Abstract
Coronavirus disease-19 caused by the novel RNA betacoronavirus SARS-CoV2 has first emerged in Wuhan, China in December 2019, and since then developed into a worldwide pandemic with >99 million people afflicted and >2.1 million fatal outcomes as of 24th January 2021. SARS-CoV2 targets the lower respiratory tract system leading to pneumonia with fever, cough, and dyspnea. Most patients develop only mild symptoms. However, a certain percentage develop severe symptoms with dyspnea, hypoxia, and lung involvement which can further progress to a critical stage where respiratory support due to respiratory failure is required. Most of the COVID-19 symptoms are related to hyperinflammation as seen in cytokine release syndrome and it is believed that fatalities are due to a COVID-19 related cytokine storm. Treatments with anti-inflammatory or anti-viral drugs are still in clinical trials or could not reduce mortality. This makes it necessary to develop novel anti-inflammatory therapies. Recently, the therapeutic potential of phytocannabinoids, the unique active compounds of the cannabis plant, has been discovered in the area of immunology. Phytocannabinoids are a group of terpenophenolic compounds which biological functions are conveyed by their interactions with the endocannabinoid system in humans. Here, we explore the anti-inflammatory function of cannabinoids in relation to inflammatory events that happen during severe COVID-19 disease, and how cannabinoids might help to prevent the progression from mild to severe disease.
Highlights
Coronavirus disease 19 (COVID-19) caused by the novel severe acute respiratory syndromecoronavirus 2 (SARS-CoV2) firstly emerged in December 2019 in Wuhan in China and has, since evolved into a global pandemic [1]
According to the current state of available clinical data, most severe COVID-19 symptoms are related to cytokine release syndrome (CRS), which is assumed to be responsible for the fatal outcome in COVID-19 patients
We discuss the hypothesis that cannabinoids may have a great potential for the inhibition of hyperinflammation leading to CRS in COVID-19 patients
Summary
Coronavirus disease 19 (COVID-19) caused by the novel severe acute respiratory syndromecoronavirus 2 (SARS-CoV2) firstly emerged in December 2019 in Wuhan in China and has, since evolved into a global pandemic [1]. It is a novel enveloped RNA betacoronavirus, which binds with its spike surface protein (S-protein) to angiotensin-converting enzyme 2 (ACE2) on the cellular host’s surface. Patients who developed acute respiratory distress syndrome (ARDS) and required mechanical ventilation had a reported mortality rate of 88.1% in the New York City area in March 2020 [9]. Elderly, and young patients with only mild comorbidities like hypertension, diabetes mellitus and obesity developed respiratory failure [10]
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