Following on from Wednesday’s post about research investigating whether antibodies to herpesvirus are associated with the symptoms of ME/CFS, today we look at another study exploring the role of viruses in the disease.
Writing in the Journal of Medical Virology, Dr Thomas Briese and colleagues aimed to determine if differences in the human virome (viruses present in the body) might be linked to the development of ME/CFS. They looked at different types of samples from people with ME/CFS and healthy controls to identify if specific viruses are connected to this debilitating condition.
Methods
Various sterile and non-sterile samples were analysed using a number of different virus detection techniques. Two groups were studied: the first group included blood samples from 285 individuals with ME/CFS and 201 healthy controls, whilst the second group included PBMCs (white blood cells), stool and saliva samples from 106 individuals with ME/CFS and 91 healthy controls.
Findings
Overall, there were no significant differences in the types of viruses present in individuals with ME/CFS and in healthy controls. The study did note a lower prevalence of anelloviruses in individuals with ME/CFS. This type of virus is thought to be influenced by the immune status of a person, hence the lower prevalence in ME/CFS cases may correlate with a heightened immune response. However, the researchers mention that further research is needed to understand the reasons behind this difference, including whether it might be related to the sample type, geographic representation, or other factors.
What does this mean?
This research suggests that there are not major differences in the viruses found in people with ME/CFS and in healthy individuals. However, more research is needed to fully understand the role of viruses in ME/CFS. It is important to note that the study was conducted before the COVID-19 pandemic, so it might not directly relate to long COVID or post-acute effects of COVID-19.
A limitation of this study is that whilst the researchers refer to ME/CFS throughout the paper, the first group utilises the Fukuda criteria which is intended for classifying chronic fatigue syndrome (CFS). As the Fukuda criteria does not require the presence of post-exertional malaise (PEM), which is now considered to be a cardinal feature of ME/CFS, it is important to consider whether the use of this criteria had an impact on the findings. Individuals in the second cohort met the Canadian Consensus Criteria (CCC) in which the presence of PEM is mandatory.
The researchers emphasise that the ‘inability to detect direct evidence of an association between viral infection and ME/CFS does not exclude a role for viral infection in its pathogenesis’, rather it does suggest that exploring the connection between viruses and ME/CFS requires more advanced testing to detect past infections, even when the virus itself is not detectable anymore.
Dr Amy Proal and her team are currently conducting a project, funded by ME Research UK, focused on using new computer-based technologies to detect viruses in tissue and nerve samples from individuals with ME/CFS. Their primary aim is to establish whether viral activity contributes to the development of ME/CFS, and to identify the specific viral species that might be most relevant.