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As covid-19 continues to evolve in the U.S., researchers are developing next-generation therapies, including a new approach that can help reduce recovery time from the disease.
Including existing treatments antivirals, antibodies, and steroids, U.S. and European scientists are focusing on creating deceptive receptors that normally bind to viruses, which can neutralize harmful effects.
To develop the new therapy, scientists first had to engineer mice to convert angiotensin to a human protein variant known as enzyme 2 or ACE2. This is located on the surface of the cells and helps regulate phenomena such as healing, inflammation and blood pressure.
Although ACE2 receptors can be found in cells throughout the body, they predominate in the lungs, heart, kidneys, and liver. usually attacks.
To protect true ACE2 receptors, here’s how it works:
Typically, spinal proteins on the skin of the virus act as the keys to ACE2 receptors, opening the door to infection. But depending on the stage of the disease, the veins, or tumors that are administered through the nose, trap the lumpy protein, moving it away from the actual receptors. After infection, treatment can reduce the viral load inside the body, which can lead to faster recovery times for patients.
In a head-to-head investigation Daniel batlle, A professor of medicine at Northwestern University, who became infected with the disease and received treatment compared to untreated animals with only mild symptoms and died.
From today, only one clinical trial It is completed in patients with moderate or severe symptoms of the ACE2 product. However, more and more researchers are contributing to the new therapeutic.
Batlle’s team began working on decoy proteins in January 2020 after learning about the first case in the U.S., based on knowledge gained from the 2003 SARS-CoV outbreak in China.
“We knew it was very likely that the SARS-CoV-2 receptor was ACE2, as it had previously been shown to be the case for SARS-CoV,” says Batlle.
But applying that knowledge was not so easy. Michael Jewett, a professor of chemical engineering at Northwestern University who did not participate in the study, compares the intricate process of deception to a particularly daunting puzzle.
“Re-engineering complex biological systems can be difficult,” says Jewett. “It’s like solving a puzzle and every time you put a piece together, the rest of the puzzle changes.”
According to Jewett, compared to antibody treatments, the attractions should be lower cost and easier to use. Some experts are optimistic about the deception’s ability to ward off the strain of the original virus and the coming mutations.
In another study, using a process called deep mutation scanning, Erik Procko, A professor of biochemistry at the University of Illinois Urbana-Champaign, he was able to see thousands of different ACE2 mutations in a single experiment and which ones could better attract and bind the virus. He then imitates those who performed best for his team. Decoys do not bind to cells, but rather float in the fluid between them to catch the virus before it binds to actual ACE2 receptors.
Using the combination of the three mutations, his team significantly increased the exchange affinity for covid-19. They created receptors that bind to the virus 50 times more strongly than ACE2.
To test the approach, Procko’s team used mouse tissue instead of live animals. “In in vitro tissue culture, we know that they are as powerful as some hand receptors – sometimes slightly better, sometimes a little less powerful, but generally as strong – like monoclonal antibodies that are allowed to use in emergencies or are in the clinic. Trials,” says Procko.
One concern was that one of these mutations would allow the so-called virus escape and protect the virus from resistance to treatment. Procker says that because viruses are so similar to natural receptors, the virus cannot evolve naturally as a result of its action.
Due to differences in infrastructure and education, access to synthetic biology technologies is distributed differently worldwide. More research — and more funding — is needed before this therapy can be made publicly available. But advances like this can eventually lead to the creation of portable and low-cost treatments for the disease.
“There are promising signs that the tubes, which are very similar to the human ACE2 receptor, will be strong and effective against all of these new variants,” Procko says. “I wouldn’t be surprised to see some of those generations of generations coming to the clinic in a couple of years.”
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