Cautiously optimistic. This is the outcome of one of the most complete and realistic studies conducted to the present date on the mutations of the SARS-CoV-2 coronavirus, just published in the scientific journal PNAS, by geneticists and virologists from the Walter Reed Army Institute of Research, the biggest biomedical research facility of the US Department of Defence.
The virus has in fact mutated and is constantly changing, but at a rate and with a number of mutations that is not worrying, and in any case, lower than those of the flu virus or HIV.
This slower rate of creating mutations is probably linked to an enzyme, found in the coronavirus, which corrects potentially fatal copying errors. The researchers reached these conclusions after analysing the genetic sequences of the SARS-CoV-2 viruses that had infected more than 27,000 patients in 84 countries.
The virologists confirmed, first of all, what has been observed in other studies: in recent months (since December 2019) to the present date, relatively few mutations have been discovered, which points towards the idea that there are random variants that are not developed for adaptation to humans, which is good news, because it means that there is less danger of having a virus that is even more difficult to fight.
On the other hand, the existence of a dominant mutation, called D614G, on the gene that encodes a key protein of the coronavirus was confirmed: the so-called Spike, needed by the virus to attach onto cells and to infect them (read more about the Spike protein here).
Today, this mutation has been found in almost all the strains in circulation. Its consequences are not well known, although several researchers believe that it makes the virus more contagious, but also, perhaps, slightly less dangerous.
In any case, D614G – in the common opinion of the experts – shouldn’t change the “rules of the game” very much. In this respect, the researchers from the Walter Reed Army Institute of Research wrote:
“There is no evidence of mutations affecting the binding of the Spike protein to the ACE2 receptor of cells (ACE2 is the point where the coronavirus usually penetrates the cells). Our results suggest that, to date, the limited diversity seen in SARS-CoV-2 should not preclude a single vaccine from providing global protection”.
This is the crux of the matter.
It means that, the vaccine, if we find one, will be (or ought to be) effective and long-lasting, because the targets for which it has been designed do not change. One vaccine in particular is being studied at the Walter Reed Army Institute of Research, which should pass the clinical trial phase in 2021: this drug is based on the Spike protein, and is reinforced by a special substance, an adjuvant, developed at the same centre.
A long and detailed article published in the scientific journal Nature also confirms that the mutations of the SARS-CoV-2 virus do not present particularly worrying characteristics, such as, for example, an increase in its lethality.
One variant however is being closely observed. This variant is almost always found together with the D614G mutation, at one of the points of the virus targeted by Remdesivir, the drug currently used, in certain circumstances, as an emergency treatment for people suffering from the coronavirus. This mutation could reduce the effectiveness of Remdesivir, bearing in mind, however, that this drug does not in any case solve the problem (initially it was created to fight Ebola).
All in all, the general situation, as we said, seems to be under control. “Despite the virus’s sluggish mutation rate”, writes Nature, “researchers have catalogued more than 12,000 mutations in SARS-CoV-2 genomes. But scientists can spot mutations faster than they can make sense of them. Many mutations will have no consequence for the virus’s ability to spread or cause disease, because they do not alter the shape of a protein, whereas those mutations that do change proteins are more likely to harm the virus than improve it”.
