Activating organ’s immunizing power against COVID–19–learning from SARS

Background Coronaviruses cause respiratory diseases in many animals, including humans. Spike protein is an important component of coronavirus structure and the formation of ACE2 (angiotensin converting enzyme 2)–spike complex mediates virus entry to host cells. C–type lectin family are widely distribute on the surface of human cells and have been shown to activate the immune system. In this article, we first illustrate why we can “learn from SARS” with phylogenetic analysis. Then, we use SARS spike protein structure, to inferring our molecular docking experiment, revealing the potential capacity of C–type lectin to directly interact with spike protein obstructs the formation of spike–ACE2 complex. Considering the expression profile of C–type lectin family changing significantly during infection, we predict certain members of this kind of protein as potential therapeutic target and verify their assumed function by inferring an C–type lectin–dependent CD4/CD28 T cell survival molecular network with endogenous molecular network theory (EMT) and comparing the predicted expression trend corresponding to each molecular with experiment data. Methods Alignments are inferred by MAFFT V7 ( G–ins–i, Blosom). Maximum likelihood analyses and bootstrap test carried out by RAXML V8.2 ML+BP online platform. Protein structure is predicted by SWISSMODELLING online platform. Molecular docking experiment is carried out by Z–dock Version 3.0.2. C–type lectin–dependent CD4/CD28 T cell Network is inferred by EMT theory. Result Our molecular docking experiment revealing the potential capacity of C–type lectin to directly interact with spike protein obstructs the formation of spike–ACE2 complex. Based on the expression profile of C–type lectin family during infection, we predicting certain member of this kind of protein as potential therapeutic target such as Clec7a, Clec12a and Clec11a, corresponding immune cell types such as CD4/CD28 T cell simulated by EMT theory and verified by experiment data, antigen adjuvant with similar C–type lectin receptor–TDM and some immune–boosting drugs–radix sophorae, lactoferrin and Astragalus membranaceus, for future testing. Conclusions C–type lectin and their corresponding immune cells predicted in this work may be the potential therapeutic targets for the disease caused by COVID–19. C–lectin with the capacity of directly interact with spike protein inhibiting the formation of ACE2–spike complex may be the way they execute anti–virus function. The corresponding cell type such as CD4/CD28 T cell may participate and against virus while Clec7a, Clec12a and Clec11a presumed capacity for facilitating CD4/CD28 T cell survival during infection being verified by EMT combining with experiment data. Our prediction at least suggest the possibility of activating organ’s immunizing power to prevent from COVID–19 and the drugs we suggested are all need to be further tested. Trial registration Retrospectively registered. Keywords C–type lectin, spike protein, coronavirus, COVID–19, TDM.