Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Post-COVID Syndrome: A Common Neuroimmune Ground?

Abstract

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating chronic disease of unknown etiology, sharing a similar clinical presentation with the increasingly recognized post-COVID syndrome. We performed the first cross-sectional study of ME/CFS in a community population in Russia. Then we described and compared some clinical and pathophysiological characteristics of ME/CFS and post-COVID syndrome as neuroimmune disorders. Of the cohort of 76 individuals who suggested themselves as suffering from ME/CFS, 56 were diagnosed with ME/CFS by clinicians according to ≥1 of the four most commonly used case definitions. Of the cohort of 14 individuals with post-COVID-19 syndrome, 14 met the diagnostic criteria for ME/CFS. The severity of anxiety/depressive symptoms did not correlate with the severity of fatigue either in ME/CFS or in post-COVID ME/CFS. Still, a positive correlation was found between the severity of fatigue and 20 other symptoms of ME/CFS related to the domains of “post-exertional exhaustion”, “immune dysfunction”, “sleep disturbances”, “dysfunction of the autonomic nervous system”, “neurological sensory/motor disorders” and “pain syndromes”. Immunological abnormalities were identified in 12/12 patients with ME/CFS according to the results of laboratory testing. The prevalence of postural orthostatic tachycardia assessed in the active orthostatic test amounted to 37.5% in ME/CFS and 75.0% in post-COVID ME/CFS (the latter was higher than in healthy controls, p = 0.02). There was a more pronounced increase in heart rate starting from the 6th minute of the test in post-COVID ME/CFS compared with the control group. Assessment of the functional characteristics of microcirculation by laser doppler flowmetry revealed obvious and very similar changes in ME/CFS and post-COVID ME/CFS compared to the healthy controls. The identified laser doppler flowmetry pattern corresponded to the hyperemic form of microcirculation disorders usually observed in acute inflammatory response or in case of systemic vasoconstriction failure.

Changing Face of Inflammatory Activation in Complex Coronary Artery Disease during the COVID-19 Pandemic

“…The median hospitalization time in the studied periods was 12 (9-15) days vs. 11 (9)(10)(11)(12)(13)(14) days (p = 0.798), respectively. The median number of performed anastomoses in each group was 2 (2-3) vs. 2 (2-3) (p = 0.950), respectively.…”

“…The SARS-CoV-2 pandemic had a significant impact on immune status in certain groups of patients, which may result in a specific immune cell response in the form of delayed-type hypersensitivity [11]. A possible increase in diseases with an inflammatory background has been reported in the COVID-19 era [12,13], suggesting an immunologically triggered etiology. Post-COVID-19 syndrome manifestations include immunological disturbances related to molecular and cellular immune abnormalities caused by the host's initial violent immune response, including cytokine release syndrome, hemophagocytic lymph histiocytosis, and macrophage activation syndrome [14].…”

Myalgic encephalomyelitis/chronic fatigue syndrome from current evidence to new diagnostic perspectives through skeletal muscle and metabolic disturbances

“…Infections have also been under magnifying lens, since infections are known to be a possible cause of long‐term impairments, including the occurrence of post‐resolution fatigue. A resemblance was found between post‐COVID syndrome and ME/CFS, leading to interpretation of ME/CFS as neuroimmune pathogenesis rather than primary mental disorders, with symptoms covering several domains, such as post‐exertional exhaustion, immune dysfunction, sleep disturbances, dysfunction of the autonomic nervous system, neurological sensory/motor disorders, and pain syndromes 170 . The high degree of similarity in the profiles of symptom scores across the so‐called post‐acute sequelae of SARS‐CoV‐2 infection (PASC) and ME/CFS can be interpreted as a result of multi‐systemic dyshomeostasis.…”

Is Pulmonary Involvement a Distinct Phenotype of Post-COVID-19?

“…PCC is defined as the continuation or development of new symptoms after 3 months from infection, lasting for a minimum period of another 2 months [9]. Its manifestations derive from multiple mechanisms that the virus has the potential of inflicting [10]; SARS-CoV-2 interacts with the host microbiome/virome, paving the way for the reactivation of pathogens such as herpesviruses or fungi under the conditions of immune dysregulation [11][12][13][14][15]; it damages the vessel endothelium and provokes clotting issues [16,17]; it alters the brainstem and vagus nerve signaling because of its neuroinvasive capabilities [18][19][20]; finally, it provokes autoimmunity due to immune cells' overactivity and molecular mimicry between pathogens and the host proteins [21,22].…”