The virus that causes Covid-19 acts as a pain reliever, suggesting new study findings that could provide a “possible explanation for the relentless spread of the disease,” the researchers said.
Researchers at the University of Arizona Health Sciences said that the virus of COVID-19 could inadvertently act as a pain reliever, which could “explain that about half of those who receive COVID-19 experience little or no experience. . Symptoms, although they are able to spread the disease, ”according to a news release on the findings.
“The spike protein completely reversed VEGF-induced pain signaling,” Khanna said. “It doesn’t matter if we used a spike or a very low dose too much – it made the pain completely the opposite.” (iStock)
“So I understand very well that the reason for the continued spread of Kovid-1 of is probably that at the initial stage you are not thinking that something is wrong as your pain has been suppressed,” said study author Rajesh Khanna in a statement. . Khanna is also a professor in the Department of Pharmacology at the College of Medicine at the University of Arizona in Tucson.
Senior Vice President of Health Sciences Dr. Michael DA added, “This research increases the likelihood that as an early symptom of COVID-19, pain can be reduced by the SARS-COVI-2 spike protein, as it calms the body’s pain signaling pathways,” said Dr. . Michael d. Deck, in a statement.
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Medical experts studying the novel virus think that SARS-CoV-2 infects humans when the virus’s spike protein binds to the ACE2 receptor on human cells. However, the virus can also use another receptor, Neuropylene-1, to infect humans. At least two studies this past summer concluded that the virus also uses the neuropilin-1 receptor, according to a press release.
“This attracts our eye because for the last 15 years my lab has been studying proteins and pathway complexes related to the pain process of neuropylene flow,” Khanna said. “So we swam back pped and realized that this could mean that maybe some kind of spike protein is involved in the pain process.”
“Many biological pathways signal the body to experience pain. Is caused by a protein called vascular endothelial growth factor-A (VEGF-A), which plays an essential role in blood vessel growth, but is also associated with diseases such as cancer, arthritis and, more recently, covid-1. “The release reads.” Like a lock key, when the VEGF-A receptor binds to neuropilin, it initiates a cascade of events that result in hyperexcitability of neurons, leading to pain. “
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The research team found that the SARS-Co-2 spike protein binds to neuropilin at exactly the same location as VEGF-A per release. The team used rats to test their theory, using VEGF-A “as a trigger to induce neuron stimulation, which produces pain, then added the SARS-Covy-2 spike protein.”
“The spike protein completely reversed VEGF-induced pain signaling,” Khanna said. “It doesn’t matter if we used a spike or a very low dose too much – it made the pain completely the opposite.”
In addition to explaining the widespread prevalence of COVID-19, the researchers said their findings could help scientists devise non-io pioid pain therapies in an effort to combat the ongoing opioid epidemic in the country.
“We are moving forward with the formation of small molecules against neuropylene, especially natural compounds, which can be important for pain relief,” Khanna said. “We have an epidemic, and we have an opioid epidemic. They are colliding. Our findings have a huge impact for both. SARS-COVI-2 is teaching us about viral spread, but COVID-1US also wants neuropilin as a new non-ioPoid method of fighting the iodide epidemic. “
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