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Lee, J.H.,Pascua, P.N.Q.,Decano, A.G.,Kim, S.M.,Park, S.J.,Kwon, H.I.,Kim, E.H.,Kim, Y.I.,Kim, H.,Kim, S.Y.,Song, M.S.,Jang, H.K.,Park, B.K.,Choi, Y.K. Elsevier Science 2015 INFECTION GENETICS AND EVOLUTION Vol.34 No.-
In 2011-2012, contemporary North American-like H3N2 swine influenza viruses (SIVs) possessing the 2009 pandemic H1N1 matrix gene (H3N2pM-like virus) were detected in domestic pigs of South Korea where H1N2 SIV strains are endemic. More recently, we isolated novel reassortant H1N2 SIVs bearing the Eurasian avian-like swine H1-like hemagglutinin and Korean swine H1N2-like neuraminidase in the internal gene backbone of the H3N2pM-like virus. In the present study, we clearly provide evidence on the genetic origins of the novel H1N2 SIVs virus through genetic and phylogenetic analyses. In vitro studies demonstrated that, in comparison with a pre-existing 2012 Korean H1N2 SIV [A/swine/Korea/CY03-1½012 (CY03-1½012)], the 2013 novel reassortant H1N2 isolate [A/swine/Korea/CY0423/2013 (CY0423-12/2013)] replicated more efficiently in differentiated primary human bronchial epithelial cells. The CY0423-12/2013 virus induced higher viral titers than the CY03-1½012 virus in the lungs and nasal turbinates of infected mice and nasal wash samples of ferrets. Moreover, the 2013 H1N2 reassortant, but not the intact 2012 H1N2 virus, was transmissible to naive contact ferrets via respiratory-droplets. Noting that the viral precursors have the ability to infect humans, our findings highlight the potential threat of a novel reassortant H1N2 SIV to public health and underscore the need to further strengthen influenza surveillance strategies worldwide, including swine populations.
Emergence of Amantadine-Resistant H3N2 Avian Influenza A Virus in South Korea
Lee, J.,Song, Y. J.,Park, J. H.,Lee, J.-H.,Baek, Y. H.,Song, M.-S.,Oh, T.-K.,Han, H.-S.,Pascua, P. N. Q.,Choi, Y.-K. American Society for Microbiology 2008 Journal of clinical microbiology Vol.46 No.11
<P>We found a relatively high frequency of unique amantadine-resistant H3N2 and H9N2 avian influenza viruses (Val27Ile on M2 protein) isolated from live poultry markets in South Korea and confirmed that a Val27Ile single substitution in the M2 protein is enough to acquire the amantadine resistance phenotype by using reverse-genetically created human-avian reassortant viruses.</P>
Evidence of Human-to-Swine Transmission of the Pandemic (H1N1) 2009 Influenza Virus in South Korea
Song, M.-S.,Lee, J. H.,Pascua, P. N. Q.,Baek, Y. H.,Kwon, H.-i.,Park, K. J.,Choi, H.-W.,Shin, Y.-K.,Song, J.-Y.,Kim, C.-J.,Choi, Y.-K. American Society for Microbiology 2010 Journal of clinical microbiology Vol.48 No.9
Song, M.S.,Cho, Y.H.,Park, S.J.,Pascua, P.N.Q.,Baek, Y.H.,Kwon, H.I.,Lee, O.J.,Kong, B.W.,Kim, H.,Shin, E.C.,Kim, C.J.,Choi, Y.K. American Association of Pathologists and Bacteriol 2013 The American journal of pathology Vol.182 No.4
Differing sensitivity of influenza A viruses to antiviral effects of the Myxovirus resistance (Mx) protein implies varying global gene expression profiles in the host. The role of Mx protein during lethal avian influenza (AI) virus infection was examined using Mx1-deficient C57BL/6 (B6-Mx1<SUP>-/-</SUP>) and congenic Mx1-expressing (B6-Mx1<SUP>+/+</SUP>) mice infected with a virulent, mouse-adapted avian H5N2 Ab/Korea/ma81/07 (Av/ma81) virus. After infection, B6-Mx1<SUP>+/+</SUP> mice were completely protected from lethal AI-induced mortality, and exhibited attenuated clinical disease and reduced viral titers and pathology in the lungs, compared with B6-Mx1<SUP>-/-</SUP> mice. Transcriptional profiling of lung tissues revealed that most of the genes up-regulated after infection are involved in activation of the immune response and host defense. Notably, more abundant and sustained expression of cytokine/chemokine genes was observed up to 3 dpi in B6-Mx1<SUP>-/-</SUP> mice, and this was associated with excessive induction of cytokines and chemokines. Consequently, massive infiltration of macrophages/monocytes and granulocytes into lung resulted in severe viral pneumonia and potentially contributed to decreased survival of B6-Mx1<SUP>-/-</SUP> mice. Taken together, our data show that dysregulated gene transcriptional activity corresponded to persistent induction of cytokine/chemokines and recruitment of cytokine-producing cells that promote inflammation in B6-Mx1<SUP>-/-</SUP> mouse lungs. Thus, we provide additional evidence of the interplay of genetic, molecular, and cellular correlates governed by the Mx1 protein that critically determine disease outcome during lethal AI virus infection.