Can SARS-CoV-2 be even more problematic than UK and South African variables?

Random differentiation is an essential part of all living things. It drives diversity, which is why there are so many different species. There are no viruses. Most viruses are known to modify genomes to adapt to their environment. We now have evidence that the virus that causes Covid, SARS-CoV-2, is not only changing, but changing in ways that are important. This is the sixth in a series of articles on how the virus changes and what that means for humanity. Read the rest: part one, part two, part three, part four, and part five.

We are quickly learning how SARS-CoV-2 moves to create changes with new features. Some of these new variables, such as those found in the UK and South Africa, could affect our ability to control the pandemic, including infectious mitigation, diagnosis , and vaccine.

Over the past few weeks, reports indicate that some variants of SARS-CoV-2 are more contagious than earlier strains. Sequential analysis of these variables reveals that their genome and proteins are originally different from the less infectious sources. The closely studied viral protein is the spike protein. Multiple independent separates port changes in the spike protein that account, at least in part, for their greater mobility.

In an introduction published on January 11, scientists from the Weizmann Institute of Science describe an experiment in which they try to mimic what happens naturally. They were looking for lab-created modifications that adhere more tightly to a structure on the surface of the cell that the virus uses to enter our bodies. They were successful. The overall winner bound the cell surface receptor, the ACE2 protein, 600 times tighter than the original virus.

The shocking result was that their lab reproduced almost exclusively changes in naturally occurring sequences in the UK and South Africa, and elsewhere. The laboratory-generated variables include the same variants, notably the named variants S477N, E484K, and N501Y. The variables give the same advantage in the test tube as in numbers.

In the laboratory-generated variant, there are seven amino acid byproducts in the spike protein receptor binding domain. Studies on the structure of the protein reveal the action. Four of the seven stabilize the spike protein structure, and three tighten the close connections that the spike makes with the ACE receptor.

These were not the only laboratory changes found by the researchers. Some carry just a little binding benefit. However, when combined with the ensemble of three winners, S477N, E484K, and N501Y, they form a spike protein that binds 600 times more tightly to the receptor than the original one. This particular combination of changes has not yet been noticed. With the rapid rate of change, it is likely that such a change will soon emerge. We may then be dealing with a more infectious virus than the UK or South African series. A public event like this has a big impact on an event like this.

A detailed analysis of the variables reveals how they develop the ability of the virus to bind the ACE2 receptor. Four of the seven modifications stabilize the spike protein structure, while three tighten the spike’s close connections to ACE2.

In considering the significance of these observations, consider that the scientists did not alter the 0.6% of the total genome and only about 12% of the spike protein. An analysis of many of the new variables that appear to be more infectious and appear to escape immune pressures reveals other spike sites and other viral proteins of interest. A similar study of the whole genome appears to reveal other tricks that the virus uses to increase infection and avoid immune detection.

Last spring SARS-CoV-2 in which the spike mutation D614G spread faster. This pressure was so successful and it has now eliminated everything else. The D614G is in all recently discovered infectious strains. In other words, these new mutations further confirm virus infection. The laboratory experiments described here show that naturally occurring changes have not yet reached the infectious stage.

It may be helpful to visualize SARS-CoV-2 mutations as a fast-growing tree. At the base of the tree, one layer of the virus infects the stock. Ascending the tree branches appear, variables in which the past changes and more of their own. Each is better suited to live in his environment, the human population, than his direct ancestor. As we climb higher, the variables become more numerous, different from each other, even more conducive to survival and prosperity. In a short time thousands of different changes began in the thousands, trying our best to alleviate disease and disease.

We have to cut the tree. We need to reduce the number of branches, the stunt of the tree. How come? With recommended methods at all times. We need to give vaccines as soon as possible; we need to strengthen public health measures – social distance, wearing mascara and social isolation. As necessary, we must encourage and, if necessary, enforce the isolation of those who are open and infectious.

But as dangerous as we thought our enemy was, until a few weeks away we were confident that we knew his form. We now understand that SARS-CoV-2 is a shape-shifting engine. Like Proteus, it changes even as we hold it in our grip. As Hercules gained the upper hand, separating Anteus from his motherland, we must clear the ever-growing forest of virus changes by reducing the numbers of people on the disease, not only in our country but everywhere it is rooted.