9 results on '"Jeong-Hyun Nam"'
Search Results
2. Surveillance of avian influenza viruses from 2009 to 2013 in South Korea
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Jeong-Hyun Nam, Erica Españo, Eun-Jung Song, Sang-Mu Shim, Woonsung Na, Seo-Hee Jeong, Jiyeon Kim, Jaebong Jang, Daesub Song, and Jeong-Ki Kim
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Multidisciplinary ,animal diseases ,Science ,virus diseases ,Article ,Birds ,Viral reservoirs ,Influenza A virus ,Virology ,Influenza in Birds ,Republic of Korea ,Animals ,Medicine ,Influenza virus - Abstract
Avian influenza viruses (AIVs) are carried by wild migratory waterfowl across migratory flyways. To determine the strains of circulating AIVs that may pose a risk to poultry and humans, regular surveillance studies must be performed. Here, we report the surveillance of circulating AIVs in South Korea during the winter seasons of 2009–2013. A total of 126 AIVs were isolated from 7942 fecal samples from wild migratory birds, with a total isolation rate of 1.59%. H1‒H7 and H9‒H11 hemagglutinin (HA) subtypes, and N1‒N3, N5, and N7‒N9 neuraminidase (NA) subtypes were successfully isolated, with H6 and N2 as the most predominant HA and NA subtypes, respectively. Sequence identity search showed that the HA and NA genes of the isolates were highly similar to those of low-pathogenicity influenza strains from the East Asian-Australasian flyway. No match was found for the HA genes of high-pathogenicity influenza strains. Thus, the AIV strains circulating in wild migratory birds from 2009 to 2013 in South Korea likely had low pathogenicity. Continuous surveillance studies such as this one must be performed to identify potential precursors of influenza viruses that may threaten animal and human health.
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- 2021
3. Inhibitory effects of aprotinin on influenza A and B viruses in vitro and in vivo
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Chong-Kil Lee, Kiho Lee, Jeong-Hyun Nam, Jiyeon Kim, Sang-Mu Shim, Eun-Jung Song, Jeong-Ki Kim, Song-Kyu Park, and Erica Españo
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0301 basic medicine ,Serine Proteinase Inhibitors ,Phenotypic screening ,Science ,viruses ,030106 microbiology ,Drug Evaluation, Preclinical ,medicine.disease_cause ,Antiviral Agents ,Virus ,Article ,Cell Line ,Madin Darby Canine Kidney Cells ,03 medical and health sciences ,Mice ,Aprotinin ,Dogs ,Influenza A Virus, H1N1 Subtype ,Orthomyxoviridae Infections ,In vivo ,medicine ,Influenza A virus ,Influenza A Virus, H9N2 Subtype ,Animals ,Humans ,Serine protease ,Multidisciplinary ,biology ,Influenza A Virus, H3N2 Subtype ,Lethal dose ,virus diseases ,Virology ,In vitro ,Mice, Inbred C57BL ,Influenza B virus ,030104 developmental biology ,Drug screening ,Viral infection ,biology.protein ,Medicine ,Influenza virus ,Influenza A Virus, H5N2 Subtype ,medicine.drug - Abstract
Influenza viruses cause significant morbidity and mortality worldwide. Long-term or frequent use of approved anti-influenza agents has resulted in drug-resistant strains, thereby necessitating the discovery of new drugs. In this study, we found aprotinin, a serine protease inhibitor, as an anti-influenza candidate through screening of compound libraries. Aprotinin has been previously reported to show inhibitory effects on a few influenza A virus (IAV) subtypes (e.g., seasonal H1N1 and H3N2). However, because there were no reports of its inhibitory effects on the other types of influenza viruses, we investigated the inhibitory effects of aprotinin in vitro on a wide range of influenza viruses, including avian and oseltamivir-resistant influenza virus strains. Our cell-based assay showed that aprotinin had inhibitory effects on seasonal human IAVs (H1N1 and H3N2 subtypes), avian IAVs (H5N2, H6N5, and H9N2 subtypes), an oseltamivir-resistant IAV, and a currently circulating influenza B virus. We have also confirmed its activity in mice infected with a lethal dose of influenza virus, showing a significant increase in survival rate. Our findings suggest that aprotinin has the capacity to inhibit a wide range of influenza virus subtypes and should be considered for development as a therapeutic agent against influenza.
