Genetic and biological properties of H10N3 avian influenza viruses: A potential pandemic candidate?
PMID: 35067005
2022
Transboundary and emerging diseases
Abstract: Importantly, several key molecular markers associated with mammalian adaptation had been detected in both avian and human-isolated H10N3 influenza viruses in the HA (G228S), PB2 (I292V and A588V), PB1 (M317V and I368V), and PA (A343S, K356R and S409N) protein.
The PB2 co-adaptation of H10N8 avian influenza virus increases the pathogenicity to chickens and mice.
PMID: 34008327
2021
Transboundary and emerging diseases
Abstract: In this study, we found that the
Abstract: The combined mutations of PB2-F6 (including PB2-I292V, PB2-R389K, PB2-A588V, PB2-T598M, PB2-L648V, and PB2-T676M) obtained higher adaptability of AIVs in avians and mammals than that of the single mutation of PB2-A588V, which suggested that the PB2 588 site is a key co-adaptation site and that synergies with other mutation sites can further enhance this co-adaptability.
Evolved avian influenza virus (H7N9) isolated from human cases in a middle Yangtze River city in China, from February to April 2017.
Discussion: Previous studies demonstrated that one or more of the Ile292Val, Ala588Val, Glu627Lys, and Asp701Asn substitutions are important for avian influenza viruses to break the host species barrier to infect mammals.
Discussion: The mutation in other sites, including Ile292Val, Ala588Val and D701N in PB2, could be found effective to compensate for the absence of E627K.
Prevailing I292V PB2 mutation in avian influenza H9N2 virus increases viral polymerase function and attenuates IFN-beta induction in human cells.
PMID: 31305236
2019
The Journal of general virology
Result: Potential mammalian adaptative mutation of PB2-I292V is predominant in avian H9N2 influenza viruses.
Discussion: PB2-I292V mutation could conceivably improve cap recognition and promote viral replication in human cells.
Discussion: In this study, we identified a new mammalian adaptive mutation, PB2-I292V, which is highly prevalent in circulating H9N2, its reassortants and pdm H1N1 virus.|m
Discussion: Interestingly, PB2-292I and PB2-292V mutations in H9N2 virus show no difference in viral polymerase activity in avian cells, suggesting that PB2-I292V mutation specifically promotes infectivity in mammalian cells.
Identification of Key Amino Acids in the PB2 and M1 Proteins of H7N9 Influenza Virus That Affect Its Transmission in Guinea Pigs.
Discussion: In other words, the I292V mutation in PB2 increases the polymerase activity of H7N9 viruses in both avian and mammalian cells.
Discussion: These findings indicate that I292V in PB2 is a host-independent mutation that promotes the transmission of H7N9 virus in mammals and facilitates the replication and spread of influenza viruses in avian species.