protectin-d1 and Influenza--Human

Influenza A viruses are the causative agents of seasonal and pandemic infections. Influenza strains have recently emerged that show resistance to anti-viral drugs. Moreover, therapies in critically ill patients with severe influenza are limited, with the current anti-viral drugs showing disappointing results even in the absence of obvious viral resistance. Given the high mortality associated with avian H5N1 or H7N9 infections and the risk of pandemic potentials, effective drugs are needed for the treatment of severe influenza. A virus-host interaction is a multidimensional host response, in which not only genes and protein but also metabolites are up- or down-regulated, and cellular pathways and networks implicated in the viral pathogenesis are perturbed. Thus, it seems an attractive strategy to overcome influenza by targeting host metabolites and/or metabolic pathways involved in viral pathogenesis. Using lipidomics and lipid libraries screening, potectin D1 isomer (PDX) derived from the 15-lipoxygenase product 17S-H(p)DHA and/or 17HDHA precursor, has recently been identified, which suppresses influenza virus replication by inhibiting the nuclear export of viral mRNA rather than regulating resolution of inflammation. Contribution of the protectins to control influenza virus replication and their therapeutic potentials are reviewed here. This article is part of a Special Issue entitled "Oxygenated metabolism of PUFA: analysis and biological relevance".

Topics: Animals; Antiviral Agents; Arachidonate 12-Lipoxygenase; Arachidonate 15-Lipoxygenase; Docosahexaenoic Acids; Host-Pathogen Interactions; Humans; Influenza A virus; Influenza, Human; Signal Transduction; Virus Replication