Highly Pathogenic Avian Influenza A(H5N8) Virus Spread by Short- and Long-Range Transmission, France, 2016–17

Abstract

I nfluenza A viruses are enveloped viruses of the Alphainfluenzavirus genus in the Orthomyxoviridae family. Their negative-stranded RNA genome consists of 8 segments encoding a total of 10-14 proteins. Avian influenza viruses (AIVs) are classified on the basis of antigenic differences in their surface glycoproteins, hemagglutinin (H1-H16) and neuraminidase (N1-N9) (1). H5 and H7 subtypes can become highly pathogenic avian influenza (HPAI) viruses after the evolution of multiple basic amino acids in the cleavage site of hemagglutinin protein (2,3). This mutation enables the virus to replicate efficiently in all organs, causing a severe and often fatal systemic disease. In contrast, the cleavage site of hemagglutinin in low pathogenicity AIVs lacks these multiple amino acids, restricting viral replication to the respiratory and digestive tracts. Low pathogenicity AIVs cause subclinical or mild disease that can be aggravated by secondary infections (4,5). Because H5 and H7 AIVs can evolve to be highly pathogenic, the diseases caused by these subtypes are notifiable to national and international bodies (6).