SARS-CoV-2 Infection: A Role for S1P/S1P Receptor Signaling in the Nervous System?

摘要: The recent coronavirus disease (COVID-19) is still spreading worldwide. severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the virus responsible for COVID-19, binds to its receptor angiotensin-converting enzyme 2 (ACE2), and replicates within cells of nasal cavity, then spreads along airway tracts, causing mild clinical manifestations, and, in a majority patients, persisting loss smell. In some individuals, SARS-CoV-2 reaches infects several organs, including lung, leading pulmonary disease. induces neurological symptoms, likely contributing morbidity mortality through unknown mechanisms. Sphingosine 1-phosphate (S1P) bioactive sphingolipid with pleiotropic properties functions many tissues, nervous system. S1P regulates neurogenesis inflammation it implicated multiple sclerosis (MS). Notably, Fingolimod (FTY720), modulator receptors, has been approved treatment MS being tested COVID-19. Here, we discuss putative role on viral infection modulation survival stem cell niche olfactory epithelium. This could help design therapeutic strategies based S1P-mediated signaling limit or overcome host-virus interaction, propagation pathogenesis complications involving