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Evolution and ecology of influenza A viruses.
Yoon, Sun-Woo,Webby, Richard J,Webster, Robert G Springer-Verlag 2014 Current topics in microbiology and immunology Vol.385 No.-
<P>Wild aquatic bird populations have long been considered the natural reservoir for influenza A viruses with virus transmission from these birds seeding other avian and mammalian hosts. While most evidence still supports this dogma, recent studies in bats have suggested other reservoir species may also exist. Extensive surveillance studies coupled with an enhanced awareness in response to H5N1 and pandemic 2009 H1N1 outbreaks is also revealing a growing list of animals susceptible to infection with influenza A viruses. Although in a relatively stable host-pathogen interaction in aquatic birds, antigenic, and genetic evolution of influenza A viruses often accompanies interspecies transmission as the virus adapts to a new host. The evolutionary changes in the new hosts result from a number of processes including mutation, reassortment, and recombination. Depending on host and virus these changes can be accompanied by disease outbreaks impacting wildlife, veterinary, and public health.</P>
Rhodri Harfoot,Richard J. Webby 한국미생물학회 2017 The journal of microbiology Vol.55 No.3
H5 influenza viruses have caused much alarm globally due to their high pathogenic potential. As yet we have not seen sustained spread of the virus amongst humans despite a high prevalence of the virus in avian populations. Nevertheless, isolated human cases of infection have demonstrated high mortality and there are substantial efforts being taken to monitor the evolution of the virus and to undertake prepar-edness activities. Here we review and discuss the evolution of the A/goose/Guangdong/1/96 (H5N1) virus with emphasis on recent events.
The evolution and future of influenza pandemic preparedness
Harrington Walter N.,Kackos Christina M.,Webby Richard J. 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-
The influenza virus is a global threat to human health causing unpredictable yet recurring pandemics, the last four emerging over the course of a hundred years. As our knowledge of influenza virus evolution, distribution, and transmission has increased, paths to pandemic preparedness have become apparent. In the 1950s, the World Health Organization (WHO) established a global influenza surveillance network that is now composed of institutions in 122 member states. This and other surveillance networks monitor circulating influenza strains in humans and animal reservoirs and are primed to detect influenza strains with pandemic potential. Both the United States Centers for Disease Control and Prevention and the WHO have also developed pandemic risk assessment tools that evaluate specific aspects of emerging influenza strains to develop a systematic process of determining research and funding priorities according to the risk of emergence and potential impact. Here, we review the history of influenza pandemic preparedness and the current state of preparedness, and we propose additional measures for improvement. We also comment on the intersection between the influenza pandemic preparedness network and the current SARS-CoV-2 crisis. We must continually evaluate and revise our risk assessment and pandemic preparedness plans and incorporate new information gathered from research and global crises.
Virological and pathological characterization of an avian H1N1 influenza A virus
Koo, Bon-Sang,Kim, Hye Kwon,Song, Daesub,Na, Woonsung,Song, Min-Suk,Kwon, Jin Jung,Wong, Sook-San,Noh, Ji Yeong,Ahn, Min-Ju,Kim, Doo-Jin,Webby, Richard J,Yoon, Sun-Woo,Jeong, Dae Gwin Springer-Verlag 2018 Archives of virology Vol.163 No.5
Song, Min-Suk,Kumar, Gyanendra,Shadrick, William R.,Zhou, Wei,Jeevan, Trushar,Li, Zhenmei,Slavish, P. Jake,Fabrizio, Thomas P.,Yoon, Sun-Woo,Webb, Thomas R.,Webby, Richard J.,White, Stephen W. National Academy of Sciences 2016 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.113 No.13
<P>The influenza endonuclease is an essential subdomain of the viral RNA polymerase. It processes host pre-mRNAs to serve as primers for viral mRNA and is an attractive target for antiinfluenza drug discovery. Compound L-742,001 is a prototypical endonuclease inhibitor, and we found that repeated passaging of influenza virus in the presence of this drug did not lead to the development of resistant mutant strains. Reduced sensitivity to L-742,001 could only be induced by creating point mutations via a random mutagenesis strategy. These mutations mapped to the endonuclease active site where they can directly impact inhibitor binding. Engineered viruses containing the mutations showed resistance to L-742,001 both in vitro and in vivo, with only a modest reduction in fitness. Introduction of the mutations into a second virus also increased its resistance to the inhibitor. Using the isolated wild-type and mutant endonuclease domains, we used kinetics, inhibitor binding and crystallography to characterize how the two most significant mutations elicit resistance to L-742,001. These studies lay the foundation for the development of a new class of influenza therapeutics with reduced potential for the development of clinical endonuclease inhibitorresistant influenza strains.</P>
Song, Min-Suk,Pascua, Philippe Noriel Q.,Lee, Jun Han,Baek, Yun Hee,Lee, Ok-Jun,Kim, Chul-Joong,Kim, Hyunggee,Webby, Richard J.,Webster, Robert G.,Choi, Young Ki American Society for Microbiology 2009 Journal of virology Vol.83 No.23
