Until now, it was known that SARS-CoV-2 enters cells using the ACE2 protein. However, a few days ago, a professor of pharmacology at the University of Arizona, Rajesh Hannah, discovered a new way of introducing a virus into cells, which allows you to infect the human nervous system, making it immune to pain.
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Studies have shown that the spike proteins located on the surface of SARS-CoV-2 bind to the neuropilin-1 protein and use it, like ACE2, to enter cells. The initial function of neuropilin-1 is to control the growth of blood vessels and the viability of neurons, but when it binds to the VEGF-A protein, it excites pain signals in cells that are transmitted through the spinal cord to the brain, causing a person to feel pain. At the same time, it is known that in patients with coronavirus, the activity of neuropilin-1 is increased, as in the pain-sensing neurons of animal models.
Through experiments in the laboratory, Rajesh Hannah's team was able to find out that the binding of SARS-CoV-2 spike proteins to neuropilin-1 minimizes the intensity of pain signals and, therefore, dulls pain. Neuropilin-1 blocks VEGF-A, suppressing the sensitivity of neurons to pain signals and thereby reducing the pain threshold.
A deeper study of this issue in the future will help to invent a cure not only for coronavirus infection, but also for cancer, experts say.
Scientists have previously stated that vitamin D does not block the severe form of COVID-19 and is dangerous for the kidneys in case of an overdose.