• Pain · Jan 2021

    SARS-CoV-2 Spike protein co-opts VEGF-A/Neuropilin-1 receptor signaling to induce analgesia.

    • Aubin Moutal, Laurent F Martin, Lisa Boinon, Kimberly Gomez, Dongzhi Ran, Yuan Zhou, Harrison J Stratton, Song Cai, Shizhen Luo, Kerry Beth Gonzalez, Samantha Perez-Miller, Amol Patwardhan, Mohab M Ibrahim, and Rajesh Khanna.
    • Departments of Pharmacology, and.
    • Pain. 2021 Jan 1; 162 (1): 243252243-252.

    AbstractGlobal 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.

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