Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

<jats:p>Surveillance of avian influenza viruses is crucial for the characterization of viral diversity in bird populations. Although virulent phenotypes are complex traits, several molecular determinants of pathogenicity in avian influenza viruses have been well characterised, particularly the polybasic proteolytic cleavage site within the Hemagglutinin protein, which allows a systemic spread of the infection in avian hosts. We hypothesise that the parallel evolution of highly pathogenic lineages, from low-pathogenic ancestors, may have been facilitated by permissive or compensatory secondary mutations occurring anywhere in the viral genome. We used a comparative phylogenetic and structural approach to detect mutations across the whole genome of avian influenza viruses of the H7NX subtype, that are shared by multiple, independent highly pathogenic lineages. Parallel mutations occur frequently among highly pathogenic outbreaks. Mutations strongly associated with the HP phenotype may function as an early detection system for transitional virulence stages.</jats:p>

Original publication

DOI

10.1101/370015

Type

Journal article

Publisher

Cold Spring Harbor Laboratory

Publication Date

16/07/2018