Abstract
The coronavirus SARS-CoV-2 at the origin of COVID-19 shares more than 70% genetic similarity with SARS-CoV-1 that was at the origin of 2003 SARS. Infection-associated symptoms are very similar between SARS and COVID-19 diseases and are the same as community-acquired pneumonia symptoms. Antibiotics were empirically given to SARS patients in the early stages of the pathology whereas a different strategy has been decided in the management of COVID-19 pandemic with a worldwide shutdown. The cytokine storm, both identified in SARS and COVID-19 severe cases, is generated through inflammasome activation, which opens therapeutic perspectives to counteract the pathogenic inflammation. As corticoids have numerous side effects that limit their use, focusing on anti-inflammasome agents could represent a safer alternative for patients with severe COVID-19.
MeSH terms
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Adrenal Cortex Hormones / therapeutic use
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Anti-Bacterial Agents / therapeutic use*
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Betacoronavirus / isolation & purification
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COVID-19
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Coronavirus Infections / drug therapy*
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Coronavirus Infections / epidemiology
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Humans
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Inflammasomes / chemistry
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Inflammasomes / metabolism
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Pandemics
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Pneumonia, Viral / drug therapy*
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Pneumonia, Viral / epidemiology
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Purinergic P2X Receptor Antagonists / therapeutic use
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Receptors, Purinergic P2X7 / chemistry
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Receptors, Purinergic P2X7 / metabolism
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SARS-CoV-2
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Severe Acute Respiratory Syndrome / drug therapy*
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Severe Acute Respiratory Syndrome / epidemiology
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Severe Acute Respiratory Syndrome / virology
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Severe acute respiratory syndrome-related coronavirus / isolation & purification
Substances
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Adrenal Cortex Hormones
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Anti-Bacterial Agents
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Inflammasomes
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Purinergic P2X Receptor Antagonists
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Receptors, Purinergic P2X7