A recent study of the COVID-19 structure reveals how the virus works throughout the human lungs. The envelope protein of the virus halts the cell-junction protein, creating damage to the body and eventually holding the door wide open for the virus to spread. On the good side, the new structure based on SARS-CoV-2 could be a potential model to speed up the process of formulating a more effective drug to repel the severe effects of the coronavirus.


Cryo-EM Shows Interaction Between Envelope Protein of SARS-CoV-2 and Lungs Cell Junction PALS1

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Cryo-electron microscopy or cryo-EM was the technology used to produce frozen samples of the interaction between the two proteins. The new, atomic-level model of the viral process shows how it actually infects protein in the human body through its very own envelope proteins. According to the study published in the journal Nature Communications entitled "Structural basis for SARS-CoV-2 envelope protein recognition of human cell junction protein PALS1", the interaction of the viral protein with the human protein leads to extensive damage of the lungs.

The genomes of the SARS-CoV-2 include an "envelope" protein which is found on the membrane of the virus. The protein is in charge of the overall development cycle of the virus, including assembly and release. The study shows that once the virus affected the human body, it will hijack specific human proteins that maintain the lining of the lungs, causing serious damage. After the lungs, the virus targets other humans organs.

The coronavirus envelope protein, also known as E protein, attacks the PALS1 or cell junctions of the lungs. This disruption of the lung cells will require immune cells to manage and fix the damage. However, the immune reaction usually triggers uncontrollable inflammation that results in a cytokine storm, SciTechDaily reports.

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Immunity Reaction of Human Body Produce Cytokine Storm

The cytokine storm is an immune response when the human body releases cytokines at a massive rate to prevent and fight off internal organ injuries, including cellular-level damage. According to the National Cancer Institute, a normal level of cytokine is essential to immunity, but when released in unnecessary amounts it can cause inflammation, fatigue, and high fever. In the worst-case scenario, a cytokine storm can escalate to hypercytokinemia when multiple organs shut down.

Brookhaven Lab's Laboratory for BioMolecular Structure, also known as LBMS, is the research facility where studies for the new molecular model of the virus were conducted. Qun Liu, Brookhaven Lab's structural biologist and lead author of the study, explained that the damage from the protein infections was successfully analyzed with the atomic-level data that the new cryo-electron microscopes provided.

LBMS, together with Brookhaven's National Synchroton Light Source II, played essential roles in identifying the effects of the virus through unique protein-imaging techniques. Deciphering the effects of COVID-19 on the proteins and the lungs was the first paper published from the research facility. LBMS is a new center that opened ahead of schedule to contribute to research against coronavirus.

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