The largest genome-wide association study to date of myalgic encephalomyelitis/chronic fatigue syndrome has identified eight genetic loci that are significantly associated with the chronic debilitating condition. Onset of ME/CFS often is traced back to an infection and four of the loci involve genes that are expressed in response to viral or bacterial infections.
The largest genome-wide association study to date of myalgic encephalomyelitis/chronic fatigue syndrome has identified eight genetic loci that are significantly associated with the chronic debilitating condition.
In a recent study in the Journal of Translational Medicine, researchers from Azrieli Research Center (Canada) and collaborating institutions hypothesized that the dysregulation of SMPDL3B may be involved in myalgic encephalomyelitis (ME) progression, and investigated its role and clinical relevance in ME pathophysiology.
Two papers in the Feb. 8, 2023, issue of Cell Host & Microbe have reported new insights into the relationship between myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and alterations in the gut microbiome, and how those relationships change over time. A reliable way to diagnose ME/CFS would be a huge step forward for the study of ME/CFS. Currently, the condition is diagnosed purely by symptoms, which are assessed via questionnaire.
In a study comparing the antibody repertoire of individuals with severe myalgic encephalopathy/ chronic fatigue syndrome (ME/CFS) to that of healthy controls, the majority of individuals with CFS showed antibody responses to specific microbiome proteins. Such responses were largely absent in healthy controls, implicating immune reactions to the microbiome in the development of ME/CFS.
When SARS-CoV-2 first emerged in 2020, with respiratory symptoms as the most obvious feature of infection, the most obvious comparison was to influenza. COVID-19, of course, was never just another flu.