Researchers believe they may have found the key to stopping the new coronary virus.

According tomedia BGR reported that there are already several drugs can be used as a treatment for new coronary pneumonia, but there is still no “magic cure” to prevent complications and significantly reduce mortality. Some researchers think they’ve come up with another way to treat COVID-19, first by treating the disease as a vascular disease. This limited exploratory experiment has provided promising results.

Some researchers believe that COVID-19 should not be seen as a respiratory disease in the first place, but as a vascular disease. The same study says it’s not a high-profile cytokine storm that causes complications and death, but a different kind of “storm” that occurs inside the body before the immune system goes into overdying.

Thomas Smith wrote on Medium that summit supercomputers at Oak Ridge National Laboratory in Tennessee analyzed more than 40,000 genes from 17,000 genetic samples to better understand COVID-19. This computer is the second fastest in the world, but it still takes more than a week to crush 2.5 billion gene combinations. After the data was processed, Dr. Daniel Jacobson and his colleagues came up with a new hypothesis that they thought could explain what might happen if the new corona virus infected the human body. They also think they know how to treat with existing drugs.

Researchers believe they may have found the key to stopping the new coronary virus.

This is the peptide hypothesis, which refers to a compound directly affected by the virus that can cause a “slow peptide storm” that can cause serious problems and lead to death.

Data from Summit’s computer show that the new crown virus does not just infect cells with ACE2 receptors that bind to the pathogen’s tingling glycogen. Instead, it “spoofs” the body into raising the ACE2 receptor, including the lungs, where ACE2 receptors are not normally found. This is where the renin-angion stress system (RAS) system works. RAS controls the level of peptides in the body and has a direct effect on blood pressure. But viruses can interact with RAS systems and then increase the number of peptide receptors. At the same time, the body stops breaking down the substance, which leads to a storm of so-called peptides.

With the accumulation of peptides, the effect begins to appear. This compound increases the permeability of blood vessels, which means that water in the blood can seep into adjacent tissues through the blood vessels. When this happens in the lungs, fluid begins to build up and cells from the immune system eventually mix in, leading to inflammation.

Jacobson and his team think COVID-19 may have another effect, complicating matters. The virus increases the production of hyaluronic acid (HLA) that absorbs large amounts of liquid. When HLA interacts with fluid in the lungs, the end result is a hydrogel that makes breathing more difficult. At this point, it’s likely that even a ventilator won’t help. “It reaches a point where no matter how much oxygen you breathe, it doesn’t matter because the lungs are full of this hydrogel,” Jacobson said. “Jacobson became like a water polo.”

The researchers believe the RAS-slow kineptide imbalance may explain heart symptoms of COVID-19, including arrhythmic disorders and low blood pressure. In addition, high doses of resorbid peptides may alter the protection provided by the blood-brain barrier, allowing some toxins to enter the brain. This may explain the neurological symptoms that occur in some COVID-19 cases. Skin diseases described as COVID toes may also be due to the compound’s ability to increase the permeability of blood vessels. The substance may also have an effect on the thyroid gland, which may explain thyroid symptoms, the researchers said.

Researchers believe they may have found the key to stopping the new coronary virus.

ACE inhibitors are a class of heart disease drugs that lower blood pressure and have similar effects on the RAS system to new coronaviruses, including increased levels of anti-kineptides. Therefore, in addition to lowering blood pressure, COVID-19 mimics ACE inhibitors to treat side effects of heart disease, including dry cough and fatigue. The peptide effect can also increase blood potassium levels. ACE inhibitors are also associated with sudden loss of taste and smell, but in cases of COVID-19, the virus infects certain cells in the nose, so the symptoms occur.

The researchers also believe that the peptide hypothesis may explain why men are more likely than women to develop COVID-19 because some RAS-related aspects are gender-related due to proteins located on the X chromosome.

Researchers believe that there is a solution to the problem of peptides, and that some FDA-approved drugs may help. The list includes danazine, styrene alcohol and Aycara peptides, which can reduce the production of anti-kinetic peptides. Aycara peptides can reduce the transmission of slow-up peptide signals. Jacobson and his team also say vitamin D may help with COVID-19 management because it involves the RAS system and can reduce a different compound. These drugs may prevent a storm of peptides. Hymecromone is then a different drug that lowers HAL levels and thus lung complications. Finally, a different drug called timbetasin can mimic the mechanisms that protect women.

It is important to note that this is only speculation based on the results of the study. More research is needed on this topic, which, of course, seems to be a hypothesis worthy of investigation. The researchers say the drugs need to be tested in clinical trials.

A team of Dutch scientists seems to agree that the virus can block the regulation of peptides, a process that has huge side effects in some patients. As The Scientist recently reported, researchers are already studying the potential efficacy of drugs that can target peptide systems, including icatibant and a monoclonal antibody called lanadelumab. A small exploratory study showed that hypoxia patients who took icatibant shortly after hospitalization had improved oxygenation and did not require oxygen supplementation compared to the control group. This is not a randomized study, and some patients who get the drug still need oxygen treatment.

The full study by jacobson’s team is available on this link and can benefit from additional review and research by experts in the field.