WILL PREVIOUS VACCINES WORK TO COMBAT THE DELTA VARIANT?

 

Scientists are trying to figure out why mutations in the delta variety of SARS-CoV-2 are spreading so fast. But new evidence shows that previous vaccines cannot prevent further transmission, but do prevent the severity of the disease.

Laboratoriesaround the world,studying the genome of the viruses that currently cause the disease, found that the Delta variant is the one that is causing  new waves of COVID-19 infections around the world. But studying the genetic sequence of this variant reveals the molecular secrets that make it more dangerous.  

So far four variants have been discovered in this virus, in South Africa, the United Kingdom, Brazil and India, but only the Delta this causing many new infections.

Theresults of data analysis of patients who have already been vaccinated and who contracted the disease again are showing that the condition is milder, compared to people who had not been vaccinated and became ill with the Delta variant. Which shows that getting vaccinated was a good idea.

Research is ongoing and the genetic information of the different variants of SARS-CoV-2 and their effects of this variant on vaccinated people is already beingcompared. The results keep coming in, but researchers are testing the variants (and their constituent mutations) by applying the new viruses to human tissue cultures and animal models to see if the Delta variant can attack individual cells in the presence of antibodies produced by vaccines in people.

How do you know it's a variant of SARS-CoV-2?

Researchers found the first two variants of the coronavirus in late November and early December 2020 thanks to genome sequencing. A genomic initiative on COVID-19 in the UK determined that the sudden increase in the number of cases in the south-east of England and London could be due to a variant of the virus now called Alpha.

On the other hand, a team led by bioinformatician Tulio de Oliveira, from the University of KwaZulu-Natal in Durban, South Africa, connected the rapid expansion of the epidemic in the Eastern Cape province with a variant of the coronavirus they called Beta. The British and South African variants emerged independently, but both carry a set of mutations (some identical) in the protein of the spicule of the coronavirus thatserves to identify and infect host cells and that constitutes the main targets of the immune response.

Epidemiologists studying the proliferation of the Delta variant have estimated that it is 50 percent more transmissible than the other viruses in circulation. This contributed to the governments of several countries deciding to order confinement. Scientists want to discover the biological underpinnings: If they know what makes the virus more transmissible, then they will be more informed to make decisions about the pandemic.

Researchers are faced with the challenge of unraveling the effect of each mutation that distinguishes the lineages of different varieties. The Alpha variant carries eight changes that affect the spicule protein and some more in other genes, while the South African variant, or Beta, carries up to nine changes in the spicule. These mutations are alter the proteins that are in contact with the blood, these changes in the spicule protein render useless to the antibodies produced by the immune system to attack an earlier variant of the protein and therefore that virus.

Antibody testing

The rapid spread of variants has fuelled efforts to contain their spread through confinement, border closures and intensified surveillance. Added to the sense of urgency is the concern that variants may weaken the immune response triggered by vaccines or a previous infection.

In a related experiment, a team of researchers also found that the 501Y mutation, at least, did not drastically alter the activity of convalescent serum neutralizing antibodies (from blood taken from people who had recovered from COVID-19).

But there are mutations that could. The main one is the E484K, which has been identified in the domain of attachment to the receiver of the Delta variant. It is being tested against convalescent serum and serum from people vaccinated in trials.

Immune escape

Indications are beginning to appear that the E484K mutation allows the virus to escape the immune response of some people. One researcher cultured SARS-CoV-2 in the presence of a small amount of convalescent serum. The goal was to select viral mutations that bypassed the repertoire of antibodies generated in response to infection. The experiment did not have to work, but in less than 90 days, by natural selection, the virus had already acquired three mutations that made it immune to this person's serum. It was surprising because it suggested that the individual's entire antibody response to SARS-CoV-2 was directed against a small part of the spicule.

The strain evolved in the laboratory turned out to be less resistant to other people's convalescent serum. For the experiment we suggest that mutations of the Delta variant and changes in the domain of the amino end that both variants carry could affect the way they are recognized by antibodies generated by vaccines or by a previous infection.