tetano
Editor, Senior Moderator
J Virol. 2012 Aug 1. [Epub ahead of print]
Incoming Influenza A Virus Evades the Early Host Recognition - Direct Interferon Induction by Influenza B Virus Entry.
Osterlund P, Strengell M, Sarin LP, Poranen MM, Fagerlund R, Mel?n K, Julkunen I.
Source
Department of Infectious Disease Surveillance and Control, Virology Unit, National Institute for Health and Welfare, Helsinki, Finland.
Abstract
Activation of interferon (IFN) system, which is triggered largely by the recognition of viral nucleic acids, is one of the most important host defense reactions against viral infection. Although influenza A and B viruses, which both have segmented negative strand RNA genome, share major structural similarities, they have evolutionary diverged with total genetic incompatibility. Here we compare antiviral-inducing mechanisms during the infection with type A and B influenza viruses in human dendritic cells. We observed that IFN responses are induced significantly faster in cells infected with influenza B virus than type A virus, and that the early induction of antiviral gene expression is mediated by the activation of transcription factor IRF3. We further demonstrate that influenza A virus infection activates the IFN responses only after the viral RNA (vRNA) synthesis, whereas influenza B virus induces IFN responses even if its infectivity is destroyed by UV treatment. Thus, initial viral transcription, replication and viral protein synthesis are dispensable for the influenza B virus-induced antiviral responses. Moreover, vRNA molecules from both type A and B virus are equally potent activators of the IFN induction, but, instead, incoming influenza B virus structures are recognized directly in the cytosol, while influenza A virus is able to evade the early recognition. Collectively, our data provide new evidence of a novel antiviral evasion strategy for influenza A virus without contribution of viral NS1 protein and this opens up new insights into different influenza virus pathogenicity.
PMID:
22855501
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22855501
Incoming Influenza A Virus Evades the Early Host Recognition - Direct Interferon Induction by Influenza B Virus Entry.
Osterlund P, Strengell M, Sarin LP, Poranen MM, Fagerlund R, Mel?n K, Julkunen I.
Source
Department of Infectious Disease Surveillance and Control, Virology Unit, National Institute for Health and Welfare, Helsinki, Finland.
Abstract
Activation of interferon (IFN) system, which is triggered largely by the recognition of viral nucleic acids, is one of the most important host defense reactions against viral infection. Although influenza A and B viruses, which both have segmented negative strand RNA genome, share major structural similarities, they have evolutionary diverged with total genetic incompatibility. Here we compare antiviral-inducing mechanisms during the infection with type A and B influenza viruses in human dendritic cells. We observed that IFN responses are induced significantly faster in cells infected with influenza B virus than type A virus, and that the early induction of antiviral gene expression is mediated by the activation of transcription factor IRF3. We further demonstrate that influenza A virus infection activates the IFN responses only after the viral RNA (vRNA) synthesis, whereas influenza B virus induces IFN responses even if its infectivity is destroyed by UV treatment. Thus, initial viral transcription, replication and viral protein synthesis are dispensable for the influenza B virus-induced antiviral responses. Moreover, vRNA molecules from both type A and B virus are equally potent activators of the IFN induction, but, instead, incoming influenza B virus structures are recognized directly in the cytosol, while influenza A virus is able to evade the early recognition. Collectively, our data provide new evidence of a novel antiviral evasion strategy for influenza A virus without contribution of viral NS1 protein and this opens up new insights into different influenza virus pathogenicity.
PMID:
22855501
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22855501