Abstract
Prolonged recovery and delayed polysymptomatic complications distinguish the COVID-19, caused by SARS-COV-2 viral infection, from other flu-like illnesses 1 . A growing number of patients report symptoms, including early and late onset neurological and psychiatric signs and symptoms, persisting, or emerging after initial recovery 2 , suggesting significant potential for retarded sequelae with poorly defined pathogenesis. Although distinct from usual flu-like illnesses, this feature of COVID-19 resembles neurological and mental disorders reported in acute or recovery phases in previous coronavirus (MERS and SARS) outbreaks 3 . We hypothesise that in the aftermath of COVID-19 reactive neuroglia, in a subset of patients, fail to return to the physiological state.
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