Analysis of post COVID-19 condition and its overlap with myalgic encephalomyelitis/chronic fatigue syndrome

Sukocheva, Olga; Maksoud, Rebekah; Beeraka, Narasimha M; Madhunapantula, SubbaRao V.; Sinelnikov, Mikhail Y.; Николенко, В.Н.; Neganova, Margarita E.; Клочков, С. Г.; Kamal, Mohammad Amjad; Marshall‐Gradisnik, Sonya; Staines, Donald

doi:10.1016/j.jare.2021.11.013

Cited by 117 publications

(90 citation statements)

References 241 publications

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“…With the long-term prognosis still not clear, it will add a highly significant new health burden. The new WHO clinical case definition for PCC is very similar to the more recently refined versions of the generic clinical case definition for ME/CFS indeed suggesting the fatigue syndromes are very closely related ( 18 ). One difference was that the condition had to persist for 3 months before confirmation of diagnosis, whereas for ME/CFS it is 6 months.…”

Section: Introductionmentioning

confidence: 72%

Molecular Mechanisms of Neuroinflammation in ME/CFS and Long COVID to Sustain Disease and Promote Relapses

et al. 2022

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Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a disease now well-documented as having arisen commonly from a viral infection, but also from other external stressors, like exposure to agricultural chemicals, other types of infection, surgery, or other severe stress events. Research has shown these events produce a systemic molecular inflammatory response and chronic immune activation and dysregulation. What has been more difficult to establish is the hierarchy of the physiological responses that give rise to the myriad of symptoms that ME/CFS patients experience, and why they do not resolve and are generally life-long. The severity of the symptoms frequently fluctuates through relapse recovery periods, with brain-centered symptoms of neuroinflammation, loss of homeostatic control, “brain fog” affecting cognitive ability, lack of refreshing sleep, and poor response to even small stresses. How these brain effects develop with ME/CFS from the initiating external effector, whether virus or other cause, is poorly understood and that is what our paper aims to address. We propose the hypothesis that following the initial stressor event, the subsequent systemic pathology moves to the brain via neurovascular pathways or through a dysfunctional blood-brain barrier (BBB), resulting in chronic neuroinflammation and leading to a sustained illness with chronic relapse recovery cycles. Signaling through recognized pathways from the brain back to body physiology is likely part of the process by which the illness cycle in the peripheral system is sustained and why healing does not occur. By contrast, Long COVID (Post-COVID-19 condition) is a very recent ME/CFS-like illness arising from the single pandemic virus, SARS-CoV-2. We believe the ME/CFS-like ongoing effects of Long COVID are arising by very similar mechanisms involving neuroinflammation, but likely with some unique signaling, resulting from the pathology of the initial SARS-CoV-2 infection. The fact that there are very similar symptoms in both ongoing diseases, despite the diversity in the nature of the initial stressors, supports the concept of a similar dysfunctional CNS component common to both.

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Section: Introductionmentioning

confidence: 72%

Molecular Mechanisms of Neuroinflammation in ME/CFS and Long COVID to Sustain Disease and Promote Relapses

et al. 2022

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“…Yet, there remains uncertainty about the sequence and direction of events, i.e., which are upstream or downstream, and which may be hubs for intersecting spokes. A similar uncertainty is common among researchers struggling to understand PASC, which in some patients is clinically indiscernible from ME/CFS ( Komaroff and Bateman, 2021 ; Komaroff and Lipkin, 2021 ; Sukocheva et al, 2021 ; Yong and Liu, 2021 ).…”

Section: Discussionmentioning

confidence: 93%

“…Due to a lack of established biomarkers, the diagnosis rests on clinical criteria and the exclusion of other entities [for reviews of ME/CFS, see ( Bested and Marshall, 2015 ; Cortes Rivera et al, 2019 ; Bateman et al, 2021 )]. An as yet undefined proportion of persons with post-acute sequelae of COVID (PASC) is predicted to also meet the criteria of ME/CFS, which may significantly add to the global disease burden ( Komaroff and Lipkin, 2021 ; Sukocheva et al, 2021 ; Wong and Weitzer, 2021 ; Morrow et al, 2022 ; von Campen et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

The Pathobiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Case for Neuroglial Failure

Renz‐Polster

Tremblay

Bienzle

et al. 2022

Front. Cell. Neurosci.

