Much is still unknown, what we know about this new type tells us important things about the virus: it may be more easily adapted to become transmissible and more difficult to neutralize and possibly outsmart the vaccine. To some extent.
To date, SARS-Cavi-2 has changed at a fairly steady rate, with only one or two variations per month. Some variations have given scientists a break, bringing change to become more variable at that time, and changing at other times makes it more effective to avoid detection by our immune system. But with this new type called B.1.1.7, the virus has achieved a total of 17 mutations that, according to the Centers for Disease Control and Prevention, alter the proteins of the virus, affecting four different viral proteins: Spike Protein, ORF1. AB, aka 8 and N proteins, the main nucleocapsids.
While the sheer number of mutations in one type is worrisome, the more worrying is how simultaneous changes can alter the management of the virus. One of the mutations, N501Y, is how tightly the spike protein binds to the human AC2 receptor, making it easier for the virus to take root in infected people. This change is possible as the new strain, first isolated in the UK in late September, now accounts for more than 60% of new infections in and around London.
The second mutation of the spike protein, — 70 Dale, kills two amino acids, which, if removed, can prevent the virus from having a few immune reactions and make it more transmissible with the second mutation. — 70 Dell mutations have been observed in a variety of other species – including stretch marks in Denmark – and when patients are exposed to the virus for several months under immune pressure, it is achieved not only by the patient’s own immune system but also by treatment. Convective plasma such as those that pump antibodies into the patient’s system.
The third mutation, P681H, is called the cleavage site of the spike protein, a field known for the effect of how the virus can easily penetrate inside cells and kill it easily. Changes in this part of the virus could increase the risk of disease and its potential for lethality – although there is no evidence that these new species are more dangerous to humans. This change alone is enough to be ambiguous. The fact that it is combined with other mutations for this variety of strains aka 8 proteins that can also increase pathogenesis is actually a cause for alarm.
Mutations that affect the other two proteins – ORF1AB and N proteins – are also suspected to allow the virus to replicate faster and avoid the immune system, although more research is needed to see how each of these 17 mutations affects them. The virus works. Still, we know enough to make a few assumptions.
First, SARS-Covy-2 knows how to adapt and adapt as quickly as the flu virus. So we should be prepared for the possibility of the virus staying with us for a long time. Like the flu vaccine, the covid-19 vaccine cannot be one and the same cannot be romantically infected. We already know from a recent study published in the New England Journal of Medicine Medicine that the half-life of at least one vaccine moderate vaccine-neutral antibody, which responds the most, decreases relatively rapidly over a three-month period. Vigorous and short in those who mount less enthusiastic feedback. Although the study was small, it raises the question of whether the vaccine taken today will be effective in the future in 12 months, 18 months or more. B.1.1..7 tells us something new – not only can the immune system be weakened, but the strength of the vaccine can also change if the virus is changed. This is not to say that modern medicine cannot contain the evolved Covid-19 virus, as it is caused by the flu. But, not as simple or easy as people would expect.
Second, with the -69–0 Dell change we may face a medical paradox. In an effort to save the lives of virus-infected immunocompromised patients, providers sometimes ran several rounds of antibody treatment for their patients. In some cases, patients recover after one round of treatment and need a second dose to stay sick again. Even in a single patient, over the course of weeks and sometimes months, immune suppression gives the virus many opportunities to learn our best defenses and to be more effective in avoiding our immune system. Antibody therapy can save a person’s life, a UK study has speculated that it also facilitates the creation of new strains of the virus.
Finally, the variant suggests that in order to respond more effectively to the changing virus, we should immediately start planning for the next generation of the covid vaccine. It should provide some hope that an official vaccine has already been tested against the new variant. Companies have expressed confidence that their vaccine could protect them, Bioentech noted, adding that its vaccine could be changed to fight the new rupee.
However, it is worthwhile to further study alternative vaccine targets that may prove more effective in protecting the population against the types of viruses. Right now, most vaccines under development target spike proteins. These include the Moderna, Novovox and Johnson and Johnson vaccines, as well as adenovirus-based vaccines such as AstraZeneca. These vaccines may work against today’s version of the virus, but if we want to stay ahead of the spread of the disease, we need to include other proteins such as ORF1AB, ORF8 and N proteins or ORF3B proteins to increase vaccine targets. , Which others have studied. Other countries have developed vaccines with more traditional methods using inactivated whole viruses. This type of vaccine, or other vaccines that target multiple proteins at once, may be the best approach to move forward.
I always compare viruses to code-cracking machines, where they don’t run consecutive numbers until they find a new way to tackle environmental specifics – millions of copies of a virus, each changing and adapting to each new challenge. Sometimes, we run against a virus that learns how to break our defenses faster than we can rebuild. I’m afraid SARS-Cavi-2 could be one of them.
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