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Sci Rep. 2019 May 10;9(1):7216. doi: 10.1038/s41598-019-43632-6.
PA-X antagonises MAVS-dependent accumulation of early type I interferon messenger RNAs during influenza A virus infection.
Rigby RE1, Wise HM2,3, Smith N2, Digard P2, Rehwinkel J4.
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Abstract
The sensing of viral nucleic acids by the innate immune system activates a potent antiviral response in the infected cell, a key component of which is the expression of genes encoding type I interferons (IFNs). Many viruses counteract this response by blocking the activation of host nucleic acid sensors. The evolutionarily conserved influenza A virus (IAV) protein PA-X has been implicated in suppressing the host response to infection, including the expression of type I IFNs. Here, we characterise this further using a PA-X-deficient virus of the mouse-adapted PR8 strain to study activation of the innate immune response in a mouse model of the early response to viral infection. We show that levels of Ifna4 and Ifnb1 mRNAs in the lungs of infected mice were elevated in the absence of PA-X and that this was completely dependent on MAVS. This therefore suggests a role for PA-X in preventing the accumulation of early type I IFN mRNAs in the lung during IAV infection.
PMID: 31076606 DOI: 10.1038/s41598-019-43632-6
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PA-X antagonises MAVS-dependent accumulation of early type I interferon messenger RNAs during influenza A virus infection.
Rigby RE1, Wise HM2,3, Smith N2, Digard P2, Rehwinkel J4.
Author information
Abstract
The sensing of viral nucleic acids by the innate immune system activates a potent antiviral response in the infected cell, a key component of which is the expression of genes encoding type I interferons (IFNs). Many viruses counteract this response by blocking the activation of host nucleic acid sensors. The evolutionarily conserved influenza A virus (IAV) protein PA-X has been implicated in suppressing the host response to infection, including the expression of type I IFNs. Here, we characterise this further using a PA-X-deficient virus of the mouse-adapted PR8 strain to study activation of the innate immune response in a mouse model of the early response to viral infection. We show that levels of Ifna4 and Ifnb1 mRNAs in the lungs of infected mice were elevated in the absence of PA-X and that this was completely dependent on MAVS. This therefore suggests a role for PA-X in preventing the accumulation of early type I IFN mRNAs in the lung during IAV infection.
PMID: 31076606 DOI: 10.1038/s41598-019-43632-6
Free full text