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Although myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) has a specific and distinctive profile of clinical features, the disease remains an enigma because causal explanation of the pathobiological matrix is lacking. Several potential disease mechanisms have been identified, including immune abnormalities, inflammatory activation, mitochondrial alterations, endothelial and muscular disturbances, cardiovascular anomalies, and dysfunction of the peripheral and central nervous systems. Yet, it remains unclear whether and how these pathways may be related and orchestrated. Here we explore the hypothesis that a common denominator of the pathobiological processes in ME/CFS may be central nervous system dysfunction due to impaired or pathologically reactive neuroglia (astrocytes, microglia and oligodendrocytes). We will test this hypothesis by reviewing, in reference to the current literature, the two most salient and widely accepted features of ME/CFS, and by investigating how these might be linked to dysfunctional neuroglia. From this review we conclude that the multifaceted pathobiology of ME/CFS may be attributable in a unifying manner to neuroglial dysfunction. Because the two key features – post exertional malaise and decreased cerebral blood flow – are also recognized in a subset of patients with post-acute sequelae COVID, we suggest that our findings may also be pertinent to this entity.

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“…Immunological and psychological causes were discussed, with a potential overlap. Under the assumption of T-cell abnormalities or autoantibodies leading to long COVID, the reported higher number of T-cells and autoantibodies during and shortly after COVID-19 could be potentially causative for ongoing symptoms 15 , 16 . On the other hand, women are more prone to depression and anxiety disorders because of their higher oestrogen levels 17 – 19 .…”

Section: Discussionmentioning

confidence: 99%

Symptom burden correlates to impairment of diffusion capacity and exercise intolerance in long COVID patients

Kersten

Wolf

Hoyo

et al. 2022

Sci Rep

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After acute infection with the SARS-CoV-2 virus, a considerable number of patients remains symptomatic with pathological changes in various organ systems. This study aimed to relate the physical and mental burden of symptoms of long COVID patients to the findings of a somatic evaluation. In patients with persistent long COVID symptoms three months after acute infection we assessed physical and mental health status using the SF-36 questionnaire. The cohort was dichotomised by the results (upper two quartiles vs. lower to quartiles) and compared with regard to transthoracic echocardiography, body plethysmography (including diffusion capacity), capillary blood gas analysis and 6-min walk test (6-MWT). From February 22 to September 13, 2021, 463 patients were prospectively examined, of which 367 completed the SF-36 questionnaire. A positive correlation between initial disease severity (need for hospitalization, intensive care medicine) and resulting symptom burden at follow-up could be demonstrated. Patients with impaired subjective physical and mental status were significantly more likely to be women. There was a significant correlation between symptom severity and reduced exercise tolerance in the 6-MWT (495.6 ± 83.7 m vs 549.7 ± 71.6 m, p < 0.001) and diffusion capacity for carbon monoxide (85.6 ± 14.3% of target vs 94.5 ± 14.4, p < 0.001). In long COVID patients, initial disease severity is correlated with symptom burden after at least 3 months of follow-up. Highly symptomatic long COVID patients show impaired diffusion capacity and 6-MWT despite average or mildly affected mechanical lung parameters. It must be further differentiated whether this corresponds to a transient functional impairment or whether it is a matter of defined organ damage.

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Analysis of post COVID-19 condition and its overlap with myalgic encephalomyelitis/chronic fatigue syndrome

Cited by 117 publications

References 241 publications

Molecular Mechanisms of Neuroinflammation in ME/CFS and Long COVID to Sustain Disease and Promote Relapses

Molecular Mechanisms of Neuroinflammation in ME/CFS and Long COVID to Sustain Disease and Promote Relapses

The Pathobiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Case for Neuroglial Failure

Symptom burden correlates to impairment of diffusion capacity and exercise intolerance in long COVID patients

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