Merck’s antiviral could be what Covid is waiting for


One comforting thing is that the short duration of the course — four pills twice a day for five days — means that there is less chance of refusing to start, compared to all other standard of care for HIV. And SARS-CoV-2 is not as active as viruses such as HIV or hepatitis C; likes to make its copies quickly, which gives them less time for solid colors to change. In addition, researchers have not yet seen any growing resistance against remdesivir, the existing anti-virus Covid-19. “I’m not worried for a while,” says Monica Gandhi, an infectious disease specialist and professor of medicine at UC San Francisco. “Right now, I see it as the beginning of the HIV epidemic, and it’s kind of a miracle to find anything.”

But if people stop taking their pills sooner, viral infections can be eliminated, as some viruses can remain in the body and deafness can spread. Mark Denison, professor of pathology, microbiology, and immunology at Vanderbilt University, is one of the leading scientists in the field of medicine, he tells Appendix that they are particularly concerned that people who have not completed all the treatment will start to feel better. “In the end, it’s not about the virus or the cure – it’s about the people,” he said. Gandhi also describes the danger of not graduating: “This can increase the level of denial.”

“As the coming nations expand the Covid-19 epidemic worldwide, we need to highlight the potential benefits of this,” Merck said. He further added that the molnupiravir trial showed “unstable stability” in both Gamma, Delta, and Mu strains, indicating that existing strains of SARS-CoV-2 had not yet succeeded in resisting the drug.

Merck is not the only player in the game. On the contrary, despite the casualties of the Covid-19 assault rifle, the competition for antiretroviral drugs has intensified. Atea Pharmaceuticals and Roche are collaborating to develop a similar nucleoside analog antiviral drug, and Pfizer is testing an antiviral with another approach: SARS-CoV-2 protease inhibitor, which works by blocking the step that the virus uses to combine. only the human skin. The effects of the two drugs are expected in the coming months.

The advent of antiretroviral drugs may be a key to preventing arrest. When the first antiretroviral drug was approved by the FDA in 1987, it soon became apparent that the virus was fast-growing; in some patients, resistance was increasing a few days. Within a few years, more and more drugs were approved, and the antiviral market became a permanent support, making it increasingly difficult for the virus to survive. In particular, the combination of drugs that interfere with the various metabolic processes of the virus makes it harder for the virus to prevent all attacks.

In the end, the same approach may be required for Covid-19. “I think the combination would make sense. Because it’s not what we do to HIV because of rejection — we also do it because it’s effective,” says Gandhi. “We have to make smart combinations of these combinations,” says Khoo.

It remains to be seen how the virus will react with molnupiravir and whether it will secretly succeed. But it is important to pay close attention, says Khoo. “There is always a chance that rejection will come. We don’t know if it will, but it is always possible.”


Information from WIRED on Covid-19



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