Incredible, I had to verify that notable, spike protein blocks a particular pain pathway, talk about a perfectly engineered bioweapon…
Pain Relief Caused by SARS-CoV-2 Infection May Help Explain COVID-19 Spread
New research shows SARS-CoV-2 promotes pain relief when it infects cells through a common protein receptor, neuropilin-1. The finding gives scientists a novel target for non-opioid pain therapeutics, while also offering an explanation for the unrelenting spread of COVID-19.
SARS-CoV-2, the virus that causes COVID-19, can relieve pain, according to a new study by University of Arizona Health Sciences researchers.
The finding may explain why nearly half of all people who get COVID-19 experience few or no symptoms, even though they are able to spread the disease, according to the study's corresponding author Rajesh Khanna, a professor in the UArizona College of Medicine – Tucson's Department of Pharmacology.
"It made a lot of sense to me that perhaps the reason for the unrelenting spread of COVID-19 is that in the early stages, you're walking around all fine as if nothing is wrong because your pain has been suppressed," Khanna said. "You have the virus, but you don't feel bad because your pain is gone. If we can prove that this pain relief is what is causing COVID-19 to spread further, that's of enormous value."
The paper, "SARS-CoV-2 Spike protein co-opts VEGF-A/Neuropilin-1 receptor signaling to induce analgesia," is published in PAIN, the journal of the International Association for the Study of Pain.
https://news.arizona.edu/story/pain-relief-caused-sars-cov-2-infection-may-help-explain-covid-19-spread
PAIN article…No coincidences…PAIN
SARS-CoV-2 spike protein co-opts VEGF-A/neuropilin-1 receptor signaling to induce analgesia
Global spread of severe acute respiratory syndrome coronavirus 2 continues unabated. Binding of severe acute respiratory syndrome coronavirus 2's spike protein to host angiotensin-converting enzyme 2 triggers viral entry, but other proteins may participate, including the neuropilin-1 receptor (NRP-1). Because both spike protein and vascular endothelial growth factor-A (VEGF-A)—a pronociceptive and angiogenic factor, bind NRP-1, we tested whether spike could block VEGF-A/NRP-1 signaling. VEGF-A-triggered sensory neuron firing was blocked by spike protein and NRP-1 inhibitor EG00229. Pronociceptive behaviors of VEGF-A were similarly blocked through suppression of spontaneous spinal synaptic activity and reduction of electrogenic currents in sensory neurons. Remarkably, preventing VEGF-A/NRP-1 signaling was antiallodynic in a neuropathic pain model. A “silencing” of pain through subversion of VEGF-A/NRP-1 signaling may underlie increased disease transmission in asymptomatic individuals.
https://journals.lww.com/pain/Fulltext/2021/01000/SARS_CoV_2_spike_protein_co_opts.21.aspx