25 January 2021>: Editorial
Selective Neuronal Mitochondrial Targeting in SARS-CoV-2 Infection Affects Cognitive Processes to Induce ‘Brain Fog’ and Results in Behavioral Changes that Favor Viral Survival
George B. Stefano ABCDEF* , Radek Ptacek ABCDEF , Hana Ptackova ABCDEF , Anders Martin ABCDEF , Richard M. Kream ABCDEFDOI: 10.12659/MSM.930886
Med Sci Monit 2021; 27:e930886
Figure 1 ‘Brain fog’ and COVID-19 targeting for long-term rehabilitation. SARS-CoV-2, which causes COVID-19, can infect the lungs, CNS, gastrointestinal system, and cardiovascular system. With time, widespread infection increases the total viral load in the infected individual. SARS-CoV-2 can integrate its genome into mitochondria to reduce energy metabolism. The brain is especially vulnerable to hypoxia because cognitive neural processes adjust poorly to hypoxic conditions. Hypoxia is also pro-inflammatory. Therefore, as the viral load increases, cognitive impairment and confusion increase, a condition known as ‘brain fog’. This ongoing cascade of neuronal dysfunction is an important factor in understanding the long-term pathogenesis of CNS infection with SARS-CoV-2. Importantly, the behaviors resulting from ‘brain fog’ may increase the spread of SARS-CoV-2. COVID-19 – coronavirus disease 2019; SARS-CoV-2 – severe acute respiratory syndrome coronavirus 2; CNS – central nervous system.