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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.
Kim, Y.I.,Park, S.J.,Kwon, H.I.,Kim, E.H.,Si, Y.J.,Jeong, J.H.,Lee, I.W.,Nguyen, H.D.,Kwon, J.J.,Choi, W.S.,Song, M.S.,Kim, C.J.,Choi, Y.K. Elsevier Science 2017 INFECTION GENETICS AND EVOLUTION Vol.53 No.-
<P>During the outbreaks of highly pathogenic avian influenza (HPAI) H5N6 viruses in 2016 in South Korea, novel H5N8 viruses were also isolated from migratory birds. Phylogenetic analysis revealed that the HA gene of these H5N8 viruses belonged to clade 2.3.4.4, similarly to recent H5Nx viruses, and originated from A/Brk/Korea/Gochang1/14(H5N8), a minor lineage of H5N8 that appeared in 2014 and then disappeared. At least four reassortment events occurred with different subtypes (H5N8, H7N7, H3N8 and H10N7) and a chicken challenge study revealed that they were classified as HPAI viruses according to OIE criteria. (C) 2017 Elsevier B.V. All rights reserved.</P>
Surveillance of avian influenza virus in wild bird fecal samples from South Korea, 2003-2008.
Kang, H M,Jeong, O M,Kim, M C,Kwon, J S,Paek, M R,Choi, J G,Lee, E K,Kim, Y J,Kwon, J H,Lee, Y J [Wildlife Disease Association] 2010 JOURNAL OF WILDLIFE DISEASES Vol.46 No.3
<P>We analyzed the results from nationwide surveillance of avian influenza (AI) from birds in South Korea's major wild bird habitats and the demilitarized zone of South Korea, 2003-2008. Of 28,214 fecal samples analyzed, 225 yielded influenza viruses, for a prevalence of 0.8%. Hemagglutinin (HA) subtypes H1-H12 and all nine neuraminidase (NA) subtypes were detected. The dominant HA subtypes were H6, H1, and H4, and the most common NA subtypes were N2, N1, and N6. Among the 38 HA/NA subtype combinations, the most common were H4N6, H6N1, and H5N2. Thirty-seven low-pathogenic AI (LPAI) viruses of the H5 and H7 subtype were detected. Among them, we identified bird species for 16 H5- and H7-positive fecal samples using a DNA bar-coding system instituted in 2007; all birds were identified as Anseriformes. The HA gene of the H5 wild bird isolates belonged to the Eurasian avian lineage, and could be clearly distinguished from the sublineage H5N1 highly pathogenic AI (HPAI) of the Eurasian and American avian lineages. Whereas H7 LPAI viruses did not group as a separate sublineage with H7 HPAI viruses, H7 isolates were closely related with the Eurasian avian lineage.</P>
Park, Y-H,Kim, S-U,Kwon, T-H,Kim, J-M,Song, I-S,Shin, H-J,Lee, B-K,Bang, D-H,Lee, S-J,Lee, D-S,Chang, K-T,Kim, B-Y,Yu, D-Y Macmillan Publishers Limited 2016 Oncogene Vol.35 No.27
<P>The current study was carried out to define the involvement of Peroxiredoxin (Prx) II in progression of hepatocellular carcinoma (HCC) and the underlying molecular mechanism(s). Expression and function of Prx II in HCC was determined using H-ras(G12V)-transformed HCC cells (H-ras(G12V)-HCC cells) and the tumor livers from H-ras(G12V)-transgenic (Tg) mice and HCC patients. Prx II was upregulated in H-ras(G12V)-HCC cells and H-ras(G12V)-Tg mouse tumor livers, the expression pattern of which highly similar to that of forkhead Box M1 (FoxM1). Moreover, either knockdown of FoxM1 or site-directed mutagenesis of FoxM1-binding site of Prx II promoter significantly reduced Prx II levels in H-ras(G12V)-HCC cells, indicating FoxM1 as a direct transcription factor of Prx II in HCC. Interestingly, the null mutation of Prx II markedly decreased the number and size of tumors in H-ras(G12V)-Tg livers. Consistent with this, knockdown of Prx II in H-ras(G12V)-HCC cells reduced the expression of cyclin D1, cell proliferation, anchorage-independent growth and tumor formation in athymic nude mice, whereas overexpression of Prx II increased or aggravated the tumor phenotypes. Importantly, the expression of Prx II was correlated with that of FoxM1 in HCC patients. The activation of extracellular signal-related kinase (ERK) pathway and the expression of FoxM1 and cyclin D1 were highly dependent on Prx II in H-ras(G12V)-HCC cells and H-ras(G12V)-Tg livers. Prx II is FoxM1-dependently- expressed antioxidant in HCC and function as an enhancer of Ras(G12V) oncogenic potential in hepatic tumorigenesis through activation of ERK/FoxM1/cyclin D1 cascade.</P>