<B>ABSTRACT</B><P>Adaptation of influenza A viruses to a new host species usually involves the mutation of one or more of the eight viral gene segments, and the molecular basis for host range restriction is still poorly understood. To investigate the molecular changes that occur during adaptation of a low-pathogenic avian influenza virus subtype commonly isolated from migratory birds to a mammalian host, we serially passaged the avirulent wild-bird H5N2 strain A/Aquatic bird/Korea/W81/05 (W81) in the lungs of mice. The resulting mouse-adapted strain (ma81) was highly virulent (50% mouse lethal dose = 2.6 log10 50% tissue culture infective dose) and highly lethal. Nonconserved mutations were observed in six viral genes (those for PB2, PB1, PA, HA, NA, and M). Reverse genetic experiments substituting viral genes and mutations demonstrated that the PA gene was a determinant of the enhanced virulence in mice and that a Thr-to-Iso substitution at position 97 of PA played a key role. In growth kinetics studies, ma81 showed enhanced replication in mammalian but not avian cell lines; the PA97I mutation in strain W81 increased its replicative fitness in mice but not in chickens. The high virulence associated with the PA97I mutation in mice corresponded to considerably enhanced polymerase activity in mammalian cells. Furthermore, this characteristic mutation is not conserved among avian influenza viruses but is prevalent among mouse-adapted strains, indicating a host-dependent mutation. To our knowledge, this is the first study that the isoleucine residue at position 97 in PA plays a key role in enhanced virulence in mice and is implicated in the adaptation of avian influenza viruses to mammalian hosts.</P>
Isolation and Genetic Characterization of H5N2 Influenza Viruses from Pigs in Korea
Lee, Jun Han,Pascua, Philippe Noriel Q.,Song, Min-Suk,Baek, Yun Hee,Kim, Chul-Joong,Choi, Hwan-Woon,Sung, Moon-Hee,Webby, Richard J.,Webster, Robert G.,Poo, Haryoung,Choi, Young Ki American Society for Microbiology 2009 Journal of virology Vol.83 No.9
<B>ABSTRACT</B><P>Due to dual susceptibility to both human and avian influenza A viruses, pigs are believed to be effective intermediate hosts for the spread and production of new viruses with pandemic potential. In early 2008, two swine H5N2 viruses were isolated from our routine swine surveillance in Korea. The sequencing and phylogenetic analysis of surface proteins revealed that the Sw/Korea/C12/08 and Sw/Korea/C13/08 viruses were derived from avian influenza viruses of the Eurasian lineage. However, although the Sw/Korea/C12/08 isolate is an entirely avian-like virus, the Sw/Korea/C13/08 isolate is an avian-swine-like reassortant with the PB2, PA, NP, and M genes coming from a 2006 Korean swine H3N1-like virus. The molecular characterization of the two viruses indicated an absence of significant mutations that could be associated with virulence or binding affinity. However, animal experiments showed that the reassortant Sw/Korea/C13/08 virus was more adapted and was more readily transmitted than the purely avian-like virus in a swine experimental model but not in ferrets. Furthermore, seroprevalence in swine sera from 2006 to 2008 suggested that avian H5 viruses have been infecting swine since 2006. Although there are no known potential clinical implications of the avian-swine reassortant virus for pathogenicity in pigs or other species, including humans, at present, the efficient transmissibility of the swine-adapted H5N2 virus could facilitate virus spread and could be a potential model for pandemic, highly pathogenic avian influenza (e.g., H5N1 and H7N7) virus outbreaks or a pandemic strain itself.</P>
Wong, Sook-San,Yoon, Sun-Woo,Zanin, Mark,Song, Min-Suk,Oshansky, Christine,Zaraket, Hassan,Sonnberg, Stephanie,Rubrum, Adam,Seiler, Patrick,Ferguson, Angela,Krauss, Scott,Cardona, Carol,Webby, Richard Elsevier 2014 Virology Vol.468 No.-
<P><B>Abstract</B></P> <P>The cleavage motif in the hemagglutinin (HA) protein of highly pathogenic H5 and H7 subtypes of avian influenza viruses is characterized by a peptide insertion or a multibasic cleavage site (MBCS). Here, we isolated an H4N2 virus from quails (Quail/CA12) with two additional arginines in the HA cleavage site, PEK<B>RR</B>TR/G, forming an MBCS-like motif. Quail/CA12 is a reassortant virus with the HA and neuraminidase (NA) gene most similar to a duck-isolated H4N2 virus, PD/CA06 with a monobasic HA cleavage site. Quail/CA12 required exogenous trypsin for efficient growth in culture and caused no clinical illness in infected chickens. Quail/CA12 had high binding preference for α2,6-linked sialic acids and showed higher replication and transmission ability in chickens and quails than PD/CA06. Although the H4N2 virus remained low pathogenic, these data suggests that the acquisition of MBCS in the field is not restricted to H5 or H7 subtypes.</P> <P><B>Highlights</B></P> <P> <UL> <LI> An H4N2 influenza virus with a multibasic cleavage site in the hemagglutinin protein was isolated from quails. </LI> <LI> This virus remained lowly pathogenic in chickens and required trypsin for <I>in vitro</I> growth. </LI> <LI> This virus showed higher preference for mammalian-type sialic acid receptors. </LI> <LI> This virus transmitted better in chicken than a duck-origin H4N2 virus. </LI> </UL> </P>