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Influenza A viruses suppress cyclooxygenase-2 expression by affecting its mRNA stability
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Influenza A viruses suppress cyclooxygenase-2 expression by affecting its mRNA stability
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Journal Article
Influenza A viruses suppress cyclooxygenase-2 expression by affecting its mRNA stability
2016
Overview
Infection with influenza A viruses (IAV) provokes activation of cellular defence mechanisms contributing to the innate immune and inflammatory response. In this process the cyclooxygenase-2 (COX-2) plays an important role in the induction of prostaglandin-dependent inflammation. While it has been reported that COX-2 is induced upon IAV infection, in the present study we observed a down-regulation at later stages of infection suggesting a tight regulation of COX-2 by IAV. Our data indicate the pattern-recognition receptor RIG-I as mediator of the initial IAV-induced COX-2 synthesis. Nonetheless, during on-going IAV replication substantial suppression of COX-2 mRNA and protein synthesis could be detected, accompanied by a decrease in mRNA half-life. Interestingly, COX-2 mRNA stability was not only imbalanced by IAV replication but also by stimulation of cells with viral RNA. Our results reveal tristetraprolin (TTP), which is known to bind COX-2 mRNA and promote its rapid degradation, as regulator of COX-2 expression in IAV infection. During IAV replication and viral RNA accumulation TTP mRNA synthesis was induced, resulting in reduced COX-2 levels. Accordingly, the down-regulation of TTP resulted in increased COX-2 protein expression after IAV infection. These findings indicate a novel IAV-regulated cellular mechanism, contributing to the repression of host defence and therefore facilitating viral replication.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/89
/ 82/29
/ 82/51
/ 82/80
/ 96/95
/ Cyclooxygenase 2 - chemistry
/ Cyclooxygenase 2 - metabolism
/ DEAD Box Protein 58 - genetics
/ DEAD Box Protein 58 - metabolism
/ Humanities and Social Sciences
/ Humans
/ Influenza A virus - physiology
/ Influenza, Human - metabolism
/ Kinases
/ Proteins
/ Science
/ Solvents
/ Tristetraprolin - metabolism
/ Viruses