Lee, D-H,Kwon, J-S,Lee, H-J,Lee, Y-N,Hur, W,Hong, Y-H,Lee, J-B,Park, S-Y,Choi, I-S,Song, C-S Poultry Science Association, etc 2011 Poultry science Vol.90 No.5
<P>The frequent economic losses incurred with H9N2 low pathogenic avian influenza viruses (LPAI) infection have raised serious concerns for the poultry industry. A 1-dose regimen with inactivated H9N2 LPAI vaccine could not prevent vaccinated poultry from becoming infected and from shedding wild viruses. A study was conducted to determine whether a 2-dose regimen of inactivated H9N2 LPAI vaccine could enhance the immunologic response in chickens. Such gel-primed and mineral oil-boosted regimen has produced encouraging results associated with improved immune responses to an H9N2 LPAI. This strategy could be cost effective and helpful for preventing avian influenza virus in the poultry industry.</P>
Kwon, J. H.,Kim, J. H.,Lee, D. h.,Cho, H.,Hwang, S. Y.,Yuk, S. S.,Erdene-Ochir, T. O.,Noh, J. Y.,Hong, W. T.,Jeong, J. H. Springer Science + Business Media 2016 BioChip Journal Vol.10 No.3
<P>Highly pathogenic avian influenza (HPAI) viruses cause economic losses in the poultry industry and pose a severe threat to human health. Rapid and accurate diagnostic methods are important because they can help prevent further spread of the virus and reduce the time required for eradication of the virus. We developed a low-density microarray for the rapid detection and identification of avian influenza virus subtypes H5, H7, and H9 and their pathotypes in a previous study. In the present study, we report the development of updated probe sets and evaluation of the diagnostic microarray using H5N8 clade 2.3.4.4 HPAI viruses including clinical samples, without the need for egg propagation. Cy3-labeled DNA targets were obtained by reverse transcription polymerase chain reaction using Cy3-labeled universal primers, and labeled amplicons were hybridized to the microarray. All positive samples from RT-PCR showed H5-specific and highly pathogenic pattern in the microarray, without purification of PCR products. Furthermore, it allowed for specific detection of the subtype and pathotype from low DNA concentration samples that did not allow direct sequence analysis. Therefore, this diagnostic microarray has enormous potential for the rapid subtyping and pathotyping from clinical samples without the need for culture.</P>
Kim, M.C.,Jeong, O.M.,Kang, H.M.,Paek, M.R.,Kwon, J.S.,Song, C.S.,Kwon, Y.K.,Lee, J.G.,Kwon, J.H.,Lee, Y.J. Elsevier Scientific Pub. Co 2010 Veterinary microbiology Vol.141 No.3
An H7N7 avian influenza virus [A/Magpie/Kr/YJD174/07 (H7N7); Mp/Kr/07 virus] was isolated from magpie feces in the north-western area (Youngjongdo) of South Korea and identified as low pathogenicity by intravenous pathogenic index and amino acid sequence of cleavage site. In genetic analysis, the genome of the Mp/Kr/07 virus was the same as those of two other H7N7 viruses isolated from the Mallard ducks in Ganghwa, 5km north of Youngjongdo, and grouped under the H7-subtype Eurasian linage with the highest similarity to recent two domestic duck isolates in South Korea. In vivo studies of the chickens and magpies, the Mp/Kr/07 virus, though did not caused any clinical signs with histological changes, could replicate in the oropharynx and cloaca of the chickens and was efficiently transmitted to contact chickens. However, the virus was restrictively identified in oropharynx of the magpies and was not spread to magpies by direct contact. These results suggest that magpie are not a biological amplifier of influenza virus and thus play a minimal role in virus transmission as intermediate host.
