COVID-19:Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism


The novel coronavirus pneumonia (COVID-19) is an infectious acute respiratory caused by the novel coronavirus. The virus is a positive-strand RNA virus with high homology to bat coronavirus. In this study, conserved domain analysis, homology modeling, and molecular docking were used to compare the biological roles of specific proteins of the novel coronavirus. The results showed that some viral structural and nonstructural proteins could bind to the porphyrin, respectively. At the same time, orf1ab, ORF10 and ORF3a proteins coordinated to attack heme on the 1-beta chain of hemoglobin, dissociating iron to form porphyrin. Deoxyhemoglobin is more vulnerable to virus attacks than oxidized hemoglobin. The attack will cause less and less hemoglobin that can carry oxygen and carbon dioxide, producing symptoms of respiratory distress. Virus attack damaged many organs and tissues. Lung cells are toxic and inflammatory due to derivatives produced by the attack, which eventually resulted in ground-glass-like lung images. Capillaries easily broken due to inflammation. Proteins such as fibrinogen filled the capillaries' cracks through the coagulation reaction. Therefore, many fibrin and thrombus gathered in the lung tissue of critically ill patients. The mechanism also interfered with the normal heme anabolic pathway of the human body, expecting to result in human disease. This paper is only for academic discussion, the correctness of the theory needs to be confirmed by other experiments. According to the reader's suggestion, the content of the drug-related efficacy analysis has been deleted. Due to the side effects of drugs, please consult a qualified doctor for detailed treatment information, and do not take the drug yourself. We look forward to these discoveries bringing more ideas to people and inspiring people's confidence in defeating the virus.

Version notes

1.Based on the reader's suggestion, we rewrote some of the content, the basic conclusions remain unchanged. 2. New discovery: 1) Some structural proteins and non-structural proteins of the virus can bind porphyrin. The detailed mechanism is unclear. 2) By molecular docking, ORF3 and ORF10 can be embedded in deoxyhemoglobin respectively. This is further proved by calculations that viral proteins can attack hemoglobin. 3. Abstract: Added explanation for coagulation and fibrosis. 4. Introduction: Explained the relationship between hypoxemia, coagulation, fibrosis, mononuclear cells and other clinical phenomena and this theory. List possible routes for red blood cell infection. The symptoms similar to porphyria are listed. 5. Method: Added COVID-19 protein list 6. Results: 1) Delete the analysis content of the drug efficacy 2) Rerun the data of model. 7. Discussion: red blood cell infection and immune hemolysis 8. Conclusion: Added explanation of pathogenic mechanism