The research team of the National Institutes of Health discovered the infection mechanism of the new coronavirus. (provided by the National Health Service)
[Reporter Lin Huiqin/Taipei Report]Uncover the mechanism of new coronavirus infection! After the new coronavirus enters the human body, it mainly infects cells through the combination of the spike protein (S protein) on the surface of the virus and the ACE2 receptor on the surface of human respiratory epithelial cells. The main reason is that the spike protein will induce the high expression of the protein kinase GLK. GLK is a key player in the chain reaction, causing a steady increase in the ACE2 protein on the cell surface, and at the same time creating ACE2 that is more susceptible to infection, successfully expanding the scope of virus invasion. Severe disease.
Zhuang Huaijia said that the expression of ACE2 in normal epithelial cells is low, but after infection with the new coronavirus, acute and severe respiratory symptoms are quickly induced. If the rapid transmission mechanism can be found, there is a chance to reduce the infection.
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The research team found that the expression of protein kinase MAP4K3 (also known as GLK) in cells infected with the new coronavirus was higher than that in normal cells, and the proportion of epithelial cells with high GLK expression was positively correlated with disease severity. The results of cellular RNA sequencing, as well as the use of proteomics and various biochemical experiments, confirmed that after the new coronavirus enters the host epithelial cells, the spike protein will induce high expression of the protein kinase GLK and trigger a chain reaction.
Zhuang Huaijia pointed out that the excessive expression of GLK will phosphorylate the ACE2 protein, so that ACE2 escapes the ubiquitination degradation mechanism of the ubiquitinase UBR4, that is, the normal UBR4 acts on ACE2, which will cause ACE2 to be decomposed, but the high expression of GLK makes ACE2 escape. Passing this level of decomposition results in a steady increase in ACE2 on the cell surface.
In addition, the overexpression of GLK induces the release of ACE2-loaded extracellular bodies. Zhuang Huaijia explained that the imagination is like the cells spewing bubbles, and the ACE2-loaded bubbles are passed on to other cells with low ACE2 expression. ACE2 cells are more likely to be infected by the new coronavirus.
The above research results confirm that GLK excess is a key factor in the pathogenesis of new coronavirus infection, as well as the cause of rapid clinical symptoms and easy transmission.
Zhuang Huaijia said that the research team also used the mouse model to conduct animal experiments. When the small molecule inhibitor of GLK (verteporfin) was used, the amount of ACE2 on the cell surface could be reduced, and the production of ACE2 extracellular bodies could be reduced, and the infection in mice was successfully inhibited. Rate. Verteporfin and other drugs that can modulate GLK and ACE2-related drugs have the potential to be candidate drugs for inhibiting infection.
The relevant research results were published in the world-renowned journal EMBO Molecular Medicine in July this year. The European Molecular Biology Organization (EMBO) is a European scientific organization engaged in life science research and promoting the exchange of international scientists. It has a strong influence in the field of molecular biology in the world. It also founded the EMBO series of academic journals.
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