tetano
Editor, Senior Moderator
Cell Microbiol. 2014 Oct 8. doi: 10.1111/cmi.12375. [Epub ahead of print]
Super-infection with Staphylococcus aureus inhibits influenza virus-induced type I IFN signaling through impaired STAT1-STAT2 dimerization.
Warnking K1, Klemm C, L?ffler B, Niemann S, van Kr?chten A, Peters G, Ludwig S, Ehrhardt C.
Author information
Abstract
Bacterial super-infections are a major complication in influenza virus-infected patients. In response to infection with influenza viruses and bacteria, a complex interplay of cellular signaling mechanisms is initiated, regulating the anti-pathogen response but also pathogen-supportive functions. Here, we show that influenza viruses replicate to a higher efficiency in cells co-infected with Staphylococcus aureus. While cells initially respond with increased induction of interferon beta upon super-infection, subsequent interferon signaling and interferon-stimulated gene expression is rather impaired due to a block of STAT1-STAT2 dimerization. Thus, Staphylococcus aureus interrupts the first line of defense against influenza viruses, resulting in a boost of viral replication, which may lead to enhanced viral pathogenicity.
This article is protected by copyright. All rights reserved.
PMID:
25293394
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25293394
Super-infection with Staphylococcus aureus inhibits influenza virus-induced type I IFN signaling through impaired STAT1-STAT2 dimerization.
Warnking K1, Klemm C, L?ffler B, Niemann S, van Kr?chten A, Peters G, Ludwig S, Ehrhardt C.
Author information
Abstract
Bacterial super-infections are a major complication in influenza virus-infected patients. In response to infection with influenza viruses and bacteria, a complex interplay of cellular signaling mechanisms is initiated, regulating the anti-pathogen response but also pathogen-supportive functions. Here, we show that influenza viruses replicate to a higher efficiency in cells co-infected with Staphylococcus aureus. While cells initially respond with increased induction of interferon beta upon super-infection, subsequent interferon signaling and interferon-stimulated gene expression is rather impaired due to a block of STAT1-STAT2 dimerization. Thus, Staphylococcus aureus interrupts the first line of defense against influenza viruses, resulting in a boost of viral replication, which may lead to enhanced viral pathogenicity.
This article is protected by copyright. All rights reserved.
PMID:
25293394
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25293394