tetano
Editor, Senior Moderator
Virus Res
. 2020 Oct 16;198186.
doi: 10.1016/j.virusres.2020.198186. Online ahead of print.
V292I Mutation in PB2 Polymerase Induces Increased Effects of E627K on Influenza H7N9 Virus Replication in Cells
Yuqing Zhou[SUP] 1 [/SUP], Xiaoxin Wu[SUP] 1 [/SUP], Danying Yan[SUP] 1 [/SUP], Can Chen[SUP] 1 [/SUP], Xiaoxiao Liu[SUP] 1 [/SUP], Chenyang Huang[SUP] 1 [/SUP], Xiaofang Fu[SUP] 1 [/SUP], Guo Tian[SUP] 1 [/SUP], Cheng Ding[SUP] 1 [/SUP], Jie Wu[SUP] 1 [/SUP], Jia Xu[SUP] 1 [/SUP], Lanjuan Li[SUP] 2 [/SUP], Shigui Yang[SUP] 3 [/SUP]
Affiliations
Abstract
Characterization of host adaptation markers among human isolates is important for recognizing the potential for cross-species transmission in avian influenza A viruses. Here, we studied two new potential adaptive mutations, V292I and D740A, in the PB2 protein that were identified by a multi-factor regression model. The study shows that the prevalence of the PB2-V292I mutation is increased in H7N9 influenza viruses isolated from both humans and birds over the past 6 years. The phylogenetic tree showed that influenza A/H7N9 has a lineage based on the strains containing PB2-292I. Polymerase complexes containing PB2-292I/627 K derived from H7N9 exhibit increased polymerase activity. PB2-292I coupled with 627 K also enhances viral transcription and replication in cells, whereas PB2-292I alone did not show the same effect in the H7N9 virus. However, PB2-740A only had a limited prevalence in 2013, and the change from D to A in PB2-740A may have a negative effect on the replication of the H7N9 virus in cells.
Keywords: Adaptive Mutation; H7N9; Influenza virus.
. 2020 Oct 16;198186.
doi: 10.1016/j.virusres.2020.198186. Online ahead of print.
V292I Mutation in PB2 Polymerase Induces Increased Effects of E627K on Influenza H7N9 Virus Replication in Cells
Yuqing Zhou[SUP] 1 [/SUP], Xiaoxin Wu[SUP] 1 [/SUP], Danying Yan[SUP] 1 [/SUP], Can Chen[SUP] 1 [/SUP], Xiaoxiao Liu[SUP] 1 [/SUP], Chenyang Huang[SUP] 1 [/SUP], Xiaofang Fu[SUP] 1 [/SUP], Guo Tian[SUP] 1 [/SUP], Cheng Ding[SUP] 1 [/SUP], Jie Wu[SUP] 1 [/SUP], Jia Xu[SUP] 1 [/SUP], Lanjuan Li[SUP] 2 [/SUP], Shigui Yang[SUP] 3 [/SUP]
Affiliations
- PMID: 33075446
- DOI: 10.1016/j.virusres.2020.198186
Abstract
Characterization of host adaptation markers among human isolates is important for recognizing the potential for cross-species transmission in avian influenza A viruses. Here, we studied two new potential adaptive mutations, V292I and D740A, in the PB2 protein that were identified by a multi-factor regression model. The study shows that the prevalence of the PB2-V292I mutation is increased in H7N9 influenza viruses isolated from both humans and birds over the past 6 years. The phylogenetic tree showed that influenza A/H7N9 has a lineage based on the strains containing PB2-292I. Polymerase complexes containing PB2-292I/627 K derived from H7N9 exhibit increased polymerase activity. PB2-292I coupled with 627 K also enhances viral transcription and replication in cells, whereas PB2-292I alone did not show the same effect in the H7N9 virus. However, PB2-740A only had a limited prevalence in 2013, and the change from D to A in PB2-740A may have a negative effect on the replication of the H7N9 virus in cells.
Keywords: Adaptive Mutation; H7N9; Influenza virus.