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New evidence of link between HHV infection and ME/CFS

Human beings are exposed to all manner of viruses, bacteria, fungi and parasites during their lives, some of the most common being human herpes viruses (HHVs).

For most people, these viruses cause no noticeable disease or else only temporary symptoms such as sore throat or fever. But, after entering the body, they slowly make their way along the nerves to the central nervous system, where they can replicate and remain for many years. The viruses are to all intents and purposes relatively silent, or at least that is what conventional medical wisdom once believed.

Viral reactivation

One hypothesis is that reactivation of HHVs in some cells may partly explain the development of disease, and this is the idea being explored by Dr Bhupesh Prusty and colleagues at Julius Maximilians University in Würzburg, Germany and other centres.

Dr Prusty is also currently undertaking a related project, funded by ME Research UK, looking at the role of infectious triggers on mitochondrial dysfunction in ME/CFS.

One of the team’s key ideas is that HHV reactivation leads to the expression of HHV-6 microRNAs (molecules that help cells create proteins), which in turn cause a reduction in the function of the mitochondria (responsible for generating energy in cells) as well as immune responses.

The researchers’ previous findings suggest that any viral activity must be localised to a specific tissue, since there is a lack of activity in commonly tested samples such as blood and serum.

HHV microRNA

For this reason, in this study (published in Frontiers in Molecular Biosciences) they looked specifically at post-mortem brain and nervous tissue obtained from three ME/CFS patients and 24 control subjects.

Their results showed abundant HHV microRNA in various regions of the brain and associated neuronal tissues, including the spinal cord, but only in samples from ME/CFS patients and not from controls.

What does it mean?

So here is some objective evidence of HHV-6 activity in the brain and spinal cord of ME/CFS patients, which could disrupt normal nerve function, induce a immune response such as inflammation, and possibly account for symptoms such as brain fog, cognitive complaints, tiredness and pain.

Unfortunately, the study involved only three patients, and it is ethically and practically difficult to acquire post-mortem tissue biopsies. The results will need to be replicated in a larger number of samples, or else new methods developed to investigate viral activity in these regions.

Nevertheless, these findings renew discussion and interest in the role of HHVs in ME/CFS.

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