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Volume 21, Number 5—May 2015

Dispatch

Genetic Characterization of Highly Pathogenic Avian Influenza (H5N8) Virus from Domestic Ducks, England, November 2014

Amanda HannaComments to Author , Jill Banks, Denise A. Marston, Richard J. Ellis, Sharon M. Brookes, and Ian H. Brown
Author affiliations: Animal and Plant Health Agency, Addlestone, UK

Main Article

Table 2

Genetic mutations identified in highly pathogenic avian influenza (H5N8) virus isolate A/duck/England/36254/2014 that might result in phenotypic consequences, England, 2014*

Protein, amino acid position/motif Phenotypic consequences†
PB1-F2,
N66S
Increased virulence, replication efficiency and antivirus response in mice
HA
S133A Increased psuedovirus binding to α2,6
T156A Increased virus binding to α2,6 and increased transmission in guinea pigs
323–330 (R-X-R/K-R)
Polybasic cleavage motif sequence required for high pathogenicity
M1
N30D Increased virulence in mice
T215A
Increased virulence in mice
M2
S31N
Reduced susceptibility to amantadine and rimantadine antiviral drugs
NS1
P42S Increased virulence in mice
I101M Increased virulence in mice

*Phenotypic consequences may include an influence on viral phenotypic characteristics of importance, adaptation to mammalian species, or altered susceptibility to existing antiviral drugs. H5N1 numbering based on the mature HA protein relative to A/Vietnam/1203/2004. PB, polymerase basic protein; HA, hemagglutinin; M, matrix; NS, nonstructural.
†The mutation to the right of the amino acid position confers the phenotypic consequence described.

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