Chronic Fatigue Initiative / Hutchins Family Foundation funds research that discovers Biological Evidence of “Atypical” Chronic Fatigue Syndrome
Scientists at the Center for Infection and Immunity (CII) at Columbia University’s Mailman School of Public Health are the first to report immune signatures differentiating two subgroups of ME/CFS: “classical” and “atypical.”
Typically, symptoms of ME/CFS begin suddenly following a flu-like infection, but a subset of cases classified by the investigators as “atypical” follows a different disease course, either from triggers preceding symptoms by months or years, or accompanied by the later development of additional serious illnesses.
First author, Mady Hornig, MD, used immunoassays to measure levels of 51 immune biomarkers in cerebrospinal fluid samples taken from 32 cases of classical and 27 cases of atypical ME/CFS. All study participants were diagnosed using the same standard.
The analysis revealed lower levels of immune molecules in individuals with atypical ME/CFS than those with a classical presentation - dramatically lower levels of interleukin 7 (IL7), a protein linked to viral infections, and interleukin 17A (IL 17A) and chemokine (C-X-C motif) ligand 9 (CXCL9), inflammatory molecules implicated in a variety of neurological disorders.
Hornig says: “Importantly, our results suggest that these early biomarker profiles may be detectable soon after diagnosis of ME/CFS, laying a foundation for better understanding of and treatments for this complex and poorly understood illness. Instead of the immune exhaustion seen in later phases of classical ME/CFS, atypical patients may be experiencing a “smoldering inflammatory process”.
The new study builds on earlier research by Hornig and collaborators that found robust evidence of distinct stages of ME/CFS, pre and post 3-years of diagnosis, by cytokine and chemokine levels. This new study showed that the dampened immune profiles previously observed after the three-year mark were only observed in individuals with the classical form of the disease, not in those with atypical ME/CFS.
“Multiple biological pathways are likely involved in the pathogenesis of ME/CFS, with a range of clinical subtypes relating to variability in the types of environmental triggers, genetic and epigenetic vulnerability, as well as comorbidity patterns,” says senior author Ian Lipkin, MD, director of CII. “Shedding light on these pathways may help us to identify the various agents that precipitate disease as well as to design more precise, targeted treatments.”
For the full article, please download the pdf Chronic Fatigue Syndrome with Atypical and Classical Presentation
