Corrigendum: Neuroinflammation and Cytokines in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A Critical Review of Research Methods

At the Root of 3 “Long” Diseases: Persistent Antigens Inflicting Chronic Damage on the Brain and Other Organs in Gulf War Illness, Long-COVID-19, and Chronic Fatigue Syndrome

“…Similarly to GWI and long-COVID, ME/CFS is associated with immune system disruption 103 including systemic inflammation 104,105 and neuroinflammation. [106][107][108] Numerous infectious agents including several human herpes viruses (eg, EBV, HHV6, CMV) have long been suspected in the pathogenesis of ME/CFS [109][110][111][112][113] ; indeed, CFS was historically known as "chronic Epstein-Barr virus syndrome." 114 Several lines of research suggest that viral reactivation or viral persistence underlies ME/CFS, 98,112 including evidence of HHV-6 antigen in peripheral blood mononuclear cells in patients with CFS, 115 evidence of active and latent HHV-6/HHV-7 infection in plasma samples of CFS patients, 116 and deficient EBV-specific B-and T-cell memory response indicative of impaired ability to control early steps involved in EBV reactivation in CFS patients.…”

“…121 Although several brain anomalies are associated with ME/ CFS, 122 brainstem abnormalities have been the most consistently documented. 108,[122][123][124] The brainstem, a central hub in inflammation neurocircuitry, 125 is implicated in sickness behaviors such as malaise, lassitude, fatigue, numbness, coldness, muscle and joint aches, and reduced appetite. 126 Like ME/ CFS, both long-COVID/PASC 22,127 and GWI 37,128 have been linked to brainstem anomalies.…”

Dry eye symptoms and signs in United States Gulf War era veterans with myalgic encephalomyelitis/chronic fatigue syndrome

“…One Belgian study conducted compared circulating blood cytokines in 16 patients with ME/CFS and 14 controls, and found that the ME/CFS group had significantly higher IL‐1β (655.7 ± 47.8 femtogram/millilitre [fg/mL] vs. 87.6 ± 21.8 fg/mL), IL‐8 (19056.5 ± 8254.0 fg/mL vs. 86.1 ± 18.1 fg/mL), IL‐10 (318.8 ± 1028.3 fg/mL vs. 86.04 ± 17.9 fg/mL), and TNFα (534.0 ± 1782.4 fg/mL vs. 89.2 ± 19.4 fg/mL) levels ( p < 0.05) 23 . Overall, findings of our and previous studies suggest that while inflammation may play a role in MF/CFS, the value of blood cytokine profiling has yet to be established 55 …”

“…On the other hand, in our paper, peripheral markers of inflammation and neuroinflammation were not different between groups. This is not entirely unexpected as previous research has suggested that cytokines propagate inflammation locally via autocrine and paracrine signalling not as endocrine signalers flowing through blood 55,56 . This property likely contributed to the heterogenous findings regarding peripheral cytokines and ME/CFS seen in previous studies conducted in various geographic locations 20,57 .…”