tetano
Editor, Senior Moderator
Viruses
. 2024 Feb 25;16(3):357.
doi: 10.3390/v16030357. Wild Bird-Origin H6N2 Influenza Virus Acquires Enhanced Pathogenicity after Single Passage in Mice
Siqi Tang[SUP] 1 [/SUP], Bing Han[SUP] 1 [/SUP], Chaofan Su[SUP] 1 [/SUP], Hailing Li[SUP] 1 [/SUP], Shiyuchen Zhao[SUP] 1 [/SUP], Haoyu Leng[SUP] 1 [/SUP], Yali Feng[SUP] 1 [/SUP], Ying Zhang[SUP] 1 [/SUP]
Affiliations
The H6 subtype of avian influenza viruses (AIVs) has emerged as one of the predominant subtypes in both wild and domestic avian species. Currently, H6 AIVs have acquired the ability to infect a wide range of mammals, though the related molecular mechanisms have yet to be fully investigated. In this study, a wild bird-origin H6N2 AIV was isolated from the East Asian-Australasian migratory flyway region located in Liaoning Province. This H6N2 virus initially expressed limited replication in mice. However, after one passage in mice, the virus acquired two mutations, PB2 E627K and HA A110V. The mutant displayed enhanced replication both in vitro and in vivo, proving lethal to mice. But the mutant retained the α-2, 3-linked sialic acid binding property and failed to transmit in guinea pigs. We explored the molecular mechanisms underlying the pathogenicity difference between the wild type and the mutant. Our findings revealed that PB2 E627K dramatically enhanced the polymerase activity of the H6N2 virus, while the HA A110V mutation decreased the pH of HA activation. This study demonstrated that the H6N2 subtype wild bird-origin AIV easily acquired the mammalian adaptation. The monitoring and evaluation of H6 wild bird-origin AIV should be strengthened.
Keywords: adaptation; enhanced; pathogenicity; wild bird-origin influenza virus.
. 2024 Feb 25;16(3):357.
doi: 10.3390/v16030357. Wild Bird-Origin H6N2 Influenza Virus Acquires Enhanced Pathogenicity after Single Passage in Mice
Siqi Tang[SUP] 1 [/SUP], Bing Han[SUP] 1 [/SUP], Chaofan Su[SUP] 1 [/SUP], Hailing Li[SUP] 1 [/SUP], Shiyuchen Zhao[SUP] 1 [/SUP], Haoyu Leng[SUP] 1 [/SUP], Yali Feng[SUP] 1 [/SUP], Ying Zhang[SUP] 1 [/SUP]
Affiliations
- PMID: 38543722
- PMCID: PMC10976067
- DOI: 10.3390/v16030357
The H6 subtype of avian influenza viruses (AIVs) has emerged as one of the predominant subtypes in both wild and domestic avian species. Currently, H6 AIVs have acquired the ability to infect a wide range of mammals, though the related molecular mechanisms have yet to be fully investigated. In this study, a wild bird-origin H6N2 AIV was isolated from the East Asian-Australasian migratory flyway region located in Liaoning Province. This H6N2 virus initially expressed limited replication in mice. However, after one passage in mice, the virus acquired two mutations, PB2 E627K and HA A110V. The mutant displayed enhanced replication both in vitro and in vivo, proving lethal to mice. But the mutant retained the α-2, 3-linked sialic acid binding property and failed to transmit in guinea pigs. We explored the molecular mechanisms underlying the pathogenicity difference between the wild type and the mutant. Our findings revealed that PB2 E627K dramatically enhanced the polymerase activity of the H6N2 virus, while the HA A110V mutation decreased the pH of HA activation. This study demonstrated that the H6N2 subtype wild bird-origin AIV easily acquired the mammalian adaptation. The monitoring and evaluation of H6 wild bird-origin AIV should be strengthened.
Keywords: adaptation; enhanced; pathogenicity; wild bird-origin influenza virus.