The good news is that compared to the life-long treatment of HIV, the short course of treatment—four capsules twice a day for five days—means that there are fewer opportunities for drug resistance. And SARS-CoV-2 is not as agile as viruses such as HIV or hepatitis C; it tends to make copies of itself at a more leisurely speed, thereby reducing the time for more difficult variants to evolve. In addition, researchers have not found any resistance to the existing Covid-19 antiviral drug Remdesivir. “I’m not worried for the time being,” said Monika Gan, an infectious disease expert and professor of medicine at the University of California, San Francisco. “Now, I think this is the early stage of HIV, and getting anything is like a miracle.”
But if people stop taking medication too early, viral resistance is more likely to occur, because some viruses may stay in the body and drug-resistant strains will multiply. Mark Denison, professor of pathology, microbiology and immunology at Vanderbilt University, is one of the scientists behind the drug. Tell Endpoint news He is particularly worried that people will not be able to complete the entire treatment once they start to feel better. “Ultimately, it does not depend on viruses or drugs-it depends on humans,” he said. Gandhi echoed the danger of not completing the course: “This will indeed increase the development of possible resistance.”
“As emerging variants exacerbate the Covid-19 pandemic globally, we must consider the potential treatments for these variants,” a Merck spokesperson said. They added that the molnupiravir trial demonstrated “consistent efficacy” in the Gamma, Delta, and Mu variants, indicating that the existing SARS-CoV-2 strains have not successfully developed resistance to the drug.
Merck is not the only participant in the game. In fact, although humans limped through most of the pandemic, treatments for Covid-19 were almost empty, but the antiviral drug race began to become tense. Atea Pharmaceuticals and Roche are collaborating to develop a similar nucleoside analog antiviral drug, while Pfizer is testing an antiviral drug with a different mechanism of action: a SARS-CoV-2 protease inhibitor, which works by blocking the virus The steps used to fuse act on itself and human cells. The results of these two drugs are expected to be announced in the next few months.
The arrival of more antiviral drugs may be the key to preventing the development of resistance. In 1987, when the first antiviral drug against HIV was approved by the FDA, it was soon discovered that the virus came too fast; in some patients, drug resistance was developing A few daysWithin a few years, more drugs were approved, and antiviral cocktails became the standard treatment, making it harder for viruses to build resistance. In particular, each drug interferes with the different points in the virus replication process, which makes it more difficult for the virus to evade all attacks.
Ultimately, Covid-19 may require the same approach. “I definitely think the combination will make more sense. Because it’s not just our resistance to HIV-we also do it because it’s more effective,” Gandhi said. The multi-pronged approach is more effective at suppressing the virus, and requires lower doses of each drug, resulting in less side effects. But we need to design these combinations reasonably, Khoo said. “In the past, we have often seen that in other diseases, the company is very, very keen to retain the portfolio internally,” Khoo said. “And I don’t think we have that luxury for Covid.”
It is too early to determine how the virus will respond to monupiravir and whether it will successfully overcome its ambush mode. But it deserves attention, Khoo said. “There is always resistance. We don’t know if it will be, but it is always possible.”
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