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Association of brain heptachlor epoxide and other organochlorine compounds with lewy pathology
Ross, G. Webster,Abbott, Robert D.,Petrovitch, Helen,Duda, John E.,Tanner, Caroline M.,Zarow, Chris,Uyehara‐,Lock, Jane H.,Masaki, Kamal H.,Launer, Lenore J.,Studabaker, William B.,White, Lon R. John Wiley Sons, Inc. 2019 Movement disorders Vol.34 No.2
<P><B>ABSTRACT</B></P><P><B>Background</B></P><P>Organochlorine pesticides are associated with an increased risk of Parkinson's disease. A preliminary analysis from the Honolulu‐Asia Aging Study suggested that heptachlor epoxide, a metabolite from an organochlorine pesticide extensively used in Hawaii, may be especially important. This was a cross sectional analysis to evaluate the association of heptachlor epoxide and other organochlorine compounds with Lewy pathology in an expanded survey of brain organochlorine residues from the longitudinal Honolulu‐Asia Aging Study.</P><P><B>Methods</B></P><P>Organochlorines were measured in frozen occipital or temporal lobes in 705 brains using gas chromatography with mass spectrometry. Lewy pathology was identified using hematoxylin and eosin‐ and α‐synuclein immunochemistry‐stained sections from multiple brain regions.</P><P><B>Results</B></P><P>The prevalence of Lewy pathology was nearly doubled in the presence versus the absence of heptachlor epoxide (30.1% versus 16.3%, <I>P</I> < 0.001). Although associations with other compounds were weaker, hexachlorobenzene (<I>P</I> = 0.003) and α‐chlordane (<I>P</I> = 0.007) were also related to Lewy pathology. Most of the latter associations, however, were a result of confounding from heptachlor epoxide. Neither compound was significantly related to Lewy pathology after adjustment for heptachlor epoxide. In contrast, the association of heptachlor epoxide with Lewy pathology remained significant after adjustments for hexachlorobenzene (<I>P</I> = 0.013) or α‐chlordane (<I>P</I> = 0.005). Findings were unchanged after removal of cases of PD and adjustment for age and other characteristics.</P><P><B>Conclusions</B></P><P>Organochlorine pesticides are associated with the presence of Lewy pathology in the brain, even after exclusion of PD cases. Although most of the association is through heptachlor epoxide, the role of other organochlorine compounds is in need of clarification. © 2018 International Parkinson and Movement Disorder Society</P>
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>
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>
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>
Pascua, Philippe Noriel Q.,Song, Min-Suk,Kwon, Hyeok-Il,Lim, Gyo-Jin,Kim, Eun-Ha,Park, Su-Jin,Lee, Ok-Jun,Kim, Chul-Joong,Webby, Richard J.,Webster, Robert G.,Choi, Young-Ki American Society for Microbiology 2013 Journal of virology Vol.87 No.19
<P>We previously reported that influenza A/swine/Korea/1204/2009(H1N2) virus was virulent and transmissible in ferrets in which the respiratory-droplet-transmissible virus (CT-Sw/1204) had acquired simultaneous hemagglutinin (HA<SUB>D225G</SUB>) and neuraminidase (NA<SUB>S315N</SUB>) mutations. Incorporating these mutations into the nonpathogenic A/swine/Korea/1130/2009(H1N2, Sw/1130) virus consequently altered pathogenicity and growth in animal models but could not establish efficient transmission or noticeable disease. We therefore exploited various reassortants of these two viruses to better understand and identify other viral factors responsible for pathogenicity, transmissibility, or both. We found that possession of the CT-Sw/1204 tripartite viral polymerase enhanced replicative ability and pathogenicity in mice more significantly than did expression of individual polymerase subunit proteins. In ferrets, homologous expression of viral RNA polymerase complex genes in the context of the mutant Sw/1130 carrying the HA<SUB>225G</SUB> and NA<SUB>315N</SUB> modifications induced optimal replication in the upper nasal and lower respiratory tracts and also promoted efficient aerosol transmission to respiratory droplet contact ferrets. These data show that the synergistic function of the tripartite polymerase gene complex of CT-Sw/1204 is critically important for virulence and transmission independent of the surface glycoproteins. Sequence comparison results reveal putative differences that are likely to be responsible for variation in disease. Our findings may help elucidate previously undefined viral factors that could expand the host range and disease severity induced by triple-reassortant swine viruses, including the A(H1N1)pdm09 virus, and therefore further justify the ongoing development of novel antiviral drugs targeting the viral polymerase complex subunits.</P>