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The most common symptoms of infection from SARS-CoV2, the virus responsible for COVID-19, include fever, cough, shortness of breath, and indications of widespread respiratory system involvement. Recent evidence suggests that SARS-CoV2 can attack other organ systems, as well. In fact, some infected patients report loss of smell and taste, potentially signaling SARS-CoV2 infiltration of the central nervous system.

SARS-CoV2 exploits the angiotensin-converting enzyme 2 (ACE2) receptor to gain entry into cells. One group of scientists described the expression of ACE2 in neurological tissue and assessed the possible contribution of neurological tissue damage to the death and disease associated with COVID-19. Previous research indicates that related coronaviruses infect the olfactory bulb in mice to promote neuronal death. In addition, viral presence and accompanying damage have been observed in human brain tissue following coronavirus infection.

The authors of the current study noted that long before the neuronal damages occur, the endothelial tissues in cerebral capillaries rupture and bleed into the surrounding tissue, which is often fatal. They suggested that early signs of impaired smell or taste in an otherwise uncomplicated early-stage COVID-19 patient should be investigated thoroughly for central nervous system involvement. They concluded that although widespread homeostatic dysfunction is the primary cause of death among COVID-19 patients, cerebral edema due to neurological damage might expedite death before the onset of homeostatic failure. These findings can influence the triaging of patients with COVID-19.

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