• 한국동물위생학회지
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• 제45권1호
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• pp.31-38
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• 2022

Swine influenza (SI) is an important respiratory disease in pigs and epidemic worldwide, which is caused by influenza A virus (IAV) belonging to the family of Orthomyxoviridae. As seen again in the 2009 swine-origin influenza A H1N1 pandemic, pigs are known to be susceptible to swine, avian, and human IAVs, and can serve as a 'mixing vessel' for the generation of novel IAV variants. To this end, the emergence of swine influenza viruses must be kept under close surveillance. Herein, we report the isolation and phylogenetic study of a swine IAV, A/swine/Korea/21810/2021 (sw21810, H3N2 subtype). BLASTN sequence analysis of 8 gene segments of the isolated virus revealed a high degree of nucleotide similarity (94.76 to 100%) to porcine strains circulating in Korea and the United States. Out of 8 genome segments, the HA gene was closely related to that of isolates from cluster I. Additionally, the NA gene of the isolate belonged to a Korean Swine H1N1 origin, and the PB2, PB1, NP and NS genes of the isolate were grouped into that of the Triple reassortant swine H3N2 origin virus. The PA and M genes of the isolate belonged to 2009 Pandemic H1N1 lineage. Human infection with mutants was most common through contact with infected pigs. Our results suggest the need for periodic close monitoring of this novel swine H3N2 influenza virus from a public health perspective.

• 생명과학회지
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• 제30권9호
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• pp.749-762
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• 2020

돼지인플루엔자는 동물에서 사람에게 감염할 수 있는 인수공통전염병이다. 우리는 2019년 한국 돼지농장에서 호흡기 증상을 보이는 돼지에서 3주의 H1N2형 인플루엔자바이러스를 분리하였다. 유전자 분석결과, 이들 바이러스의 8개 유전자 중 PA 및 NP 유전자는 2009 대유행 H1N1 인플루엔자 유래였고, 나머지 유전자는 돼지에 유행하는 H3N2 및 H1N2 인플루엔자 유래 유전자를 가진 재조합 바이러스 이었다. 분리된 H1N2 바이러스를 마우스에 접종한 결과, 마우스는 17% 정도 체중이 감소하였고, 염증 세포들이 침윤한 간질성 폐렴 증상을 보였다.

• Journal of Veterinary Science
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• 제22권4호
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• pp.43.1-43.10
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• 2021

Background: The H5 avian influenza viruses (AIVs) of clade 2.3.4.4 circulate in wild and domestic birds worldwide. In 2017, nine strains of H5N6 AIVs were isolated from aquatic poultry in Xinjiang, Northwest China. Objectives: This study aimed to analyze the origin, reassortment, and mutations of the AIV isolates. Methods: AIVs were isolated from oropharyngeal and cloacal swabs of poultry. Identification was accomplished by inoculating isolates into embryonated chicken eggs and performing hemagglutination tests and reverse transcription polymerase chain reaction (RT-PCR). The viral genomes were amplified with RT-PCR and then sequenced. The sequence alignment, phylogenetic, and molecular characteristic analyses were performed by using bioinformatic software. Results: Nine isolates originated from the same ancestor. The viral HA gene belonged to clade 2.3.4.4B, while the NA gene had a close phylogenetic relationship with the 2.3.4.4C H5N6 highly pathogenic avian influenza viruses (HPAIVs) isolated from shoveler ducks in Ningxia in 2015. The NP gene was grouped into an independent subcluster within the 2.3.4.4B H5N8 AIVs, and the remaining six genes all had close phylogenetic relationships with the 2.3.4.4B H5N8 HPAIVs isolated from the wild birds in China, Egypt, Uganda, Cameroon, and India in 2016-2017, Multiple basic amino acid residues associated with HPAIVs were located adjacent to the cleavage site of the HA protein. The nine isolates comprised reassortant 2.3.4.4B HPAIVs originating from 2.3.4.4B H5N8 and 2.3.4.4C H5N6 viruses in wild birds. Conclusions: These results suggest that the Northern Tianshan Mountain wetlands in Xinjiang may have a key role in AIVs disseminating from Central China to the Eurasian continent and East African.

• Clinical and Experimental Pediatrics
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• 제52권8호
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• pp.862-868
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• 2009

Since its identification in April 2009, a swine-origin H1N1 influenza A virus (S-OIV) which is a reassortment of gene segments from both North American triple-reassortant and Eurasian swine influenza has been widely spread among humans in unexpected rapidity. To date, each gene segment of the 2009 influenza A (H1N1) outbreak viruses have shown high (99.9%) neucleotide sequence identity. As of July 6, 94,512 people have been infected in 122 countries, of whom 429 have died with an overall case-fatality rate of <0.5%. Most confirmed cases of S-OIV infection have been characterized by self-limited, uncomplicated febrile respiratory illness and 38% of cases have also included vomiting or diarrhea. Standard plus droplet precautions should be adhered to at all times. Tests on S-OIV have indicated that current new H1N1 viruses are sensitive to neuraminidase inhibitors (oseltamivir). However, current less virulent S-OIV may evolve into a pathogenic strain or acquire antiviral resistance, potentially with more severe clinical consequences. Efforts to control these outbreaks would be based on our understanding of novel S-OIV and previous influenza pandemics.

