Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.17.209288v1?rss=1 Authors: Moutal, A., Martin, L. F., Boinon, L., Gomez, K., Ran, D., Zhou, Y., Stratton, H. J., Song, C., Luo, S., Gonzalez, K. B., Perez-Miller, S., Patwardhan, A., Ibrahim, M., Khanna, R. Abstract: Global spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues unabated. Binding of SARS-CoV-2's Spike protein to host angiotensin converting enzyme 2 triggers viral entry, but other proteins may participate, including neuropilin-1 receptor (NRP-1). As both Spike protein and vascular endothelial growth factor-A (VEGF-A) - a pro-nociceptive and angiogenic factor, bind NRP-1, we tested if Spike could block VEGF-A/NRP-1 signaling. VEGF-A-triggered sensory neuronal firing was blocked by Spike protein and NRP-1 inhibitor EG00229. Pro-nociceptive behaviors of VEGF-A were similarly blocked via 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 via subversion of VEGF-A/NRP-1 signaling may underlie increased disease transmission in asymptomatic individuals. Copy rights belong to original authors. Visit the link for more info