지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2019.6
- 수록면
- 25 - 32 (8page)
- DOI
- 10.17262/KJPH.2019.06.56.1.25
이용수
초록· 키워드
오류제보하기
Objectives: Recent outbreaks caused by Middle East respiratory syndrome coronavirus (MERS-CoV), such as the May 2015 outbreak in Korea, highlight the urgency of studying new mutant viruses that may be introduced in the future and preparing effective countermeasures to prevent large-scale infections. Most coronaviruses that infect humans cause only mild respiratory infections, but research on coronaviruses has increased in the wake of large-scale epidemics of MERS and severe acute respiratory syndrome (SARS). Therefore, we conducted a comparative analysis of the major human coronaviruses using genetic information and performed a network analysis to investigate the interactions between viruses and host immune proteins.
Methods: Phylogenetic and structural analyses were performed using the spike protein sequences of six coronaviruses (HCoV-OC43, HCoV-HKU1, MERS-CoV, SARS-CoV, HCoV-229E, and HCoV-NL63) causing diseases in humans. Network analysis was performed using Cytoscape 3.3.0 to analyze the interactions of viral proteins with host immune proteins.
Results: The phylogenetic analysis showed that although HCoV-OC43 and MERS belong to different lineages (lineages A and C, respectively), the evolutionary distance between spike proteins in these two viruses is relatively close. The structural analysis confirmed that the structure of the spike protein of HCoVOC43 was similar to those of SARS-CoV and MERS-CoV, which are both highly transmissible. Finally, the network analysis confirmed interactions between the human IC1 protein, which is involved in the activation of the C1 complex, and non-structural proteins in SARS-CoV.
Conclusion: The similarity of SARS-CoV and MERS-CoV with other coronaviruses suggests the need for continued study of mutations in coronaviral genomes. In particular, the IC1 protein, which interacts with nonstructural proteins in SARS-CoV, may have a major effect on the host immune response to viral infection because it has functions related to complement system activation. Studies of these viruses and host immune proteins will assist the development of vaccines and therapeutic agents against coronaviruses by enhancing our understanding of the detailed immune mechanisms against viral infections.
Methods: Phylogenetic and structural analyses were performed using the spike protein sequences of six coronaviruses (HCoV-OC43, HCoV-HKU1, MERS-CoV, SARS-CoV, HCoV-229E, and HCoV-NL63) causing diseases in humans. Network analysis was performed using Cytoscape 3.3.0 to analyze the interactions of viral proteins with host immune proteins.
Results: The phylogenetic analysis showed that although HCoV-OC43 and MERS belong to different lineages (lineages A and C, respectively), the evolutionary distance between spike proteins in these two viruses is relatively close. The structural analysis confirmed that the structure of the spike protein of HCoVOC43 was similar to those of SARS-CoV and MERS-CoV, which are both highly transmissible. Finally, the network analysis confirmed interactions between the human IC1 protein, which is involved in the activation of the C1 complex, and non-structural proteins in SARS-CoV.
Conclusion: The similarity of SARS-CoV and MERS-CoV with other coronaviruses suggests the need for continued study of mutations in coronaviral genomes. In particular, the IC1 protein, which interacts with nonstructural proteins in SARS-CoV, may have a major effect on the host immune response to viral infection because it has functions related to complement system activation. Studies of these viruses and host immune proteins will assist the development of vaccines and therapeutic agents against coronaviruses by enhancing our understanding of the detailed immune mechanisms against viral infections.
목차
Abstract
Introduction
Methods
Results
Discussion
Conclusion
References
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UCI(KEPA) : I410-ECN-0101-2019-517-000909841