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- 2021
4. Lipophilic statins inhibit Zika virus production in Vero cells
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Erica Españo, Jeong-Hyun Nam, Eun-Jung Song, Daesub Song, Chong-Kil Lee, and Jeong-Ki Kim
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0301 basic medicine ,Phenotypic screening ,Atorvastatin ,Drug Evaluation, Preclinical ,lcsh:Medicine ,Pharmacology ,Virus Replication ,Article ,Zika virus ,Time-to-Treatment ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Mevastatin ,Chlorocebus aethiops ,medicine ,Animals ,Humans ,cardiovascular diseases ,lcsh:Science ,Fluvastatin ,Vero Cells ,Multidisciplinary ,biology ,Dose-Response Relationship, Drug ,Cholesterol ,business.industry ,Zika Virus Infection ,lcsh:R ,nutritional and metabolic diseases ,Cerivastatin ,Zika Virus ,biology.organism_classification ,Antivirals ,030104 developmental biology ,chemistry ,Simvastatin ,Viral infection ,lcsh:Q ,lipids (amino acids, peptides, and proteins) ,Lovastatin ,Hydroxymethylglutaryl-CoA Reductase Inhibitors ,business ,Hydrophobic and Hydrophilic Interactions ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Zika virus (ZIKV) is a mosquito-borne member of the Flaviviridae family. ZIKV infection has been associated with neurological complications such as microcephaly in newborns and Guillain-Barré syndrome in adults; thus, therapeutic agents are urgently needed. Statins are clinically approved for lowering cholesterol levels to prevent cardiovascular disease but have shown potential as antiviral drugs. In this study, we explored the possibility of utilizing statins as anti-ZIKV drugs. We found that, generally, lipophilic statins (atorvastatin, cerivastatin, fluvastatin, lovastatin, mevastatin, and simvastatin) could reduce ZIKV production in vitro and result in smaller foci of infection. Time-of-drug-addition assay revealed that early treatment with statins is more beneficial than late treatment; however, statins could not completely inhibit the entry stage of ZIKV infection. Furthermore, individual lipophilic statins differed in anti-ZIKV capacity, with fluvastatin being the most efficient at low concentrations. Taken together, this study shows that statins or their derivatives have the potential to be used as anti-ZIKV therapeutic agents.
- Published
- 2019
5. Rapid virulence shift of an H5N2 avian influenza virus during a single passage in mice
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Jeong-Ki Kim, Sang-Mu Shim, Daesub Song, Jeong-Hyun Nam, Erica Españo, Eun-Jung Song, and Dae-Gwin Jeong
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0301 basic medicine ,Virulence ,Biology ,medicine.disease_cause ,Virus ,Microbiology ,03 medical and health sciences ,Mice ,Orthomyxoviridae Infections ,Virology ,Influenza A virus ,medicine ,Animals ,H5N2 Avian Influenza Virus ,Phylogeny ,Mutation ,Host (biology) ,virus diseases ,General Medicine ,Adaptation, Physiological ,Influenza A virus subtype H5N1 ,030104 developmental biology ,Host adaptation ,Influenza A Virus, H5N2 Subtype - Abstract
Influenza A viruses must undergo adaptation to acquire virulence in new host species. In mouse models, host adaptation for virulence is generally performed through 5 to 20 lung-to-lung passages. However, highly pathogenic avian influenza viruses (e.g., H5N1 and H7N7 subtypes) have been observed to acquire virulence in mice after only a few in vivo passages. In this study, a low-pathogenic avian influenza H5N2 virus, A/Aquatic Bird/Korea/CN2/2009, which was a prevalent subtype in South Korea in 2009, was serially passaged in mice to evaluate its potential to become highly pathogenic. Unexpectedly, the virus became highly pathogenic in mice after a single lung-to-lung passage, resulting in 100% lethality with a mean death time (MDT) of 6.1 days postinfection (DPI). Moreover, the pathogenicity gradually increased after subsequent in vivo passages with an MDT of 5.2 and 4.2 DPI after the second and third passage, respectively. Our molecular analysis revealed that two amino acid changes in the polymerase complex (a glutamate-to-lysine substitution at position 627 of PB2 and a threonine-to-isoleucine substitution at position 97 of PA) were associated with the increased pathogenicity; the PB2 E627K mutation was responsible for the initial virulence conversion (0 to 100% lethality), while the PA T97I mutation acted as an accessory for the increased virulence.
