It has always been predicted that the genetic mutation in SARS-Cowie-2 would change. After all, viruses and other microbes do just that. The Sars-CoV-2 gene involves one or two mutations per month. In fact, its conversion rate is much lower than that of other viruses that we know of. For example, seasonal flu changes at the rate at which a new vaccine must be introduced each year.
However, over time, the viral population will accumulate reasonable mutations in different combinations. A notable feature of the SARS-Cowie-2 1.1.7 strain, which we find in the Covid-19 Genomics UK consortium (now better known in the headlines as the ‘new variant’), is that it has many mutations compared to other generations we took in UK. It has 23 in total, which sets it apart.
Most mutations are not involved because they do not change any of the amino acids that make up the proteins that make up the virus. When they do, it deserves a lot of attention, especially when mutations (or deletions) occur in an area of the virus that can alter the way it interacts with its human host. In particular, the changes in the spike protein, which stimulates the exterior of the virus and the way it binds to the host cell, are replicable and of great interest.
What scientists say about 1.1.7 inheritance is that there are 17 mutations (14 mutations and three mutations), with six mutations that don’t change any protein. Initial genetic analysis of inheritance 1.1.7 These mutations have been described previously in many other genera and have been shown to alter the functioning of the virus. A mutation (called 501Y) demonstrates how tightly a protein binds to a receptor on the surface of human cells. A second mutation (69-70 tel) has been identified in viruses that develop to prevent a natural immune response in some immunocompromised patients. But nothing can be considered about the new variant and what these mutations mean. We need more scientific evidence to understand how this particular version of the virus works compared to others.
Here we need to check: if the variant spreads so easily among people, if it causes more (or less) serious illnesses, and if it can bypass our body’s immune system. Heredity 1.1.7 At present, there is no evidence that it causes very serious disease or weakens the immune system. There is no reason to believe that any vaccines are launched or under development. But what is emerging more and more is that this line is very contagious.
In the UK, the body examining new sources of the virus is the New and Emerging Respiratory Virus Threat Advisory Group (Nervtok). o Recent publicly available minutes show that Nervtalk has “moderate confidence” that this new variant will be much more prevalent. The data you see includes genetic analysis showing that this particular strain grows 70% faster. In addition, he found a correlation between a higher R-value and the detection of a new variant in the test samples. (The value of R, remember, is the number of people sending it per person. It is high and widespread.) They also noted that this variation has increased exponentially during a period of nationwide blocking measures. were in place. It is still possible that there are other explanations for this rapid spread, but the idea that this variant is highly contagious is plausible, and it seems more and more. Laboratory studies currently being carried out will certainly answer this.
In practice, this means that all of our efforts to prevent the spread – washing hands, wearing masks and creating social distancing – are even more important. There’s nothing to suggest that the new generation can somehow avoid them, we’re just doing them the right way.
One question that can never be answered is where the new variant came from. Looking at the virus samples, the first place we found it was in Kent and London. But it is not clear whether he actually appeared there. It’s important to note that the UK runs a higher SARS-Cowie-2 streak than many other countries, and the fact that we found it here may say more about it than its final appearance. Interestingly, this variation may have occurred in a person whose immune system is infected for a long time, and the virus may copy and grow in that person for a long time. But, as always, more work is needed to understand if this really exists.
For the future, we need to review our systems to predict whether mutations will have health implications. On the basis of 126,219 genes from positive samples, a recent study of mutations by our federation identified 1,777 different amino acid mutations in the gene for the spike protein.
Identifying mutations is an imperfect process. There are tools that can model changes in the structure and function of the virus for any mutation, but this modeling still needs to be confirmed by evidence. Not only that, but the sheer number of mutations that need to be modeled is huge as well. For now, we can identify mutations that are important to human health by monitoring the rate of virus transmission, carefully monitoring the severity of the disease, and having systems that alert us when the virus may be preventing the development of. immunity in the past. Infection or vaccination. A new variant appeared first In early December, we combined this observation with genetic data while examining why Kendall’s infection rates have not declined, despite public health restrictions in the UK.
The story of the new variant shows how important genetic sequencing is, but highlights the fact that it is only when genetic data is combined with epidemiological and clinical information that it can make a difference in controlling the disease. disease. Fortunately, unlike previous epidemics, this tool can be used quickly and on an unprecedented scale. We should be grateful for this, as it’s safe to assume that this won’t be the last time we need it.