Chronic fatigue syndrome from vagus nerve infection: a psychoneuroimmunological hypothesis.

Abstract The full article is behind a paywall. Chronic fatigue syndrome (CFS) is an often-debilitating condition of unknown origin. There is a general consensus among CFS researchers that the symptoms seem to reflect an ongoing immune response, perhaps due to viral infection. Thus, most CFS research has focused upon trying to uncover that putative immune…

Screening NK-, B- and T-cell phenotype and function in patients suffering from Chronic Fatigue Syndrome

CFS individuals analyzed in this study show no differences in B-cell compartment, skewed NK cells and poorly responsive T cells.
The observed immunological defaults do not provide any causative link to the illness, but could explain some of the symptoms and in particular the poor control of viral infections reported in these individuals. Some of these biomarkers may be useful for the characterization of CFS. (But you have to distinguiesh between ME, CFS ,or both).

Disease Mechanisms and Clonidine Treatment in Adolescent Chronic Fatigue Syndrome.

At baseline, patients with CFS had a lower number of steps per day, digit span backward score, and urinary cortisol to creatinine ratio. They had a higher fatigue score, heart rate responsiveness, plasma norepinephrine level , and serum C-reactive protein concentration compared with healthy controls. There were no significant differences regarding blood microbiology evaluation.

Adolescent CFS is associated with enhanced sympathetic nervous activity, low-grade systemic inflammation, attenuated hypothalamus-pituitary-adrenal axis function, cognitive impairment, and large activity reduction, but not with common microorganisms. Low-dose clonidine attenuates sympathetic outflow and systemic inflammation in CFS but has a concomitant negative effect on physical activity; thus, sympathetic and inflammatory enhancement may be compensatory mechanisms. Low-dose clonidine is not clinically useful in CFS.

Role of adaptive and innate immune cells in chronic fatigue syndrome/myalgic encephalomyelitis.

Significant changes were observed in B-cell subsets, Tregs, CD4+CD73+CD39+ T cells, cytotoxic activity, granzyme B, neutrophil antigens, TNF-α and IFN-γ in the CFS/ME patients in comparison with the non-fatigued controls. Alterations in B cells, Tregs, NK cells and neutrophils suggest significant impairments in immune regulation in CFS/ME and these may have similarities to a number of autoimmune disorders.