Targeting eicosanoid pathways in the development of novel anti-influenza drugs

The constant new emergence of life-threatening human respiratory viral pathogens presents new challenges to clinicians who are left with no available therapeutic interventions. Highly pathogenic strains of influenza A virus (IAV) share an enhanced capacity to propagate to the lower airways and paralyze alveolar macrophage antiviral capacity in order to replicate efficiently and cause pathologic inflammation. Following a century of using NSAIDs for the management of influenza symptoms, a number of studies have interrogated their function in the host response to IAV infection. We herein provide an overview of these studies as well as further insight of how pathogenic IAV hijacks the microsomal prostaglandin E synthase-1-dependent prostaglandin E-2 pathway in order to evade host type I interferon-mediated antiviral immunity. We also reflect on the potential beneficial action of microsomal prostaglandin E synthase-1 inhibitory compounds in the treatment of IAV infections and potentially other RNA viruses.