechanisms by which RSV modulates the host cell response to infection. In the present study, we investigate suppressor of cytokine signaling (SOCS)-1 and SOCS3 expression associated with the type I IFN and IFN-stimulated gene (ISG)-15 response following infection of mouse lung epithelial (MLE-15) cells with RSV or RSV mutant viruses lacking the G gene, or NS1 and NS2 gene deletions. Studies in MLE-15 cells are important as this cell line represents the distal bronchiolar and alveolar epithelium of mice, the most common animal model used to evaluate the host cell response to RSV infection, and exhibit morphologic characteristics of alveolar type II cells, a primary cell type targeted during RSV infection. These results show an important role for SOCS1 regulation of the antiviral host response to RSV infection, and demonstrate a novel role for RSV G protein manipulation of SOCS3 and modulation of ISG15 and IFNbeta mRNA expression.

Show MeSH
Related in: MedlinePlus