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Med Sci Monit ; 27: e933015, 2021 May 10.
Article in English | MEDLINE | ID: covidwho-1239178


Persistent comorbidities occur in patients who initially recover from acute coronavirus disease 2019 (COVID-19) due to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). 'Long COVID' involves the central nervous system (CNS), resulting in neuropsychiatric symptoms and signs, including cognitive impairment or 'brain fog' and chronic fatigue syndrome. There are similarities in these persistent complications between SARS-CoV-2 and the Ebola, Zika, and influenza A viruses. Normal CNS neuronal mitochondrial function requires high oxygen levels for oxidative phosphorylation and ATP production. Recent studies have shown that the SARS-CoV-2 virus can hijack mitochondrial function. Persistent changes in cognitive functioning have also been reported with other viral infections. SARS-CoV-2 infection may result in long-term effects on immune processes within the CNS by causing microglial dysfunction. This short opinion aims to discuss the hypothesis that the pathogenesis of long-term neuropsychiatric COVID-19 involves microglia, mitochondria, and persistent neuroinflammation.

COVID-19/complications , Central Nervous System/pathology , Cognitive Dysfunction/etiology , Inflammation/pathology , Microglia/pathology , Mitochondria/pathology , COVID-19/pathology , Cognitive Dysfunction/pathology , Humans , Neurons/pathology , SARS-CoV-2
Med Sci Monit ; 27: e930886, 2021 Jan 25.
Article in English | MEDLINE | ID: covidwho-1045272


Alterations in brain functioning, especially in regions associated with cognition, can result from infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and are predicted to result in various psychiatric diseases. Recent studies have shown that SARS-CoV-2 infection and coronavirus disease 2019 (COVID-19) can directly or indirectly affect the central nervous system (CNS). Therefore, diseases associated with sequelae of COVID-19, or 'long COVID', also include serious long-term mental and cognitive changes, including the condition recently termed 'brain fog'. Hypoxia in the microenvironment of select brain areas may benefit the reproductive capacity of the virus. It is possible that in areas of cerebral hypoxia, neuronal cell energy metabolism may become compromised after integration of the viral genome, resulting in mitochondrial dysfunction. Because of their need for constant high metabolism, cerebral tissues require an immediate and constant supply of oxygen. In hypoxic conditions, neurons with the highest oxygen demand become dysfunctional. The resulting cognitive impairment benefits viral spread, as infected individuals exhibit behaviors that reduce protection against infection. The effects of compromised mitochondrial function may also be an evolutionary advantage for SARS-CoV-2 in terms of host interaction. A high viral load in patients with COVID-19 that involves the CNS results in the compromise of neurons with high-level energy metabolism. Therefore, we propose that selective neuronal mitochondrial targeting in SARS-CoV-2 infection affects cognitive processes to induce 'brain fog' and results in behavioral changes that favor viral propagation. Cognitive changes associated with COVID-19 will have increasing significance for patient diagnosis, prognosis, and long-term care.

COVID-19/metabolism , Cognitive Dysfunction/metabolism , Health Behavior , Hypoxia, Brain/metabolism , Mitochondria/metabolism , Neurons/metabolism , SARS-CoV-2/physiology , COVID-19/complications , COVID-19/physiopathology , COVID-19/psychology , COVID-19/transmission , Cognitive Dysfunction/physiopathology , Cognitive Dysfunction/psychology , Energy Metabolism , Humans , Hypoxia, Brain/physiopathology , Hypoxia, Brain/psychology , Microbial Viability , Viral Load , Virus Replication , Post-Acute COVID-19 Syndrome
Med Sci Monit ; 26: e930340, 2020 Dec 16.
Article in English | MEDLINE | ID: covidwho-979224


Alterations in complex behavioral patterns during the extended period of the COVID-19 pandemic are predicted to promote a variety of psychiatric disease symptoms due to enforced social isolation and self-quarantine. Accordingly, multifaceted mental health problems will continue to increase, thereby creating a challenge for society and the health care system in general. Recent studies show that COVID-19 can directly or indirectly influence the central nervous system, potentially causing neurological pathologies such as Alzheimer disease and Parkinson disease. Thus, chronic COVID-19-related disease processes have the potential to cause serious mental illnesses, including depression, anxiety, and sleep disorders. Importantly, mental health problems can foster systemic changes in functionally-linked neuroendocrine conditions that heighten a person's susceptibility to COVID-19 infection. These altered defense mechanisms may include compromised "self-control" and "self-care", as well as a "lack of insight" into the danger posed by the virus. These consequences may have serious social impacts on the future of COVID-19 survivors. Compounding the functionally related issues of altered mental health parameters and viral susceptibility are the potential effects of compromised immunity on the establishment of functional herd immunity. Within this context, mental health takes on added importance, particularly in terms of the need to increase support for mental health research and community-based initiatives. Thus, COVID-19 infections continue to reveal mental health targets, a process we must now be prepared to deal with.

COVID-19/complications , Mental Health , SARS-CoV-2/pathogenicity , Survivors/psychology , Alzheimer Disease/epidemiology , Alzheimer Disease/prevention & control , Alzheimer Disease/virology , Anxiety/epidemiology , Anxiety/prevention & control , Anxiety/psychology , COVID-19/epidemiology , COVID-19/psychology , Depression/epidemiology , Depression/prevention & control , Depression/psychology , Disease Susceptibility/psychology , Humans , Pandemics , Parkinson Disease/epidemiology , Parkinson Disease/prevention & control , Parkinson Disease/virology , Physical Distancing , Self Care/psychology , Self-Control/psychology , Social Isolation/psychology