Can you see the fake receptor? The corona virus can’t either.

As Covid 19 continues in the United States, researchers are now developing the next generation of treatments, including a new approach that could help reduce the time it takes to recover from the disease.

Although current treatments include antivirals, antibodies, and steroids, scientists in the United States and Europe are now focusing on making decoys of receptors that neutralize the virus’s harmful effects in general.

To develop the new therapy, scientists first had to engineer mice with a type of human protein called angiotensin converting enzyme 2 or ACE2. It stays on the surface of the cells and helps regulate healing, inflammation and blood pressure.

Although ACE2 receptors are found in cells throughout the body, they are found mainly in the lungs, heart, kidneys, and liver organs that are most commonly attacked by the disease.

To protect genuine ACE2 receptors, Deco does its job:

In general, spike proteins on the surface of the virus act like keys to ACE2 receptors, opening the door to infection. But depending on the stage of the disease, decoctions through the vein or through the nose, spikes block the protein, which takes it away from the real receptors. After infection, treatment can reduce the viral load on the body, which may mean faster recovery time for patients.

In a study led by Daniel Butley, a professor of medicine at Northwestern University, mice that were infected and treated had only milder symptoms than untreated animals that died. ۔

To date, only one clinical trial of the ACE2 product has been completed in patients with mild to severe symptoms. Nevertheless, more and more researchers are supporting new therapies.

The Beetle team began working on Deco Protein in January 2020 after learning of the first U.S. case, based on knowledge gained from the 2003 Sars-Kovi epidemic in China.

“We knew it was very possible that the SARS-CoV-2 receptor was ACE2, because the SARS-CoV case had been shown before,” Butley said.

But applying this knowledge was not so straightforward. Michael Jewett, a professor of chemical engineering at Northwestern University who was not involved in the study, compares the complex process of creating a complex to a particularly obsessive puzzle.

“It can be difficult to rearrange complex biological systems,” says Jewett. “It’s like solving a puzzle, and every time you put a piece together, the rest of the puzzle changes.”

Jewett also says that decoctions should be cheaper and easier to use than antibody treatments. And some experts are optimistic about Deco’s ability to prevent both actual viral strains and upcoming changes.

In another study, using a process called deep mutation scanning, Eric Proco, a professor of biochemistry at the University of Illinois at Urbana-Champaign, was able to see thousands of different ACE2 mutations in a single experiment and see which one works best. Can attract and bind to. To the virus. Then his team made a deco imitating the best performers. The decoys do not attach to the cells but float in the fluid between them so that they attach to the real ACE2 receptors before catching the virus.

Using a combination of three variations, his team was able to significantly extend Deco’s relationship to Cove 19. They made deco receptors that are 50 times more binding to the virus than ACE2.

To test the approach, Proco’s team used mouse tissue instead of live animals. “In vitro tissue culture, we know that some of the deco receptors are just as powerful بعض sometimes a little better, sometimes a little less, but overall just as powerful م as monoclonal antibodies used in emergencies. Permission or medical trials are allowed, “says Proko.

One concern was that one of these mutations could allow so-called viral escape and help speed up the virus’s resistance to treatment. But because decoys are similar to natural receptors, Proco says their action is unlikely to cause the virus to develop unnaturally.

Due to differences in infrastructure and education, access to artificial biotechnology technologies is unequally distributed around the world. More research and more funding is needed before such therapy becomes publicly available. But such advances could ultimately help create a low-cost, portable, easy-to-use treatment for the disease.

“There are promising signs that closely resemble the human ACE2 receptor will be powerful and effective against all these new conditions,” Proco said. “I wouldn’t be surprised if we had some next-generation Davis clinics.”

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