Merck’s Antiviral Could Be What Covid Has Been Waiting For
One source of relief is that the short course of treatment — four pills twice a day for five days — means that there is little chance of developing resistance, compared to lifelong courses of treatment for of HIV. And SARS-CoV-2 is less active against viruses such as HIV or hepatitis C; it tends to make copies of itself at a more comfortable pace, giving it less time for a more difficult variant to develop. In addition, the researchers have not yet seen any resistance developed against remdesivir, the existing Covid-19 antiviral. “I wasn’t worried for a while,” said Monica Gandhi, an infectious disease specialist and professor of medicine at UC San Francisco. “Now, I think it’s very early stages of HIV, and it’s like a miracle to get anything.”
But if people stop taking their pills too early, virus resistance may be more likely to occur, as some of the viruses may remain in the body and resistance strains may increase. Mark Denison, a professor of pathology, microbiology, and immunology at Vanderbilt University and one of the scientists behind medicine, told Latest News that he is specifically concerned about people not being able to complete the entire course of treatment once they start feeling well. “Ultimately, it doesn’t depend on the virus or the drugs – it depends on the people,” he said. Gandhi echoed the danger of not completing courses: “That would definitely add to the development of possible resistance.”
“As evolving variants exacerbate the Covid-19 pandemic worldwide, we need to examine potential treatments with these variants in mind,” said a Merck spokesperson. They added that molnupiravir trials showed “consistent efficacy” across Gamma, Delta, and Mu variants, suggesting that existing SARS-CoV-2 strains have not yet succeeded in developing resistance. against medicine.
Merck isn’t the only player in the game. In fact, even though the public is claiming most of the pandemic has an almost empty arsenal of treatments for Covid-19, the antiviral drug race is starting to tighten. Atea Pharmaceuticals and Roche collaborated to create the same nucleoside analog antiviral drug, and Pfizer tested an antiviral with a different mechanism of action: an inhibitor of the protease SARS-CoV-2, which acts by blocking a step used by the fuse virus. of itself with a human cell. Results of both treatments are expected in the coming months.
The advent of multiple antiviral drugs may be the key to preventing build-up resistance. When the first antiviral drug against HIV was approved by the FDA in 1987, it quickly became clear that the virus was highly contagious; in some patients, resistance improved how many days. Within a few years, many medications were approved, and an antiviral cocktail became the standard treatment, making it difficult for the virus to build resistance. In particular, a combination of drugs that each interfere at different points in the virus replication process makes it even more difficult for a virus to evade all attacks.
Finally, a similar approach may be necessary for Covid-19. “I think absolutely that a combination makes more sense. Because that’s not just what we do with HIV because of resistance — we also do it because it’s more effective,” Gandhi said. A multi-prong approach it’s better to suppress a virus, and requires a lower dose of each drug, which results in a milder effect. But we have to reasonably design these combinations, says Khoo. “Most of the past, in the other diseases, we see, companies are very keen to keep the combinations inside, “Khoo said.” And I don’t think we have that luxury for Covid. “
Soon tell how the virus reacts to molnupiravir and if it can successfully overcome the ambush method. But it’s worth watching, says Khoo. “There’s always the possibility that resistance could arise. We don’t know it’s going to happen, but there’s always the possibility that it could.”
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