Emerging neurotropic features of SARS-CoV-2

Abstract

The prevailing coronavirus disease-19 (COVID-19) caused by a novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) has presented some neurological manifestations including hyposmia, hypogeusia, headache, stroke, encephalitis, Guillain-Barre syndrome, and some neuropsychiatric disorders. Although several cell types in the brain express angiotensin-converting enzyme-2 (ACE2), the main SARS-CoV-2 receptor, and other related proteins, it remains unclear whether the observed neurological manifestations are attributed to virus invasion into the brain or just comorbidities caused by dysregulation of systemic factors. Here, we briefly review the neurological manifestations of SARS-CoV-2, summarize recent evidence for the potential neurotropism of SARS-CoV-2, and discuss the potential mechanisms of COVID-19-associated neurological diseases.

Keywords: ACE2; SARS-CoV-2; brain invasion; neurological manifestations.

Figure 1

Possible mechanism for the effects of SARS-CoV-2 on the nervous system. SARS-CoV-2 may cause damage to the nervous system through direct or indirect pathways. The direct infection of SARS-CoV-2 into sustentacular cells and horizontal basal cells impairs the function of olfactory neurons, which leads to the loss of smell sense and may further cause brain damage. SARS-CoV-2 induces an immune response after it enters the human body. The cytokine storm formed in the process of immune response can cause thrombosis and destruction of the BBB, and thus indirectly cause brain damage. When the BBB is broken, SARS-CoV-2 may cross the barrier and directly infect nerve cells by binding to specific receptors on nerve cells.