tetano
Editor, Senior Moderator
J Immunother
. 2023 Feb 20.
doi: 10.1097/CJI.0000000000000455. Online ahead of print.
COVID-19: Attacks Immune Cells and Interferences With Antigen Presentation Through MHC-Like Decoy System
Wenzhong Liu[SUP] 1 2 [/SUP], Hualan Li[SUP] 2 [/SUP]
Affiliations
Abstract
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.
. 2023 Feb 20.
doi: 10.1097/CJI.0000000000000455. Online ahead of print.
COVID-19: Attacks Immune Cells and Interferences With Antigen Presentation Through MHC-Like Decoy System
Wenzhong Liu[SUP] 1 2 [/SUP], Hualan Li[SUP] 2 [/SUP]
Affiliations
- PMID: 36799912
- DOI: 10.1097/CJI.0000000000000455
Abstract
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.