For all its deadly effects, the novel coronavirus may actually have one unexpected side effect.
It could block pain, potentially allowing the virus to lurk undetected in a body in its earliest stages.
A new study from scientists at the University of Arizona Health Sciences center shows that the novel coronavirus has a second receptor that is linked to pain signaling. The coronavirus spike attaches to receptors to enter and infect cells.
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By attaching to this receptor, called the neuropilin-1 receptor, the virus seems to decrease or stop pain entirely, according to the study’s lead researcher, Rajesh Khanna.
“The pathway for pain is shut off,” Khanna said.
In its recent study, Khanna’s team tested the ability of the virus to provide pain relief in over 100 mice. They injected some of the mice with an inactivated spike of the novel coronavirus that cannot cause infection but that still attaches to the neuropilin-1 receptor. The other mice received placebos.
The mice receiving the coronavirus spikes experienced pain relief within 30 minutes, which persisted for about nine hours, according to Khanna.
He theorizes that this mechanism could allow the virus to fly under the radar earlier on in the course of a COVID-19 infection, before symptoms occur and when people are the most infectious.
“Maybe in the first stages, the first critical stages, you’re resilient to that, you have pain relief,” he said. “It’s fooling you into believing that you’re fine.”
This is just a theory, Khanna said, and he is not a coronavirus expert. Even if the virus blocks feelings of pain, Khanna said, people can still get sick.
He has received dozens of anecdotal emails since his study published from patients who had chronic pain conditions before getting sick.
“Then they got COVID and now their pain is gone,” he said. “I fully acknowledge that these are anecdotes … but it’s a recurrent theme. It’s mind boggling!”
Once the COVID-19 infection subsides in the patients, their chronic pain comes back, he said.
While these are anecdotal cases, Khanna believes it shows that it may be important to study this receptor further.
Rather than blocking all types of pain, the receptor seems to be most related to chronic inflammatory pains such as arthritis, back pain, or pain as a result of chemotherapies.
He also theorized that the virus may attach more often to the neuropilin-1 receptor in asymptomatic COVID-19 patients than to the main receptor. The main receptor for the virus is the ACE2 receptor, which is found in a variety of organs such as the lung, kidney, heart and intestines.
As a UA professor of pharmacology who specializes in researching pain and pain treatments, Khanna is excited about the implications of the study beyond this pandemic. His team had already been studying the neuropilin-1 receptor for the last 18 months to gauge potential pain management treatments.
“What this virus did was reveal this receptor as a new player in pain signaling,” he said.
He plans to use the findings to further study the receptor and target this area for future pain management therapies or treatments.
Amanda Morris covers all things bioscience, which includes health care, technology, new research and the environment. Send her tips, story ideas, or dog memes at [email protected] and follow her on Twitter @amandamomorris for the latest bioscience updates.
Independent coverage of bioscience in Arizona is supported by a grant from the Flinn Foundation.
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This article originally appeared on Arizona Republic: UA scientists study theory that the coronavirus may briefly block pain, masking illness