tetano
Editor, Senior Moderator
Biochem Biophys Res Commun. 2014 Oct 22;454(1):189-195. doi: 10.1016/j.bbrc.2014.10.067. [Epub ahead of print]
Type I interferon-mediated immune response against influenza A virus is attenuated in the absence of p53.
Zhu Z1, Yang Y2, Wei J2, Shao D2, Shi Z2, Li B2, Liu K2, Qiu Y2, Zheng H3, Ma Z4.
Author information
Abstract
Influenza A virus (IAV) infection induces secretion of type I interferon (IFN) and activation of p53, which play essential roles in the host defense against tumor development and viral infection. In this study, we knocked down p53 expression by RNA interference. The expression levels of IFN-stimulated genes (ISGs) including IFN regulatory factor (IRF) 5, IRF9, ISG15, ISG20, guanylate-binding protein 1, retinoic acid-inducible gene-I and 2'-5'-oligoadenylate synthetase 1 were significantly attenuated in response to IAV infection and IFN-α stimulation in p53-knockdown cells. This attenuated expression of ISGs was associated with enhanced replication of IAV. Pretreatment of p53-knockdown cells with IFN-α failed to inhibit IAV replication, indicating impaired antiviral activity. These findings indicate that p53 plays an essential role in the enhancement of the type I IFN-mediated immune response against IAV infection.
Copyright ? 2014 Elsevier Inc. All rights reserved.
KEYWORDS:
Antiviral immune response; Influenza A virus; Interferon-stimulated genes; Type I interferon; p53
PMID:
25450379
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25450379
Type I interferon-mediated immune response against influenza A virus is attenuated in the absence of p53.
Zhu Z1, Yang Y2, Wei J2, Shao D2, Shi Z2, Li B2, Liu K2, Qiu Y2, Zheng H3, Ma Z4.
Author information
Abstract
Influenza A virus (IAV) infection induces secretion of type I interferon (IFN) and activation of p53, which play essential roles in the host defense against tumor development and viral infection. In this study, we knocked down p53 expression by RNA interference. The expression levels of IFN-stimulated genes (ISGs) including IFN regulatory factor (IRF) 5, IRF9, ISG15, ISG20, guanylate-binding protein 1, retinoic acid-inducible gene-I and 2'-5'-oligoadenylate synthetase 1 were significantly attenuated in response to IAV infection and IFN-α stimulation in p53-knockdown cells. This attenuated expression of ISGs was associated with enhanced replication of IAV. Pretreatment of p53-knockdown cells with IFN-α failed to inhibit IAV replication, indicating impaired antiviral activity. These findings indicate that p53 plays an essential role in the enhancement of the type I IFN-mediated immune response against IAV infection.
Copyright ? 2014 Elsevier Inc. All rights reserved.
KEYWORDS:
Antiviral immune response; Influenza A virus; Interferon-stimulated genes; Type I interferon; p53
PMID:
25450379
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25450379