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One source of convenience is that the short course of treatment — four pills twice a day for five days — is less likely to develop resistance compared to HIV treatment cycles. And SARS-CoV-2 is not as mild as viruses like HIV or hepatitis C; it tends to make copies of itself at a slower pace, giving less time to a harder variant to evolve. In addition, researchers have not yet seen the development of resistance to remdesivir, an antidote to the existing Covid-19 virus. “I’m not worried for a while,” says Monica Gandhi, an infectious disease specialist and UC San Francisco medical professor. “Right now, I think it’s the early stages of HIV, and it’s like a miracle to get anything done.”
But if people stop taking the pills too early, viral resistance can occur because some viruses can persist in the body and strain resistance can increase. Mark Denison, a professor of pathology, microbiology and immunology at Vanderbilt University and one of the scientists behind the drug, say Endpoints News that he is specifically concerned with not finishing the entire treatment when people start to feel better. “Ultimately, it’s not about the virus or the drugs, it’s about the humans,” he said. Gandhi echoes the risk of not completing the course: “This can really increase the development of possible resistance.”
“As developing strains worsen the Covid-19 pandemic around the world, we need to assess potential treatments for these variants,” a Merck spokesman said. They added that trials of molnupiravir have demonstrated “consistent efficacy” in the Gamma, Delta, and Mu variants, suggesting that SARS-CoV-2 strains have not yet achieved the development of drug resistance.
Merck isn’t the only player in the game. In fact, despite the fact that most of the pandemic has passed through the almost empty treatment arsenal for Covid-19, the race for antiviral drugs has begun to tighten. Atea Pharmaceuticals and Roche are collaborating on the development of a similar antiviral drug analog, and Pfizer is testing an anti-virus with a different mechanism of action: the SARS-CoV-2 protease inhibitor, which works by blocking a step used to fuse the virus. the same with a human cell. The results of both medications are expected in the coming months.
The advent of more antiviral drugs may be key to preventing resistance. When the FDA approved the first anti-HIV drug in 1987, it quickly became clear that the virus was too fast; in some patients, resistance was developing account of days. Within a few years, more drugs were accepted, and an anti-virus cocktail became the standard treatment, making it much more difficult for viruses to create resistance. In particular, a mixture of medications that interfere at different points in the replication process of the virus makes it much more difficult for a virus to prevent all attacks.
After all, the same approach would be needed for Covid-19. “I think a combination would make more sense. Not only do we do this because of our resistance to HIV, we also do it because it is more effective, ”says Gandhi. A multi-point approach is best to get rid of a virus, and requires lower doses of each drug, causing milder side effects. But we need to design these combinations rationally, says Khook. “Often in the past, in other diseases, we’ve seen companies that are very, very enthusiastic about keeping combinations within,” says Khook. “And I don’t think we have that luxury for Covid.”
It remains to be seen how the virus will react to molnupiravir and whether it will successfully overcome its ambush mode. But it’s worth paying attention to, says Khook. “There is always the opportunity to create resistance. We don’t know if it will be, but there is always that possibility. “
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