Lyme disease is caused by the bacteria Borrelia burgdorferi, transmitted through the bite of an infected tick.
Although Lyme disease can be treated using antibiotics, research has suggested that 10% to 20% of cases do not resolve following the course of medication, leading to a collection of symptoms such as debilitating fatigue, muscle and joint pain, headaches, sleep difficulties, cognitive issues, and paraesthesia (‘pins and needles’), referred to as Post-treatment Lyme disease syndrome (PTLDS).
Some symptoms of PTLDS have been found to overlap with those of ME/CFS, including brain fog (a non-medical term used to describe cognitive issues such as difficulty concentrating or thinking clearly) and fatigue.
There is also some evidence to suggest that there may be overlap between the underlying disease mechanisms for ME/CFS and PTLDS – such as increased markers of inflammation, and metabolic differences (differences in chemical processes in the body), however more research is needed.
To investigate whether specific genes – which carry information needed to specify physical and biological traits in the body, may provide an insight into disease mechanisms for PTLDS, researchers in America have published a study which aimed to:
- Investigate whether specific genetic variations are associated with PTLDS using a genome wide association study (GWAS).
- Compare the findings from the GWAS for PTLDS with those for people with ME/CFS, and those for people with fibromyalgia – another illness with symptoms that overlap with PTLDS.
Results of the study showed that there were two genetic loci – the term used to describe the genetic makeup of an individual at a specific location, linked with PTLDS, but that these loci were not associated with either ME/CFS or fibromyalgia.
One of the loci found to be associated with PTLDS has been linked to a protein on immune cells which regulate the body’s immune response. Although this was not linked to ME/CFS in this study, the results do not rule out the potential role of the immune system in ME/CFS disease mechanisms, only that the the specific genetic loci linked to PTLDS was not common to ME/CFS in this specific group of participants.
This study used information from medical records to define cases of ME/CFS and of fibromyalgia. Medical codes used in clinical practice may not accurately capture “ME/CFS” – or at the very least, the terminology used is inconsistent. Where possible future research should use ME/CFS case definitions — such as the Canadian Consensus Criteria or the Institute of Medicine 2015 criteria, which include post exertional malaise as a required symptom for disease diagnosis.
More research is needed to understand the potential role of the immune response in PTLDS – and to identify the specific genetic variations associated with ME/CFS, and how these relate to disease mechanisms.
Gemma Samms, under the supervision of Professor Chris Ponting, is currently conducting PhD level research at the University of Edinburgh – funded by ME Research UK, which aims to use data from the DecodeME study to identify which specific genes are involved in ME/CFS, what types of cell are affected by those genes, and how those changes may lead to alterations in cellular function in people with ME/CFS.
