Experiments on Syrian gold hamsters have shown that the most common of the new type of coronavirus mutations, the D614G, makes it more infectious in the nasopharynx, trachea and upper respiratory tract. An article with the conclusions of scientists published in the scientific journal Nature.
“In the nasopharynx and trachea of hamsters infected with the mutated form of SARS-CoV-2, we found an increased amount of viral particles. However, this was not typical for their lungs. This discovery confirms the results of patient observations and suggests that due to the mutation of D614G, the virus can indeed spread better from one victim to another,” the researchers write.
Since the outbreak of Covid-19 in China, scientists are trying to understand the direction and evolution of the coronavirus causing it SARS-CoV-2. It is known to accumulate mutations at about the same rate as the influenza agent. However, scientists cannot yet fully understand what these mutations are leading to.
The first major change in the coronavirus genome was recorded by scientists in early March. Then in Europe began to spread new strains of coronavirus, which was characterized by a general mutation in the gene S, which governs the production of proteins of that part of the shell SARS-CoV-2, which is directly related to its penetration into the body.
Now this mutation – D614G – is present in almost all variations of the new coronavirus type, which circulates among the population of all continents of the Earth. Judging by its rapid spread, this mutation can make coronavirus infectious from 2.5 to 8 times.
American molecular biologists, led by virologist from the University of Texas at Galveston (USA) Jessica Plante, tested this hypothesis in experiments on the Syrian hamsters (Mesocricetus auratus). These animals are as prone to SARS-CoV-2 infection as humans and ferrets.
For the experiments, scientists have created a new version of coronavirus based on one of the very first strains, which penetrated into the U.S. back in January this year and therefore has not yet acquired a mutation of D614G. By inserting it into the genome of the strain, the scientists infected the hamsters with both versions of the virus. They then compared how the infection happened in both cases.
It turned out that the mutant version of the virus multiplied much more actively in the trachea and nasopharynx of rodents. This was well noticeable already on the second day after the infection of the animals. Because of this, by the fourth or fifth day of the disease, the number of viral particles in the upper respiratory tract of animals was several dozen times greater than in the control group hamsters.
The biologists then checked what would happen if they tried to infect the animals simultaneously with both versions of SARS-CoV-2. It turned out that in the first week after infection, the number of viral particles with the mutation of D614G in hamsters was 1.5 to 2.5 times higher.
Scientists do not yet know exactly how this mutation works. However, the experiments of Plante and her colleagues show that it can simultaneously make the virus more stable under adverse environmental conditions, and particularly affect the interaction of antibodies and coronavirus particles, hiding the virus from immunity.
On the other hand, the same experiences indicate that D614G has not made coronavirus more dangerous to the lower respiratory tract and other lung areas, nor has it increased its resistance to vaccines and drugs. Future mutations of SARS-CoV-2 may not have such positive features, so scientists should actively monitor new changes in its RNA and study their impact on the nature of the course of infection, conclude Plante, and her colleagues.