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People who are infected with a virus commonly report having aches and pains. Most people who are infected with SARS-CoV-2, the virus that causes COVID-19, exhibit symptoms such as fever, cough, and difficulty breathing, but not pain. Findings from a new study demonstrate that SARS-CoV-2 blocks pain receptors.
Robust evidence suggests that SARS-CoV-2 exploits the ACE2 receptor to gain entry into cells. A specific region of the virus called a spike protein binds to a cell’s ACE2 receptor, and the virus injects its genetic material – RNA – into the cytosol. Once inside, the virus hijacks the body’s natural replicating processes to promote viral reproduction.
Other evidence points to the possibility that ACE2 is not the sole means of entry, however, and that other proteins, such as the neuropilin-1 receptor (NRP-1), may be involved. NRP-1 participates in pain sensing and angiogenesis (the development of new blood vessels) and is a receptor for vascular endothelial growth factor-A (VEGF-A). When VEGF-A binds to NRP-1, it elicits neuronal hyperexcitability, producing pain.
The authors of the study wanted to see if the spike protein would interfere with VEGF-A/NRP-1 signaling in a rodent model of nerve pain. They used VEGF-A as a trigger to induce pain, and then they administered the SARS-CoV-2 spike protein.
They found that the spike protein interfered with pain signaling and effectively blocked the VEGF-A-induced pain. They saw this effect regardless of how much spike protein was present.
These findings suggest that SARS-CoV-2 blocks pain, which may have relevance for disease spread via asymptomatic people. Learn more about COVID-19 in these Q&As featuring Dr. Rhonda Patrick, released April 14 and June 10.
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