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- 2017
6. Nontoxic outer membrane vesicles efficiently increase the efficacy of an influenza vaccine in mice and ferrets
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Dae Gwin Jeong, Chong-Kil Lee, Sang-Mu Shim, Doo-Jin Kim, Jeong-Hyun Nam, Eun-Jung Song, Jeong-Ki Kim, Tae-Young Lee, Sang-Hyun Kim, and Daesub Song
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0301 basic medicine ,Influenza vaccine ,medicine.medical_treatment ,Cross Protection ,030106 microbiology ,Heterologous ,Biology ,Antibodies, Viral ,Virus ,Microbiology ,03 medical and health sciences ,Mice ,Immunogenicity, Vaccine ,Influenza A Virus, H1N1 Subtype ,Adjuvants, Immunologic ,Orthomyxoviridae Infections ,medicine ,Escherichia coli ,Animals ,Lung ,Attenuated vaccine ,General Veterinary ,General Immunology and Microbiology ,Lethal dose ,Public Health, Environmental and Occupational Health ,Ferrets ,Th1 Cells ,Viral Load ,Virology ,Immunity, Humoral ,030104 developmental biology ,Infectious Diseases ,Influenza Vaccines ,Humoral immunity ,Molecular Medicine ,Viral load ,Adjuvant ,Bacterial Outer Membrane Proteins - Abstract
In this study, we developed a further-modified outer membrane vesicle (fmOMV) from the ΔmsbB/ΔpagP mutant of Escherichia coli transformed with the plasmid, pLpxF, in order to use it as an adjuvant for pandemic H1N1 (pH1N1) influenza vaccine. We evaluated the efficacy of the pH1N1 influenza vaccine containing the fmOMV in animal models as compared to the commercial adjuvants, alum or AddaVaxTM. The fmOMV-adjuvanted pH1N1 influenza vaccine induced a significant increase in the humoral immunity; however, this effect was less than that of the AddaVaxTM. The fmOMV-adjuvanted vaccine displayed pronounced an enhanced protective efficacy with increased T cell immune response and reduced the viral load in the lungs of the infected mice after challenging them with a lethal dose of the homologous virus. Moreover, it resulted in a significantly higher cross-protection against heterologous virus challenge than that of the pH1N1 vaccine with alum or with no adjuvants. In ferrets, the fmOMV-adjuvanted vaccine elicited a superior antibody response based on the HI titer and efficiently protected the animals from the lethal viral challenges. Taken together, the nontoxic fmOMV could be a promising adjuvant for inducing robust T cell priming into the pH1N1 vaccine and might be broadly applicable to the development of preventive measures against influenza virus infection.
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- 2016
7. Genetic Characterization of an Ancestral Strain of the Avian-Origin H3N2 Canine Influenza Virus Currently Circulating in East Asia
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Bo-Kyu Kang, Woonsung Na, Hyoungjoon Moon, Eun-Jung Song, Daesub Song, Dong-Jun An, Dae Gwin Jeong, Kwang-Soo Lyoo, Jeong-Ki Kim, Jeong-Hyun Nam, Minjoo Yeom, and Sang-Mu Shim
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0301 basic medicine ,China ,Genotype ,viruses ,Canine influenza ,Biology ,Applied Microbiology and Biotechnology ,Virus ,Evolution, Molecular ,03 medical and health sciences ,Dogs ,Orthomyxoviridae Infections ,Phylogenetics ,Republic of Korea ,Animals ,East Asia ,Dog Diseases ,Phylogeny ,Transmission (medicine) ,Strain (biology) ,Influenza A Virus, H3N2 Subtype ,virus diseases ,General Medicine ,Sequence Analysis, DNA ,Thailand ,Virology ,030104 developmental biology ,Cats ,Biotechnology - Abstract
H3N2 canine influenza virus emerged in South Korea in 2007 and subsequently spread to China and Thailand, causing epidemic or endemic respiratory diseases in dogs. Through intermammalian species transmission, the virus has also infected cats. However, no direct evidence of significant genetic evolution has been reported since its first emergence. Here, we describe in depth the genetic and molecular characteristics of the ancestral strain (i.e., the first virus isolate from South Korea) of the H3N2 canine influenza virus currently circulating in East Asia.
