With that knowledge, they performed a series of experiments in the laboratory and in rodent models to test their hypothesis that the SARS-CoV-2 spike protein acts on the VEGF-A/neuropilin pain pathway. They used VEGF-A as a trigger to induce neuron excitability, which creates pain, then added the SARS-CoV-2 spike protein.
"The spike protein completely reversed the VEGF-induced pain signaling," Dr. Khanna said. "It didn't matter if we used very high doses of spike or extremely low doses—it reversed the pain completely."
