![]() ![]() Many of these symptoms remain long after the acute illness has passed, a phenomenon described as “long-COVID”, post-COVID-19 condition or post-acute sequelae of SARS-CoV-2 infection (PASC). Various neurologic signs and symptoms have been reported, such as headache, nausea, anosmia, myalgia, hemorrhage, syncope, seizure, and stroke. ![]() The penetration of SARS-CoV-2 into the brain could account for the neurological symptoms observed in a large majority of people with COVID-19. Despite some initial controversies, an increasing number reports the presence of SARS-CoV-2 in the central nervous system (see Ref. Although COVID-19, the acute respiratory disease caused by the SARS-CoV-2 virus, targets primarily the lungs leading to an acute respiratory disease, increasing evidence indicates a more widespread infection of other organs including the heart and blood vessels, kidneys, gut, and brain. Our findings open new perspectives for the repurposing of melatonergic drugs and its clinically used analogs in the prevention of brain infection by SARS-CoV-2 and COVID-19-related long-term neurological symptoms.Īs of February 17, 2022, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is estimated to have infected globally approximately 410 million people, with more than 5 million deaths and currently more than 2,000,000 new confirmed infected cases per 24 h, as reported by WHO ( ). Molecular modeling analyses complemented by experimental studies in cells showed that SARS-CoV-2 entry in endothelial cells is prevented by melatonin binding to an allosteric-binding site on human angiotensin-converting enzyme 2 (ACE2), thus interfering with ACE2 function as an entry receptor for SARS-CoV-2. Here, we show that treatment of K18- hACE2 mice with melatonin and two melatonin-derived marketed drugs, agomelatine and ramelteon, prevents SARS-CoV-2 entry in the brain, thereby reducing virus-induced damage of small cerebral vessels, immune cell infiltration and brain inflammation. We previously showed that melatonin or two prescribed structural analogs, agomelatine and ramelteon delay the onset of severe clinical symptoms and improve survival of SARS-CoV-2-infected K18-hACE2 mice. Prevention of brain infection in the acute phase of the disease might thus be of therapeutic relevance to prevent long-lasting symptoms of COVID-19. Brain infection is particularly pronounced in the K18- hACE2 mouse model of COVID-19. ![]() Invasion of the brain by SARS-CoV-2 has been observed in humans and is postulated to be involved in post-COVID state. COVID-19 is a complex disease with short- and long-term respiratory, inflammatory and neurological symptoms that are triggered by the infection with SARS-CoV-2. ![]()
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