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

Stefano, George B.; Ptáček, Radek; Ptáčková, Hana; Martin, Andrew; Kream, Richard M.

doi:10.12659/msm.930886

Cited by 99 publications

(104 citation statements)

References 11 publications

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“… 19 , 59 It is thought to be secondary to the SARS-CoV-2 causing hypoxia and mitochondrial dysfunction that leads to microstructural brain damage and resultant symptoms of brain fog. 58 …”

Section: Manifestations Of Long-covid-19mentioning

confidence: 99%

The Conundrum of ‘Long-COVID-19ʹ: A Narrative Review

Garg¹,

Maralakunte²,

Garg³

et al. 2021

IJGM

152

117

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COVID-19 is an ongoing pandemic with many challenges that are now extending to its intriguing long-term sequel. ‘Long-COVID-19ʹ is a term given to the lingering or protracted illness that patients of COVID-19 continue to experience even in their post-recovery phase. It is also being called ‘post-acute COVID-19ʹ, ‘ongoing symptomatic COVID-19ʹ, ‘chronic COVID-19ʹ, ‘post COVID-19 syndrome’, and ‘long-haul COVID-19ʹ. Fatigue, dyspnea, cough, headache, brain fog, anosmia, and dysgeusia are common symptoms seen in Long-COVID-19, but more varied and debilitating injuries involving pulmonary, cardiovascular, cutaneous, musculoskeletal and neuropsychiatric systems are also being reported. With the data on Long-COVID-19 still emerging, the present review aims to highlight its epidemiology, protean clinical manifestations, risk predictors, and management strategies. With the re-emergence of new waves of SARS-CoV-2 infection, Long-COVID-19 is expected to produce another public health crisis on the heels of current pandemic. Thus, it becomes imperative to emphasize this condition and disseminate its awareness to medical professionals, patients, the public, and policymakers alike to prepare and augment health care facilities for continued surveillance of these patients. Further research comprising cataloging of symptoms, longer-ranging observational studies, and clinical trials are necessary to evaluate long-term consequences of COVID-19, and it warrants setting-up of dedicated, post-COVID care, multi-disciplinary clinics, and rehabilitation centers.

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“… 19 , 59 It is thought to be secondary to the SARS-CoV-2 causing hypoxia and mitochondrial dysfunction that leads to microstructural brain damage and resultant symptoms of brain fog. 58 …”

Section: Manifestations Of Long-covid-19mentioning

confidence: 99%

The Conundrum of ‘Long-COVID-19ʹ: A Narrative Review

Garg¹,

Maralakunte²,

Garg³

et al. 2021

IJGM

152

117

View full text Add to dashboard Cite

show abstract

“…Furthermore, THOP1 appears to play a crucial role in the regulation of MHC I cell-surface expression [72][73][74]. Due to the shown high expression of THOP1 in several brain compartments and in the effector CD8 T-cells of COVID-19 patients [71], it raises the question about a possible relationship between different SARS-CoV-2 immune responses [75,76], neurological disorders observed in long covid patients, and THOP1 involvement in MHC-class I regulation in COVID-19 patients [77][78][79].…”

Section: Discussionmentioning

confidence: 99%

A modular molecular framework for quickly estimating the binding affinity of the spike protein of SARS-CoV-2 variants for ACE2, in presence of mutations at the spike receptor binding domain

Tragni

Laera

et al. 2021

Preprint

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The rapid spread of new SARS-CoV-2 variants needs the development of rapid tools for predicting the affinity of the mutated proteins responsible for the infection, i.e., the SARS-CoV-2 spike protein, for the human ACE2 receptor, aiming to understand if a variant can be more efficient in invading host cells. Here we show how our computational pipeline, previously used for studying SARS-CoV-2 spike receptor-binding domain (RBD)/ACE2 interactions and pre-/post-fusion conformational changes, can be used for predicting binding affinities of the human ACE2 receptor for the spike protein RBD of the characterized infectious variants of concern/interest B.1.1.7-UK (carrying the mutations N501Y, S494P, E484K at the RBD), P.1-Japan/Brazil (RBD mutations: K417N/T, E484K, N501Y), B.1.351-South Africa (RBD mutations: K417N, E484K, N501Y), B.1.427/B.1.429-California (RBD mutations: L452R), the B.1.141 variant (RBD mutations: N439K), and the recent B.1.617.1-India (RBD mutations: L452R; E484Q) and the B.1.620 (RBD mutations: S477N; E484K). Furthermore, we searched for ACE2 structurally related proteins that might be involved in interactions with the SARS-CoV-2 spike protein, in those tissues showing low ACE2 expression, revealing two new proteins, THOP1 and NLN, deserving to be investigated for their possible inclusion in the group of host-cell entry factors responsible for host-cell SARS-CoV-2 invasion and immunity response.

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“…In 2020, Goldstein proposed that chronic activation of the extended autonomic system (EAS), which includes the neuroendocrine and neuroimmune systems, is associated with an increased risk of developing ‘long COVID’ [ 8 ]. Long-term, viral-induced disease pathogenesis is associated with conditions that include myalgic encephalomyelitis, chronic fatigue syndrome, and postural orthostatic tachycardia syndrome (POTS) [ 3 , 9 – 11 ]. Acute cognitive impairment, similar to ‘brain fog,’ may also occur in Lyme disease and infection with influenza, West Nile virus, and Ebola virus [ 10 , 12 – 16 ].…”

Section: A Hypothesis For the Pathogenesis Of Long-term Neuropsychiatric Covid-19mentioning

confidence: 99%

“…Long-term COVID-19, or ‘long COVID,’ can include compromise to integrative neurological functions that regulate key cognitive and affective processes in the CNS, resulting in neuropsychiatric disease [ 1 ]. Based on recent empirical data, SARS-CoV-2 infection may functionally divert the bioenergetics capacity of infected cells to support viral replication [ 1 – 3 ]. It is possible that mitochondrial targeting by the virus may be the substrate for the emergence of cognitive impairment or ‘brain fog’ [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Editorial: The Pathogenesis of Long-Term Neuropsychiatric COVID-19 and the Role of Microglia, Mitochondria, and Persistent Neuroinflammation: A Hypothesis

et al. 2021

Self Cite

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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.

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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

Cited by 99 publications

References 11 publications

The Conundrum of ‘Long-COVID-19ʹ: A Narrative Review

The Conundrum of ‘Long-COVID-19ʹ: A Narrative Review

A modular molecular framework for quickly estimating the binding affinity of the spike protein of SARS-CoV-2 variants for ACE2, in presence of mutations at the spike receptor binding domain

Editorial: The Pathogenesis of Long-Term Neuropsychiatric COVID-19 and the Role of Microglia, Mitochondria, and Persistent Neuroinflammation: A Hypothesis

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