How the H7N9 influenza a virus adapted to become a human pathogen?

Abstract

The influenza A (H7N9) virus is a zoonotic disease that arose in China in 2013. Most previously studied H7N9 viruses were found to have low pathogenicity; however, the genetic reassortment of several avian-origin influenza viruses gave rise to a novel H7N9 pathogen that could spread to humans to cause severe pneumonia, acute respiratory distress syndrome and, in some cases, death. Akin to other influenza viruses, the H7N9 virus, could induce strong inflammatory immune responses with the increased secretion of cytokines and chemokines, and pre-existing immunity to the influenza subtype in humans appeared to be limited. In this review, we will examine the changes that occurred in the H7N9 virus, namely the potential mutations in hemagglutinin, polymerase basic protein 2, and neuraminidase, that led to the virus' increased pathogenicity and virulence. The H7N9 virus could bind to both avian type and human type sialic acid receptors, but person-person transmission of the H7N9 virus was low. These findings raise the importance for continual vigilance in maintaining enhanced surveillance of H7N9 viruses to monitor their spread and limit the chance of pandemic infections.

Keywords

influenza virus, H7N9, HA, basic protein 2, immune response

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