UArizona researchers study pain relief caused by coronavirus
PHOENIX – New research from the University of Arizona could explain why nearly half of all people who get coronavirus show few or no symptoms.
“This research raises the possibility that pain, as an early symptom of COVID-19, may be reduced by the SARS-CoV-2 spike protein as it silences the body’s pain signaling pathways,” UArizona Health Sciences Senior Vice President Michael Dake said in a press release.
Researchers at UArizona discovered SARS-CoV-2, the virus that causes COVID-19, has the ability to reduce pain by blocking the pain pathway at the cellular level. Viruses infect cells through protein receptors, and coronavirus is no different.
Usually, when the body is affected by infection, a protein called vascular endothelial growth factor, binds to the pain receptor on the surface of the cell, or neuropilin, which signals a series of events that trigger the sensation of pain.
UArizona researchers found in rodent and laboratory models that when COVID-19 proteins bind to cells, the pain pathway is blocked.
“The spike protein completely reversed the VEGF-induced pain signaling,” UArizona College of Medicine and research Rajesh Khanna said. “It didn’t matter if we used very high doses of spike or extremely low doses – it reversed the pain completely.”
Because the pathway is blocked, it could explain why some people who are infected with coronavirus have no pain symptoms.
Khanna is working with immunologists and virologists at UArizona Health Science to continue studying the role that neuropilin plays in the spread of COVID-19.
Researchers are also studying neuropilin as a new target for non-opioid pain relief.
“We have a pandemic, and we have an opioid epidemic. They’re colliding. Our findings have massive implications for both,” Khanna said. “SARS-CoV-2 is teaching us about viral spread, but COVID-19 has us also looking at neuropilin as a new non-opioid method to fight the opioid epidemic.”