Open AccessSuper‐infection with S taphylococcus aureus inhibits influenza virus‐induced type I IFN signalling through impaired STAT1 ‐ STAT2 dimerization
Author(s) -
Warnking Kathrin,
Klemm Carolin,
Löffler Bettina,
Niemann Silke,
Krüchten Andre,
Peters Georg,
Ludwig Stephan,
Ehrhardt Christina
Publication year - 2015
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12375
Subject(s) - biology , interferon , virology , stat2 , pathogen , stat1 , microbiology and biotechnology , staphylococcus aureus , virus , influenza a virus , viral replication , bacteria , gene , stat , biochemistry , genetics , stat3
Summary 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 signalling 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 S taphylococcus aureus ( S. aureus ). While cells initially respond with increased induction of interferon beta upon super‐infection, subsequent interferon signalling and interferon‐stimulated gene expression are rather impaired due to a block of STAT1 ‐ STAT2 dimerization. Thus, S . aureus interrupts the first line of defence against influenza viruses, resulting in a boost of viral replication, which may lead to enhanced viral pathogenicity.