{"title":"COVID-19:通过mhc样诱饵系统攻击免疫细胞并干扰抗原呈递","authors":"Wenzhong Liu, Hualan Li","doi":"10.1097/CJI.0000000000000455","DOIUrl":null,"url":null,"abstract":"<p><p>The high mortality of coronavirus disease 2019 is related to poor antigen presentation and lymphopenia. Cytomegalovirus and the herpes family encode a series of major histocompatibility complex (MHC)-like molecules required for targeted immune responses to achieve immune escape. In this present study, domain search results showed that many proteins of the severe acute respiratory syndrome coronavirus 2 virus had MHC-like domains, which were similar to decoys for the human immune system. MHC-like structures could bind to MHC receptors of immune cells (such as CD4 + T-cell, CD8 + T-cell, and natural killer-cell), interfering with antigen presentation. Then the oxygen free radicals generated by E protein destroyed immune cells after MHC-like of S protein could bind to them. Mutations in the MHC-like region of the viral proteins such as S promoted weaker immune resistance and more robust transmission. S 127-194 were the primary reason for the robust transmission of delta variants. The S 144-162 regulated the formation of S trimer. The mutations of RdRP: G671S and N: D63G of delta variant caused high viral load. S 62-80 of alpha, beta, lambda variants were the important factor for fast-spreading. S 616-676 and 1014-1114 were causes of high mortality for gamma variants infections. These sites were in the MHC-like structure regions.</p>","PeriodicalId":15996,"journal":{"name":"Journal of Immunotherapy","volume":"46 3","pages":"75-88"},"PeriodicalIF":3.2000,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9987643/pdf/cji-46-75.pdf","citationCount":"1","resultStr":"{\"title\":\"COVID-19: Attacks Immune Cells and Interferences With Antigen Presentation Through MHC-Like Decoy System.\",\"authors\":\"Wenzhong Liu, Hualan Li\",\"doi\":\"10.1097/CJI.0000000000000455\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The high mortality of coronavirus disease 2019 is related to poor antigen presentation and lymphopenia. Cytomegalovirus and the herpes family encode a series of major histocompatibility complex (MHC)-like molecules required for targeted immune responses to achieve immune escape. In this present study, domain search results showed that many proteins of the severe acute respiratory syndrome coronavirus 2 virus had MHC-like domains, which were similar to decoys for the human immune system. MHC-like structures could bind to MHC receptors of immune cells (such as CD4 + T-cell, CD8 + T-cell, and natural killer-cell), interfering with antigen presentation. Then the oxygen free radicals generated by E protein destroyed immune cells after MHC-like of S protein could bind to them. Mutations in the MHC-like region of the viral proteins such as S promoted weaker immune resistance and more robust transmission. S 127-194 were the primary reason for the robust transmission of delta variants. The S 144-162 regulated the formation of S trimer. The mutations of RdRP: G671S and N: D63G of delta variant caused high viral load. S 62-80 of alpha, beta, lambda variants were the important factor for fast-spreading. S 616-676 and 1014-1114 were causes of high mortality for gamma variants infections. These sites were in the MHC-like structure regions.</p>\",\"PeriodicalId\":15996,\"journal\":{\"name\":\"Journal of Immunotherapy\",\"volume\":\"46 3\",\"pages\":\"75-88\"},\"PeriodicalIF\":3.2000,\"publicationDate\":\"2023-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9987643/pdf/cji-46-75.pdf\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Immunotherapy\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1097/CJI.0000000000000455\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Immunotherapy","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/CJI.0000000000000455","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
COVID-19: Attacks Immune Cells and Interferences With Antigen Presentation Through MHC-Like Decoy System.
The high mortality of coronavirus disease 2019 is related to poor antigen presentation and lymphopenia. Cytomegalovirus and the herpes family encode a series of major histocompatibility complex (MHC)-like molecules required for targeted immune responses to achieve immune escape. In this present study, domain search results showed that many proteins of the severe acute respiratory syndrome coronavirus 2 virus had MHC-like domains, which were similar to decoys for the human immune system. MHC-like structures could bind to MHC receptors of immune cells (such as CD4 + T-cell, CD8 + T-cell, and natural killer-cell), interfering with antigen presentation. Then the oxygen free radicals generated by E protein destroyed immune cells after MHC-like of S protein could bind to them. Mutations in the MHC-like region of the viral proteins such as S promoted weaker immune resistance and more robust transmission. S 127-194 were the primary reason for the robust transmission of delta variants. The S 144-162 regulated the formation of S trimer. The mutations of RdRP: G671S and N: D63G of delta variant caused high viral load. S 62-80 of alpha, beta, lambda variants were the important factor for fast-spreading. S 616-676 and 1014-1114 were causes of high mortality for gamma variants infections. These sites were in the MHC-like structure regions.
期刊介绍:
Journal of Immunotherapy features rapid publication of articles on immunomodulators, lymphokines, antibodies, cells, and cell products in cancer biology and therapy. Laboratory and preclinical studies, as well as investigative clinical reports, are presented. The journal emphasizes basic mechanisms and methods for the rapid transfer of technology from the laboratory to the clinic. JIT contains full-length articles, review articles, and short communications.