Heterogeneity in the haemagglutinin gene and emergence of the highly pathogenic phenotype among recent H5N2 avian influenza viruses from Mexico

First field evidence of the evolution from a non-virulent HPR0 to a virulent HPR-deleted infectious salmon anaemia virus

“…This is consistent with the hypothesis that these two mutations, the HPR deletion in the HE gene and the Q 266 L substitution in the F gene, represent necessary mutational steps for the transition to virulence in ISAV [18,22]. This is also in agreement with observations in avian influenza (AI) where highly pathogenic AI viruses (HPAIV) arise from low-pathogenic AI viruses (LPAIV) by mutations of specific virulence markers and where the acquisition and increase in virulence is a stepwise process [36][37][38][39][40][41]. Although the role of other proteins than HE and F in ISAV pathogenesis so far remains elusive, further mutations of other proteins are expected to increase virulence [11,22,42,43] as demonstrated in other members of the orthomyxovirus family, e.g.…”

Human influenza A H5N1 virus related to a highly pathogenic avian influenza virus

“…None of the other sera inhibited haemagglutination, indicating that the isolate was of the H5 subtype. Oligonucleotide primers were selected on the basis of published H5 gene sequences 12,13 and fragments of the expected length were amplified from the viral RNA in a RT-PCR assay. Nucleotide sequence analysis of the haemagglutinin gene confirmed the H5 genotype of the HK97 virus.…”

Evaluation of interventions and vaccination strategies for low pathogenicity avian influenza: spatial and space–time analyses and quantification of the spread of infection

“…However, HPAI viruses may emerge by mutation from low pathogenicity AI (LPAI) viruses of the H5 and H7 subtypes circulating in domestic poultry [2,3], and both LPAI and HPAI viruses can infect humans [4][5][6], which stresses the need for the monitoring and control of LPAI viruses in poultry.…”