2026/04/01 by Yurui Dong, Ying Bian, Chenzhi Huo +8 · 1 voice
Medicine · Immunology and Microbiology · #Influenza Virus Research Studies #interferon and immune responses #Virology and Viral Diseases
paper · doi:10.1016/j.jia.2026.04.004
openalex publication_date 2026/04/01 · openalex created_date 2026/04/08 · openalex updated_date 2026/07/23
Highly pathogenic avian influenza viruses (AIV) primarily circulate within poultry populations. However, continuous evolution and mutation accumulation drive antigenic drift and may enable the virus to evade host immunity and cross the species barrier. To identify residues associated with antigenic changes and virulence in the H5N1 virus under immune selection pressure, SPF chickens, SPF chicken embryos, and chicken embryo fibroblast cells were used as model to serially passage the SY (Re-5 like) virus in the presence of homologous chicken antiserum. Progeny viruses escaped the neutralizing capacity of the antiserum were sequenced. A total of twelve amino acid mutation sites were identified in the HA, PB2, and PB1 proteins. The results showed that in the HA of the H5N1 virus, both K205N and K205T mutation patterns resulted in a significant reduction in HI titers and microneutralization titers when tested with chicken antisera. The K32M and E69K mutations in PB2, along with the M246I mutation in PB1 could effectively attenuate viral pathogenicity in mice, whereas the S155N mutation in PB2 significantly enhanced it. Notably, under the immune pressure, the S155N mutation in PB2 delayed the emergence of K205N substitution in HA. This in vivo and in vitro method for selecting immune-escape mutants provides a valuable tool for predicting emerging antigenic variants and mammalian adaptive mutations, as well as elucidating the co-evolution dynamics between surface and internal genes in H5N1 viruses.