COVID-19 may not be all doom and gloom after all. In fact, it may even lead to the creation of a new kind of pain medication. I know this sound counterintuitive considering how painful getting the coronavirus actually is but the research seems to indicate that it’s possible.
Scientist Rajesh Kanna from the University of Arizona explains in Discover Magazine:
“You might be wondering how my lab began to probe the connection between SARS-CoV-2 and pain. We were inspired by two preliminary reports that appeared on the preprint server BioRxiv that showed that the infamous spike proteins on the surface of the SARS-CoV-2 virus bound to a protein called neuropilin-1. This means that the virus can also use this protein to invade nerve cells as well as through the ACE2 protein.
For the past year, some six months before the pandemic took hold, my colleagues and I had been studying the role of neuropilin-1 in the context of pain perception. Because neuropilin-1, like the ACE2 receptor, allowed spike to enter the cells, we wondered if this alternate gateway could also be related to pain.
Under normal circumstances, the neuropilin-1 protein controls the growth of blood vessels, and as well as the growth and survival of neurons.
However, when neuropilin-1 binds to a naturally occurring protein called called Vascular endothelial growth factor A (VEGF-A), this triggers pain signals. This signal is transmitted via the spinal cord into higher brain centers to cause the sensation we all know as pain.
Staring at this jigsaw puzzle – neuropilin-1 and VEGF-A and neuropilin and spike – we wondered if there was a link between spike and pain.
Previous research has shown a link between VEGF-A and pain. For people with osteoarthritis, for instance, studies have shown that increased activity of the VEGF gene in fluids lubricating joints, like the knee, is associated with higher pain scores.
Although activity of the neuropilin-1 gene is higher in biological samples from COVID-19 patients compared to healthy controls and activity of the neuropilin-1 gene is increased in pain-sensing neurons in an animal model of chronic pain, the role of neuropilin-1 in pain has never been explored until now.
In in vitro studies done in my lab using nerve cells, we showed that when spike binds to neuropilin-1 it decreases pain signaling, which suggests that in a living animal it would also have a pain-dulling effect.
When the spike protein binds to the neuropilin-1 protein, it blocks the VEGF-A protein from binding and thus hijack’s a cell’s pain circuitry. This binding suppresses the excitability of pain neurons, leading to lower sensitivity to pain.”
In fact, this may explain why the disease has been spread so easily as a ton of people who may have had it may have not felt any pain or discomfort, thought they were fine, and continued to go about their business. So if this is true that could be a significant game-changer, both for how we understand and treat the disease, and also for the chance that it could lead to something positive like a new pain medication.
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