Significant alteration of cognitive and affective behaviors mediated by neural pathways in the central nervous system (CNS), currently referred to as “brain fog”, is a major long-term complication following recovery from an acute infectious event.1-3 Persistent cognitive deficits have been identified in patients who have recovered from acute infection with severe acute respiratory syndrome-coronavirus 2 (SARS-CoV- 2), the etiologic agent of coronavirus disease-2019 (COVID-19). Post-infectious cognitive dysfunction has been observed in previous pandemics, including those associated with the widespread transmission of Asiatic (Russian) influenza, myalgic encephalomyelitis, Spanish influenza, diphtheria, encephalitis lethargica, and chronic fatigue syndrome (also known as post- viral fatigue syndrome).3 Furthermore, chronic cognitive behavioral deficits have been listed as significant complications of Ebola, Zika, influenza A, and human immunodeficiency virus (HIV) infections.4 Collectively, these data strongly suggest that secondary targeting of brain neural structures by viruses that have previously-
Stefano GB, Büttiker P, Kream RM. Reassessment of the blood-brain barrier: a potential target for viral entry into the immune-privileged brain. 2022. Germs. 2022 Mar 31;12(1):99-101.