Imagine being infected by a virus that makes you immune to pain, and that, when detected, is already too late, as it has spread everywhere. this suggests a recent discovery by Rajesh Khanna, professor of pharmacology at the University of Arizona, about Sars-Cov-2.
So far, most reports of the disease focus on the idea that the virus is spread to cells through the ACE2 protein. However, recent studies, which have not yet been peer-reviewed, indicate that there is an alternative route to the disease – one that takes you directly to the nervous system.
Based on these reports, the professor’s team conducted some tests and found a link between a specific cell protein and pain – an interaction that is interrupted by the coronavirus. Now, the study led by Khanna has been revised and is about to be published in the journal Pain.
Link between Sars-Cov-2 and pain
The idea of investigating the relationship between pain and swelling arose after two surveys were registered with BioRxiv, a pre-printed server, which showed that the famous proteins present on the surface of the virus can bind to a second protein, called neuropilin-1.
This means that the virus can use this form to invade nerve cells present in the body, as well as infect the individual in the already known way, through the ACE2 protein.
Since neuropilin-1, like ACE2, allowed the virus to invade the body, the researchers raised the hypothesis that it could be related to pain. Under normal circumstances, the protein controls the growth of blood vessels and neurons.
However, when neuropilin-1 binds to a natural protein called vascular endothelial growth factor A (VEGF-A), it triggers pain signals that are transmitted through the spinal cord directly to the upper centers of the brain.
Until then, infecting the ACE2 protein was the best known way for the disease to invade the body. Photo: Kateryna Kon / Shutterstock
In in vitro conditions, created by Khanna’s team, samples of nerve cells infected by the disease showed that when the virus binds to neuropilin-1, it decreases pain signaling. This suggests that, under normal conditions, that is, in a live animal, the effect may be similar.
What exactly happens is that when the neuropilin-1 protein is invaded, its binding with VEGF-A is blocked, “hijacking” the circuit that signals pain. This connection suppresses the excitability of the neurons that receive the signal, making the patient less sensitive to pain.
If it is confirmed that the virus also acts in this way in humans, science may have a new approach to develop treatments against Covid-19. As raised by the professor, one of the possibilities to fight the disease would be to create a compound that blocks neuropilin-1 to limit the entry of the virus into the cells. In any case, further studies are still needed.
Via: Science Alert
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