Coronavirus does not become more harmless with time
At the beginning of the coronavirus pandemic, it was repeatedly heard that the virus could possibly disappear in the summer. Unfortunately, this did not prove to be the case. On the contrary, the new pathogen continues to spread and, according to experts, is not becoming any more harmless. In addition, mutations keep appearing, which probably make it necessary for new vaccines to be developed.
The worldwide vaccinations against the coronavirus SARS-CoV-2 and the disease COVID-19 triggered by the pathogen give cause for hope. Nevertheless, experts believe that we will have to live with the virus for a long time to come.
Highly modified coronavirus variants
Corona research faces a puzzle, according to a recent article in “scilog,” the magazine of the Austrian Science Fund FWF (Fonds zur Förderung der wissenschaftlichen Forschung).
Since the beginning of the pandemic, it has been known that the SARS-CoV-2 coronavirus will mutate over time. This behavior had been expected by experts; flu viruses also behave this way. According to the data, there were on average two mutations per month, until the end of 2020.
But then, suddenly, highly modified coronavirus variants appeared, with not just one or two new mutations, but as many as 30 at once – enough to reduce the effectiveness of certain vaccines and cause higher infection rates.
The question of how such mutations in the virus arise is therefore more pressing than ever. A group led by Andreas Bergthaler is now working on a research project to answer this question.
Mutations are not only a disadvantage for the virus
“Coronaviruses are RNA viruses,” explains the virologist and immunologist at CeMM, the Research Center for Molecular Medicine of the Austrian Academy of Sciences. “They inherently have a relatively error-prone copying mechanism,” Bergthaler said.
As explained in the paper, RNA’s function in living cells is to transport genetic information stored in DNA to ribosomes, where protein molecules are produced according to the blueprints they contain. At this point, RNA viruses intervene in the process.
Because coronaviruses have the largest RNA genomes of all known viruses, they have developed their own correction mechanisms to reduce the error rate. “Nevertheless, errors or mutations are not only a disadvantage for the virus,” Bergthaler says.
“On the contrary, such new mutations allow the virus to adapt to new conditions. If we compare today’s virus genomes with the reference sequence, i.e. the genetic information from Wuhan 2019, we see that circa one to two mutations were accumulated every month,” the expert explains.
Virus can mutate faster
But since the end of December 2020, researchers around the world have been observing a new phenomenon. “We keep encountering new variants that are more mutated, with up to 30 additional mutations at once.”
We are talking, for example, about the British variant B 1.1.7 as well as the South African variant B 1.351. The coronavirus has found a way to mutate faster. Whether this is a coincidence or there is a common cause behind this development is not yet clear.
Researchers have two hypotheses for this. “One assumption is that there was an animal intermediate host and that these mutations accumulated there, but there’s not much evidence for that,” says Bergthaler, who has been tracking the mutation dynamics of the coronavirus in Austria since the pandemic broke out.
The second conjecture is that “the viruses could have replicated in individual infected individuals for a very long time without being controlled by the immune system.” Thus, the pathogen would have had enough time to accumulate so many mutations. This could be the case in people with weakened immune systems, among others.
“But it still doesn’t adequately explain, in our opinion, why so many mutations have accumulated,” the virologist said. “That’s one of the questions we want to address.”
Hundreds of viral genomes in one infected person
The goal of the new basic research project is to understand, on the one hand, how mutations accumulate in a single organism and, on the other hand, how many of those mutations are passed on to another person through the “bottleneck” of infection.
The range of mutations in a single infected person is sometimes much higher than that of viruses actually transmitted between people. “In each person, there can be hundreds of viral genomes with small differences,” explains the project leader.
“It is important for us to be able to detect even these low-frequency mutations. We are able to detect mutations that are present in only one out of 100 genomes in a sample,” Bergthaler says.