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- 2016
8. A novel reassortant canine H3N1 influenza virus between pandemic H1N1 and canine H3N2 influenza viruses in Korea
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Seong-Jun Park, Manki Song, Hye-Young Jeoung, Hyoungjoon Moon, Minjoo Yeom, Bo-Kyu Kang, Minki Hong, Daesub Song, Dong-Jun An, Hyekwon Kim, Jeong-Hyun Nam, Robert G. Webster, Jeong-Ki Kim, Bong-Kyun Park, and Jinsik Oh
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Canine influenza ,viruses ,Molecular Sequence Data ,Biology ,medicine.disease_cause ,Genetic analysis ,H5N1 genetic structure ,Virus ,Viral Proteins ,Dogs ,Orthomyxoviridae Infections ,Virology ,Reassortant Viruses ,Pandemic ,Republic of Korea ,Influenza A virus ,medicine ,Animals ,Cluster Analysis ,Viral shedding ,Phylogeny ,Sequence Homology, Amino Acid ,Animal ,virus diseases ,Sequence Analysis, DNA ,Virus Shedding ,Carrier State ,RNA, Viral - Abstract
During recent canine influenza surveillance in South Korea, a novel H3N1 canine influenza virus (CIV) that is a putative reassortant between pandemic H1N1 2009 and H3N2 CIVs was isolated. Genetic analysis of eight genes of the influenza virus revealed that the novel H3N1 isolate presented high similarities (99.1–99.9 %) to pandemic influenza H1N1, except for in the haemagglutinin (HA) gene. The HA gene nucleotide sequence of the novel CIV H3N1 was similar (99.6 %) to that of CIV H3N2 isolated in Korea and China. Dogs infected with the novel H3N1 CIV did not show any notable symptoms, in contrast to dogs infected with H3N2 CIV. Despite no visible clinical signs of disease, nasal shedding of virus was detected and the infected dogs presented mild histopathological changes.
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- 2011
9. Emergence of mammalian species-infectious and -pathogenic avian influenza H6N5 virus with no evidence of adaptation
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Eun-Ha Kim, Young Ki Choi, Daesub Song, Jeong-Hyun Nam, Haryoung Poo, and Jeong-Ki Kim
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animal structures ,Swine ,viruses ,Immunology ,Reassortment ,Virulence ,Hemagglutinin (influenza) ,Chick Embryo ,medicine.disease_cause ,Microbiology ,H5N1 genetic structure ,Antigenic drift ,Virus ,Birds ,Feces ,Mice ,Viral Proteins ,Orthomyxoviridae Infections ,Virology ,medicine ,Influenza A virus ,Animals ,Lung ,biology ,Ferrets ,virus diseases ,RNA-Dependent RNA Polymerase ,Influenza A virus subtype H5N1 ,Mice, Inbred C57BL ,Ducks ,Genetic Diversity and Evolution ,Insect Science ,Influenza in Birds ,biology.protein ,Chickens - Abstract
The migratory waterfowl of the world are considered to be the natural reservoir of influenza A viruses. Of the 16 hemagglutinin subtypes of avian influenza viruses, the H6 subtype is commonly perpetuated in its natural hosts and is of concern due to its potential to be a precursor of highly pathogenic influenza viruses by reassortment. During routine influenza surveillance, we isolated an unconventional H6N5 subtype of avian influenza virus. Experimental infection of mice revealed that this isolate replicated efficiently in the lungs, subsequently spread systemically, and caused lethality. The isolate also productively infected ferrets, with direct evidence of contact transmission, but no disease or transmission was seen in pigs. Although the isolate possessed the conserved receptor-binding site sequences of avian influenza viruses, it exhibited relatively low replication efficiencies in ducks and chickens. Our genetic and molecular analyses of the isolate revealed that its PB1 sequence showed the highest evolutionary relationship to those of highly pathogenic H5N1 avian influenza viruses and that its PA protein had an isoleucine residue at position 97 (a representative virulence marker). Further studies will be required to examine why our isolate has the virologic characteristics of mammalian influenza viruses but the archetypal receptor binding profiles of avian influenza viruses, as well as to determine whether its potential virulence markers (PB1 analogous to those of H5N1 viruses or isoleucine residue at position 97 within PA) could render it highly pathogenic in mice.
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- 2011
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