Lee, D.H.,Park, J.K.,Yuk, S.S.,Erdene-Ochir, T.O.,Kwon, J.H.,Lee, J.B.,Park, S.Y.,Choi, I.S.,Lee, S.W.,Song, C.S. Elsevier Science 2014 INFECTION GENETICS AND EVOLUTION Vol.26 No.-
In 2011, we isolated a natural recombinant H9N2 avian influenza virus from fecal droppings of bean goose (Anser fabalis) in Korea. Phylogenetic analyses showed that the A/bean goose/Korea/220/2011(H9N2) isolate is a reassortant of Eurasian and North American lineages of avian influenza virus. In addition, the complete genome sequence, including all 8 gene segments, was associated with Chinese H9N2 viruses isolated from wild birds in the Hunan East Dongting Lake National Nature Reserve. These data provide direct evidence for the exchange of avian influenza viruses between Korea and China via wild birds.
NO₂Sensing Properties of CuPc and H₂Pc LB Films
Kwon, H.J.,Lee, Y.-J.,Chang, Y.K.,Kim, J.-D. 경북대학교 센서기술연구소 1998 센서技術學術大會論文集 Vol.9 No.1
Characteristics of CuPc and H_(2)Pc Langmuir-Blodgett(LB) films were examined and their NO_(2) sensing properties were investigated on a gas sensor using 9 MHz quartz crystal microbalance(QCM). The monolayer behavior of H_(2)Pc in air-water interface was observed by inspecting its UV absorption spectra as the surface pressure was increased. On ellipsometry measurement for CuPc and H_(2)Pc LB films, the thickness of H_(2)Pc LB film was almost twice as thick as that of CuPc. X-ray photoelectronic spectroscopy (XPS) spectra of CuPc LB film showed that Cu2p(1/2) and Cu2p(3/2) peak shifts arised from new bond formation by NO_(2) adsorption. Both CuPc and H_(2)Pc LB film produced significant frequency changes in low ppm range of NO_(2).
Lee, J. W.,Park, J. W.,Kwon, O. K.,Lee, H. J.,Jeong, H. G.,Kim, J. H.,Oh, S. R.,Ahn, K. S. Springer Science + Business Media 2017 INFLAMMATION Vol.40 No.1
<P>Mucus overproduction is a fundamental hallmark of COPD that is caused by exposure to cigarette smoke. MUC5AC is one of the main mucin genes expressed in the respiratory epithelium, and its transcriptional upregulation often correlates with increased mucus secretion. Calcium-sensing receptor (CaSR) antagonists have been reported to possess anti-inflammatory effects. The purpose of the present study was to investigate the protective role of NPS2143, a selective CaSR antagonist on cigarette smoke extract (CSE)-stimulated NCI-H292 mucoepidermoid human lung cells. Treatment of NPS2143 significantly inhibited the expression of MUC5AC in CSE-stimulated H292 cells. NPS2143 reduced the expression of MMP-9 in CSE-stimulated H292 cells. NPS2143 also decreased the release of proinflammatory cytokines such as IL-6 and TNF-alpha in CSE-stimulated H292 cells. Furthermore, NPS2143 attenuated the activation of MAPKs (JNK, p38, and ERK) and inhibited the nuclear translocation of NF-kappa B in CSE-stimulated H292 cells. These results indicate that NPS2143 had a therapeutic potential in COPD.</P>