Neurotropism of SARS-CoV-2 and neurological diseases of the central nervous system in COVID-19 patients

Abstract

The devastating COVID-19 pandemic is caused by the SARS-CoV-2 virus. It primarily affects the lung and induces acute respiratory distress leading to a decrease in oxygen supply to the cells. This lung insufficiency caused by SARS-CoV-2 virus contributes to hypoxia which can affect the brain and other organ systems. The heightened cytokine storm in COVID-19 patients leads to an immune reaction in the vascular endothelial cells that compromise the host defenses against the SARS-CoV-2 virus in various organs. The vascular endothelial cell membrane breach allows access for SARS-CoV-2 to infect multiple tissues and organs. The neurotropism of spike protein in SARS-CoV-2 rendered by furin site insertion may increase neuronal infections. These could result in encephalitis and encephalopathy. The COVID-19 patients suffered severe lung deficiency often showed effects in the brain and neural system. The early symptoms include headache, loss of smell, mental confusion, psychiatric disorders and strokes, and rarely encephalitis, which indicated the vulnerability of the nervous system to SARS-CoV-2. Infection of the brain and peripheral nervous system can lead to the dysfunction of other organs and result in multi-organ failure. This review focuses on discussing the vulnerability of the nervous system based on the pattern of expression of the receptors for the SARS-CoV-2 and the mechanisms of its cell invasion. The SARS-CoV-2 elicited immune response and host immune response evasion are further discussed. Then the effects on the nervous system and its consequences on neuro-sensory functions are discussed. Finally, the emerging information on the overall genetic susceptibility seen in COVID-19 patients and its implications for therapy outlook is discussed.

BCG-Based Vaccines Elicit Antigen-Specific Adaptive and Trained Immunity against SARS-CoV-2 and Andes orthohantavirus

“…SARS-CoV-2 infects the upper and lower respiratory tracts, and this disease is characterized by several systemic symptoms [ 23 ]. Among the most common symptoms fever, cough, fatigue, headache, sore throat, shortness of breath; although, Acute Respiratory Distress Syndrome (ARDS), acute cardiac injury, anaemia, predisposition to secondary infections, and central nervous system damage (CNS) are reported [ 23 , 24 , 25 ].…”

COVID-19 infection enhances susceptibility to oxidative-stress induced parkinsonism

“…Given recent reports of COVID-19-induced parkinsonism [15][16][17] , where the parkinsonian symptoms appear similar to those described after the 1918 H1N1 outbreak, it would be derelict to not consider that these two vastly different pandemic viruses may share a common mechanism that leads to these neurological sequalae. Both influenza and SARS-CoV-2 are respiratory viruses, both have been shown to infect epithelial cells in the lung and gut 28 and both the 1918 H1N1 influenza virus 29 and SARS-CoV-2 30 do not appear to have significant neurotropic potential (except in cases where there is a breach in the blood-brain barrier). Related to a possible mechanism, both the 1918 influenza and SARS-CoV-2 appear to induce an enhanced program of induction of pro-inflammatory cytokines and chemokines, known as a cytokine storm 31 .…”

Transparente Darstellung von Kasuistiken nach COVID-19-Erkrankung oder COVID-19-Impfung – eine zeitliche Koinzidenz

“…Die Mannigfaltigkeit der COVID-19-Erkrankung 1 wird anhand der direkten Zellinteraktion des Coronavirus SARS-CoV-2 nach Invasion über den Rezeptor Angiotensin-Converting-Enzyme-2 2 mit immunologischen und thromboembolischen Folgereaktionen erklärt 3 , 4 , wobei das Virus sich u. a. durch einen Neurotropismus auszeichnet, was vielseitige neurologische Symptome verursachen kann 5 . Manifestationen im Rahmen von COVID-19 sind für letztlich jede okuläre Struktur beschrieben worden 6 , 7 , 8 .…”