• Journal of Microbiology and Biotechnology
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• 제20권11호
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• pp.1500-1505
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• 2010

The novel swine-origin influenza A/H1N1 virus (S-OIV) first detected in April 2009 has been identified to transmit from humans to humans directly and is the cause of the currently emerged pandemic. In this study, nucleotide and deduced amino acid sequences of the hemagglutinin (HA) and neuraminidase (NA) of the S-OIV and other influenza A viruses were analyzed through bioinformatic tools for phylogenetic analysis, genetic recombination, and point mutation to investigate the emergence and adaptation of the S-OIV in humans. The phylogenetic analysis showed that the HA comes from triple reassortant influenza A/H1N2 and the NA from Eurasian swine influenza A/H1N1, indicating that HA and NA descend from different lineages during the genesis of the S-OIV. Recombination analysis ified the possibility of occurrence of recombination in HA and NA, denoting the role of reassortment in the outbreak. Several conservative mutations were observed in the amino acid sequences of the HA and NA, and these mutated residues were identical in the S-OIV. The results reported herein suggest the notion that the recent pandemic is the result of reassortment of different genes from different lineages of two envelope proteins, HA and NA, which are responsible for the antigenic activity of the virus. This study further suggests that the adaptive capability of the S-OIV in humans is acquired by the unique mutations generated during emergence.

• 대한수의학회지
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• 제51권2호
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• pp.129-137
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• 2011

Swine diseases could be caused by unrecognized or minor pathogens. In this study, two unknown cytopathogenic agents were isolated from swine, through cell culture. In order to identify these two cytopathogenic agent (designated CP129 and #2045-7), a particle associated nucleic acids PCR (PANPCR) from previous paper was used with simple modification. The cloning procedure was more specified in this study by adding cell control system. According to the modified PAN-PCR, two and four agentsspecific DNA sequences were obtained from CP129 and #2045-7, respectively, and they were identified as Mycoplasma (M.) hyorhinis and Mammalian orthoreovirus by nucleotide BLAST. Since M. hyorhinis (CP129) was filterable and non-visible by microscope, this unusual virus-like nature of M. hyorhinis (CP129) was discussed. Especially, the reovirus (#2045-7) was a serotype 3 and a triple reassortant among three serotypes of reoviruses. It was grouped with recently reported reoviruses from disease cases (swine, human and feline), based on the genetic analysis of L1 and S1 partial sequences. In conclusion, two unknown cytopathogenic agents were successfully identified using modified PAN-PCR with cell control system and they were characterized in this study.

• 생명과학회지
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• 제20권3호
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• pp.365-373
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• 2010

2006년 10월부터 2008 년 6월까지 총 인플루엔자 의사 환자 1,822건의 인후도찰물 및 비인후도찰물에서 277건의 인플루엔자바이러스를 분리했다. 절기별로는 2006~2007 절기의 1,154검체 중 52건(4.5%), 2007~2008절기의 668검체 중 210건(31.4%)에서 인플루엔자바이러스를 분리하였다. 인플루엔자바이러스 A/H1N1의 HA 유전자의 경우, 2008~2009 절기의 백신주인 A/Brisbane/59/2007과는 96.7%~97.7%, A/Solomon Islands/3/2006 96.5%~97.3%, A/New Caledonia/20/99와는 95.6%~96.6%의 유사성을 나타냈으며, NA 유전자의 경우, A/Brisbane/59/2007과는 97.8%~98.5%, A/Solomon Islands/3/2006과는 96.7%~97.6%, A/New Caledonia/20/99와는 96.8%~97.7%의 유사성을 보여 2008~2009절기의 백신주인 A/Brisbane/59/07과 가장 유사성이 컸다. 인플루엔자바이러스 A/H3N2의 분리주 중 1주를 제외한 모든 분리주가 HA 유전자에서 2008~2009 절기 백신주인 A/Brisbane/10/2007과는 98.4%~99.7%의 유사성을 보였고, A/Wisconsin/67/2005와는 96.5%~97.5%의 유사성을 보였으며, NA 유전자에서는 A/Brisbane/10/2007과는 98.9%~99.4%, A/Wisconsin/67/2005와는 98.0%~98.6%, A/California/7/2004와는 98.3%~98.9%의 유사성을 보였다. 인플루엔자바이러스 B의 HA 유전자의 경우는 2주를 제외하고는 2008~2009 절기의 백신주인 B/Florida/4/2006과는 96.5%~99.7%의 유사성을 보였으며, B/Malaysia/2506/2004와는 86.7%~87.7%의 유사성을 보여 B/Florida/4/2006과의 유사성이 크게 나타났다. NA 유전자의 경우는 reassortant분리주가 96.7%와 97.3%의 유사성을 나타내는 것을 제외하고는 B/Florida/4/2006에 98.9%~100%의 유사성을 나타냈으며, 분리주 유행시기의 백신주인 B/Malaysia/2506/2004와는 94.5%~96.7%의 유사성을 나타내어 2008~2009 절기의 백신주와 더 큰 유사성을 보였다. HA 유전자에서는 conserverd receptor binding site는 아미노산의 치환 없이 모든 분리주에서 잘 보존되어 있었으며, N-linked glycosylation site도 인플루엔자바이러스 A/H1 1주, A/H3 1주를 제외하고는 모두 같은 수의 N-linked glycosylation sites를 가졌으며, 인플루엔자바이러스 B의 경우는 2008~2009 절기의 백신주보다 1개가 많은 4개의 N-linked glycosylation sites를 가지고 있었다. Antigenic sites의 경우는 인플루엔자바이러스 A/H1의 Sb의 3개의 아미노산에서 백신주들과 다른 아미노산을 가지고 있으며, A/H3에서는 A, B, E 부위에서 는 아미노산의 변화가 나타났고, C, D 부위에서는 변화가 없었다. 인플루엔자바이러스 B의 4개의 분리주에서는 150 loop와 160 loop에서 B/Florida/4/2006과 비교하여 1개의 아미노산에서 치환이 나타났으며, 190 helix에서 모든 분리주가 B/Florida/4/2006과 비교하여 1개의 아미노산에서 치환이 나타났다.