Middle East Respiratory Syndrome Coronavirus (MERS-CoV) was first identified in 2012 at the Middle East which is an emerging pathogen that caused outbreak in South Korea in 2015; a total 186 cases have been infected, with a death 38 people. Evasion of the innate immunity would contribute to MERS-CoV...
Middle East Respiratory Syndrome Coronavirus (MERS-CoV) was first identified in 2012 at the Middle East which is an emerging pathogen that caused outbreak in South Korea in 2015; a total 186 cases have been infected, with a death 38 people. Evasion of the innate immunity would contribute to MERS-CoV pathogenesis, but the mechanism is largely unclear. Furthermore, MERS-CoV encodes many viral genes, but still unidentified. The goal of this study is to construction and expression of viral proteins, structural (E, M, N, S-N-terminal, S-RBD, Spike full), nonstructural (nsp1 to nsp16, PLpro), and accessory (ORF3, ORF4a, ORF4b) proteins and to determine which proteins involved in immune evasion mechanism. We synthesized viral gene products by PCR with MERS-CoV whole genome and cloned into N-terminal Flag-tagged plasmid, then transiently transfected into 293T cells. Among viral proteins, non-structural protein 1 inhibits MDA5- induced IFN-β promoter activity, whereas MDA5 protein is degraded by NSP1. Here, we further explore the antiviral effect and pathogenic role of MERS-CoV NSP1. Our results suggest new finding that MERS-CoV NSP1 150-193 domain inhibits MDA5.
Middle East Respiratory Syndrome Coronavirus (MERS-CoV) was first identified in 2012 at the Middle East which is an emerging pathogen that caused outbreak in South Korea in 2015; a total 186 cases have been infected, with a death 38 people. Evasion of the innate immunity would contribute to MERS-CoV pathogenesis, but the mechanism is largely unclear. Furthermore, MERS-CoV encodes many viral genes, but still unidentified. The goal of this study is to construction and expression of viral proteins, structural (E, M, N, S-N-terminal, S-RBD, Spike full), nonstructural (nsp1 to nsp16, PLpro), and accessory (ORF3, ORF4a, ORF4b) proteins and to determine which proteins involved in immune evasion mechanism. We synthesized viral gene products by PCR with MERS-CoV whole genome and cloned into N-terminal Flag-tagged plasmid, then transiently transfected into 293T cells. Among viral proteins, non-structural protein 1 inhibits MDA5- induced IFN-β promoter activity, whereas MDA5 protein is degraded by NSP1. Here, we further explore the antiviral effect and pathogenic role of MERS-CoV NSP1. Our results suggest new finding that MERS-CoV NSP1 150-193 domain inhibits MDA5.
주제어
#Middle East respiratory syndrome coronavirus Non-structural protein 1 Type I interferon MDA5 중동 호흡기 코로나 바이러스 비구조 단백질 1 인터페론 1형 흑색 종 분화 관련 단백질 5
학위논문 정보
저자
윤슬기
학위수여기관
전북대학교 일반대학원
학위구분
국내석사
학과
생리활성소재과학과
지도교수
명진종
발행연도
2018
총페이지
viii, 48 p.
키워드
Middle East respiratory syndrome coronavirus Non-structural protein 1 Type I interferon MDA5 중동 호흡기 코로나 바이러스 비구조 단백질 1 인터페론 1형 흑색 종 분화 관련 단백질 5
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