A drug and a vaccine in development to stop covid

The Francis Crick Institute and the University of Cambridge have presented two new studies that could provide answers to one of the most important current medical issues: the future of viruses and how drugs act in our body. The first of them has discovered mutations in the SARS-CoV 2 virus caused by an antiviral, while the one carried out in Cambridge reveals a technology that could protect us from future viruses and their variants. Let's go one by one.
A team of scientists from the Francis Crick Institute along with other universities in the United Kingdom and South Africa have discovered a link between an antiviral drug for Covid infections called molnupiravir and a pattern of mutations in the SARS-CoV-2 virus. According to the results, published in "Nature", this drug acts by inducing mutations in the genetic information or genome of the virus during replication. Many of these mutations will damage or kill the virus, reducing the viral load in the body. Molnupiravir was one of the first antivirals available on the market during the pandemic and was widely adopted by many countries.
To reach this conclusion, the authors used global sequencing databases to map mutations in the SARS-CoV-2 virus over time. In total, they analyzed a family tree of 15 million SARS-CoV-2 sequences to see what mutations had occurred at each point in the evolutionary history of each virus.
While it is true that viruses mutate all the time, the researchers identified mutational events in the global sequencing database that appeared very different from typical Covid mutation patterns and that were strongly associated with individuals who had taken molnupiravir.
These mutations increased in 2022, coinciding with the introduction of molnupiravir. They were also more likely to be seen in older age groups, consistent with the use of antivirals to treat people who are at higher risk, and in countries known to have high use of molnupiravir.
The authors also observed small clusters of mutations that suggest subsequent transmission from one person to another, although there are currently no variants of concern in this regard.
In the conclusions, the authors highlight that it is difficult to understand the impact of treatment with molnupiravir on the risks of new variants and, at the same time, it is important to take into account that chronic covid infections for which molnupiravir is used, can cause new mutations. “Covid continues to have a significant effect on human health and some people have difficulty eliminating the virus, so it is important that we develop drugs that aim to shorten the time,” concludes the leader of the study, Theo Sanderson. "But our evidence shows that a specific antiviral drug, molnupiravir, also produces new mutations, increasing genetic diversity in the surviving viral population. The findings are useful for continued evaluation of the risks and benefits of treatment with molnupiravir, a drug that can cause the virus to mutate so much that it is fatally weakened. But what we have discovered is that in some patients, this process does not kill all viruses and some mutated viruses can spread. “It is important to keep this in mind when evaluating the overall benefits and risks.”
For its part, the second study, also published in "Nature", revolves around a vaccine "prepared for the future." The authors, from the University of Cambridge, have shown that a single antigen can be modified to provide a broadly protective immune response in animals. Studies suggest that a single vaccine with combinations of these antigens (a substance that causes the immune system to produce antibodies against it) could protect against an even wider variety of current and future coronaviruses.
Studies in mice, rabbits and guinea pigs, an important step before starting human clinical trials currently underway in Southampton and Cambridge, showed that the vaccine candidate provided a strong immune response against a variety of coronaviruses by attacking parts of the virus. essential for its replication.