Keeping track of each new SARS-CoV-2 strain and variant may feel like learning a new language. The myriad of Greek letters used to designate each one quickly turns science into classics, so it’s understandable how one may get lost in the confusing terms. But keep calm, these identifiers are crucial for understanding how COVID-19 evolves. They help scientists organize the virus’ different traits and open a window into understanding its behavior at the molecular level. A recent experimental study has just discovered how one of the determining factors that contribute to virulence could be the strength with which the virus binds to the host cell. In a joint effort between the University of Auburn, University of Munich, and Utrecht University, scientists analyzed the virus’ atomic structure.
The team observed how the different variants’ spike proteins interacted with the human ACE-2 protein and found that Alpha’s docking sequence is much stronger than those of Beta and Gamma. However, these latter variants appeared equally virulent as Alpha, leading researchers to conclude that it was their ability to evade immune responses that compensated for their relatively weak adhesion. The lead experimental scientist, Dr. Bauer, took an innovative approach by using force stability – essentially the net force with which the virus binds to the protein receptor of the host cell – as a means of determining the strength of adhesion.
Being a respiratory virus, the cells to which COVID-19 primarily binds are those along the path air takes from the nostrils to the lungs. After making contact with one of these cells, the virus begins a docking sequence that will allow it to assume control of the cell’s replicative mechanisms. In one of the universe’s most fascinating existential tricks, the virus is neither living nor dead: it is simply an envelope filled with genetic material. If it wants to replicate itself, it can’t do it alone. The virus binds to an ACE-2, a common receptor protein on the outside of the phospholipid bilayer. Once firmly connected, the host cell sends lysosomes to digest the envelope, revealing the virus’ genetic information, which enters the cell through a pinocytotic vacuole. Once inside, the virus then hijacks the existing cell structures to replicate itself. After assembling an army of fellow viruses, the host cell ruptures, releasing legions of viruses to neighboring cells in an attempt to repeat and amplify the process. This rupturing is often the source of the soar throats from which infected patients suffer.
As someone who has in the past gone toe-to-toe with COVID-19, I can say that it is a formidable opponent. It is clever, elusive, and stubborn. For a while I felt only the most bitter animosity towards this microscopic speck, but after developing an understanding of its behavior and anatomy, I can now respect its sophisticated biological processes that aid in its reproduction. I still view it as the most heinous and lowest “life” forms in the universe, but at least I understand its point of view. Let me know what you think about this groundbreaking research! Will it prove pivotal for engineering future vaccines for specific variants? How fascinating and haunting that the severity of the illness can be determined by how firmly the virus snatches at your cells!
Leave a Reply