Abstract
The recent coronavirus disease (COVID-19) is still spreading worldwide. The 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 the cells of the nasal cavity, then spreads along the airway tracts, causing mild clinical manifestations, and, in a majority of patients, a persisting loss of smell. In some individuals, SARS-CoV-2 reaches and infects several organs, including the lung, leading to severe pulmonary disease. SARS-CoV-2 induces neurological symptoms, likely contributing to morbidity and mortality through unknown mechanisms. Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid with pleiotropic properties and functions in many tissues, including the nervous system. S1P regulates neurogenesis and inflammation and it is implicated in multiple sclerosis (MS). Notably, Fingolimod (FTY720), a modulator of S1P receptors, has been approved for the treatment of MS and is being tested for COVID-19. Here, we discuss the putative role of S1P on viral infection and in the modulation of inflammation and survival in the stem cell niche of the olfactory epithelium. This could help to design therapeutic strategies based on S1P-mediated signaling to limit or overcome the host–virus interaction, virus propagation and the pathogenesis and complications involving the nervous system.
Highlights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a positive-sense single-stranded RNA virus, has been included by the Coronaviridae Study Group (CSG) of the International Committee on Taxonomy of Viruses, into the family of Coronaviridae SARS-CoV-2, causes the pandemic coronavirus disease (COVID-19) started in China at the end of 2019.The most prevalent symptoms of COVID-19 are cough, fever, tiredness, breathlessness, conjunctivitis and, in the severe cases, acute respiratory distress syndrome characterized by diffuse damage of alveolar cells [1]
The aim of the present review is to present the properties of Sphingosine 1-phosphate (S1P) that are interesting, spreading from the regulation of virus infection/replication to cell survival, stem cell proliferation and inflammation
Olfactory receptor mature neurons do not present angiotensin-converting enzyme 2 (ACE2) [49], it is possible that SARS-CoV-2 enters and damages the sustentacular and stem cells in the nasal epithelium, which are required for normal olfactory functions and/or regeneration of damaged neurons
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a positive-sense single-stranded RNA virus, has been included by the Coronaviridae Study Group (CSG) of the International Committee on Taxonomy of Viruses, into the family of Coronaviridae SARS-CoV-2, causes the pandemic coronavirus disease (COVID-19) started in China at the end of 2019. COVID-19 patients showed neurological signs, such as headache, nausea and vomiting [6,7], stroke, isolated cases of Guillain–Barré syndrome [8] and demyelination [9] It is unclear whether the neurological symptoms are the result of a direct infection of neurons (via a transynaptical transport to the peripheral or central nervous system (CNS) or of an indirect infection (i.e., of the endothelial cells of the blood-brain-barrier, and/or of inflammatory cells, which reach the CNS). Regarding SARS-CoV-2, it has been described as a case of a COVID-19 patient under Fingolimod (FTY720) treatment for MS (a 57-year-old female) with a positive outcome [36], indicating that the immunomodulation might be beneficial to reduce mortality. Exploring the effects of S1P in the olfactory epithelium as well as in sensorial pathways may open new windows on the therapeutic opportunities against the neurological symptoms and the excessive immune responses that characterize this novel, overwhelming and worldwide infection
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