2025: looking back on a year of ME/CFS research
In 2025, scientists made a significant step towards understanding the pathophysiology of ME/CFS. It may not be a breakthrough, but we’re uncovering more pieces of the puzzle. It’s like fitting the corners and outer layer: we cannot yet see what the puzzle is, but we’re starting to get a glimpse of what it will show.
https://mecfsscience.org/2025-looking-back-on-a-year-of-me-cfs-research/
DecodeME
2025 was the year of the gene. We had genetic studies on natural killer cell receptors, herpesviruses, metabolism, cytokines, and the Olduvai domain. There was one study, however, that dwarfed all others: DecodeME.
DecodeME is the largest ME/CFS study ever conducted; more than 15,000 in the United Kingdom participated by sending their DNA through the mail. Their genetic code was compared to that of 250,000 control participants. The results show that ME/CFS has a modest heritability. Genes can increase the risk of developing the illness, but they play a lesser role than in, for example, schizophrenia, Crohn’s disease, or type 1 diabetes. Further analysis by PrecisionLife suggests that ME/CFS is also highly polygenic meaning that the risk of getting the disease is spread out across many different genes, each contributing only a tiny effect.
Rare mutations
Before DecodeME, there was already a fascinating genetics study that had generated excitement and discussion. Mark Snyder’s team at Stanford University applied a different approach but found similar results.
DecodeME looked at common DNA variants that slightly influence how much of a protein is made. The effects are small and gradual, like turning on a volume knob. Snyder’s group, however, zoomed in on rare DNA variants that have more dramatic effects, such as making a defective protein that no longer functions properly.
Virus hunt
DecodeME and Snyder’s study also had genetic signals pointing to the immune system. Unfortunately, most immunology studies in 2025 found null results.
Let’s start with the hunt for viruses and other pathogens. This year, the severely ill patient study from Ronald Davis’ team finally published its findings on virus sequencing. They looked at 185 human viruses in the blood but found traces of only 17. These weren’t more frequent in patients than in controls. In fact, the authors wrote that “surprisingly, more viruses were found in the healthy controls than in the ME/CFS patients.”
Antibodies
2025 also saw the most extensive study on antibodies in ME/CFS. Maureen Hanson’s group at Cornell used two advanced techniques to measure hundreds of antibodies simultaneously. The first was a 1134 autoantibody Luminex panel. This method uses microscopic beads that are dyed with specific colors so that they act as unique barcodes for different targets. The second method is called Rapid Extracellular Antigen Profiling (REAP) and was developed quite recently by Aaron Ring (who was an author on this paper). Instead of colored beads, REAP uses a library of living yeast cells where each cell displays a specific protein on its surface with a matching DNA barcode inside the cell. Using REAP, the authors could test antibodies against 6183 extracellular human proteins and 225 human viral pathogen proteins.
B-cell repertoires
A study by Audrey Ryback and Graeme Cowen replicated abnormalities in B-cells found by two earlier studies, namely an increase in Immunoglobulin Heavy Variable IGHV3-30.
B-cells are the immune cells that recognize pathogens and make targeted antibodies to neutralize them. These antibodies also sit on the surface of B-cells, where they act as receptors. Our immune system creates an almost endless diversity of these receptors so that it can respond to all sorts of pathogens. One way to do this is to select and rearrange the building blocks for antibodies in new B-cells, a bit like shuffling cards. IGHV3-30 is one of these building blocks. Researchers found that B-cells of ME/CFS patients used it more often in their receptors than controls.
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