IACFS/ME 2022 Virtual Medical and Scientific Conference July 27 – 30, 2022
Day 3 (29 July 2022) of the IACFS/ME Annual Conference provided a continuous stream of fascinating and illuminating talks and presentations. The final two days of the conference had a particular focus on the immunology and management of Long-Covid with relevance to ME/CFS.
Dr. Daiki Takewaki at the National Institute of Science Japan talked about clearly identifiable gut dysbiosis (imbalance of gut microbiota involving the loss of beneficial microbial input or signal and an expansion of pathogenic microbes – pathobionts) that correlate with symptoms and immune markers in ME/CFS patients. A number of speakers provided patient case work from clinical practice, including Melissa Siller and Susan Levine MD, Lucina Bateman MD talked on follow-up of identical twins and the risk of family members also developing ME/CFS, and Leigh Jerome PhD on the care and management of Long-Covid patients.
One of the stand-out talks was given by Akiko Iwasaki PhD, a Professor of Immunobiology and Molecular, Cellular and Developmental Biology at Yale Medical School. Dr. Iwasaki provided an especially insightful talk on the biochemical signatures of Long-Covid syndrome. Dr. Iwasaki stated that it was fairly easy to differentiate Long-Covid sufferers simply by examining their symptom profiles on simple symptom surveys, and that Long-Covid was a female dominant illness, just like ME/CFS; symptoms were largely the same as in ME/CFS, with some exceptions, such as breathlessness being more prevalent in Long-Covid but post-exertional malaise (PEM), brain-fog, sleep disturbances, and fatigue all being dominant features of Long-Covid.
Using structural equation modelling and principal components analysis (PCA) Dr. Iwasaki was able to identify three clusters of patients, one being Long-Covid patients, and despite considerable heterogeneity between patients in terms of symptoms and immune profiles, she was able to visualise the Long-Covid patients among the healthy controls based on their immunological assays, serology and other tests. Long-Covid patients exhibited raised CD4 and CD8 cells – these are a type of immune cell, T-cell or Lymphocyte, that are often raised following infection. What was remarkable was that these cells remained elevated over a relatively long period following initial infection, even after 1 year in some Long-Covid patients. Long-Covid patients also tended to exhibit lower cortisol levels than healthy control patients. The reasons for this were unclear, but we do know from prior ME/CFS studies that low cortisol is identifiable in some ME/CFS patients.
Dr. Iwasaki plans to apply for funding to replicate her work on Long-Covid in ME/CFS, using larger numbers of patients.
Day 4 (30 July 2022), the final day, saw an insightful talk by Lauren Stiles in which she reviewed Postural Orthostatic Tachycardia Syndrome (POTs) and autonomic dysfunction research in ME/CFS. POTs and autonomic dysfunction were perhaps one of the central themes of this year’s conference, given many speakers across the four days either were examining this complaint directly in their research or referred to POTs and the autonomic system and neurological inflammation as cardinal features of both ME/CFS and Long-Covid syndrome.
Dr. Gunnar Gottschalk PhD of the Simmaron Research Centre, USA (whose institute works to advance translational science in treating neuroimmune diseases) talked about autophagy-related protein ATG13. This protein is involved in causing damaged or infected cells to die off, and is strongly upregulated in the serum of ME/CFS patients, indicating impairment in this process.
Dr. Gottschalk has also identified a microglia-based oxidative stress response in ME/CFS patients, with the production of reactive oxygen species (ROS) and nitric oxide in human HMC3 microglial cells. This production is diminished after neutralization of ATG13, suggesting that ATG13 plays a role in the observed stress response in microglial cells. This work ties in with the focus on POTs and dysautonomia, and may partly explain some of the disruption of brain pathophysiology-chemistry in ME/CFS.
PhD candidate, Brandon Cox of Ohio State talked about the role of Epstein-Barr Virus and Human Herpes Virus-6A in ME/CFS, Luke Liu MD of Neuroversion Inc. talked about the possible role of stellate ganglion block (SGB), and presented the results of treating Long-Covid patients using this method. Again, control of dysautonomia was mentioned. Other speakers at the conference talked about using vagal nerve stimulation devices to moderate the same sorts of processes.
Dr. Nicola Clague-Baker of the University of Liverpool talked about the role physiotherapists and allied health professionals could play in helping ME/CFS patients manage their condition, again with a focus on POTs, movement, dysautonomia and more. Dr. Nancy Klimas MD at Nova Southeastern talked about how to involve patients in research, and Cathy Kline and Gloria Grey ran a workshop on how to engage caregivers and health professionals. Dr. Lily Chu, conference organiser, closed the conference with a round-up of the key themes across the many presentations.
The conference is clearly growing in numbers and is now attracting a wider array of research scientists who are now participating in ME/CFS research or looking to translate their current research, often on Long-Covid, into ME/CFS studies. Like many of the talks given at the conference, raised immune markers and inflammation that impacts the neurobiology of the central nervous system, appeared to be central themes of this year’s conference. Infection is the most likely culprit in this story, but given many ME sufferers are unwell for many years, sometimes decades, the key question remains whether ongoing infection, be that active viral or bacterial infection, such as EBV or intracellular bacterial stealth infections are at work, or whether some viral remnants remain, pieces of RNA that are not active virus, but continue to stimulate an immune response; or are we witnessing a sort of auto-immune disease response in ME/CFS and Long-Covid patients, perhaps triggered by an initial virus some-time in the past?