Research review: The enterovirus theory of disease etiology in ME/CFS

The enterovirus theory of disease etiology in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome: a critical review, by Adam J O’Neal and Maureen R Hanson in Front. Med., 18 June 2021 []


Research review abstract:

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex, multi-system disease whose etiological basis has not been established.

Enteroviruses (EVs) as a cause of ME/CFS have sometimes been proposed, as they are known agents of acute respiratory and gastrointestinal infections that may persist in secondary infection sites, including the central nervous system, muscle, and heart.

To date, the body of research that has investigated enterovirus infections in relation to ME/CFS supports an increased prevalence of chronic or persistent enteroviral infections in ME/CFS patient cohorts than in healthy individuals. Nevertheless, inconsistent results have fuelled a decline in related studies over the past two decades.

This review covers the aspects of ME/CFS pathophysiology that are consistent with a chronic enterovirus infection and critically reviews methodologies and approaches used in past EV-related ME/CFS studies. We describe the prior sample types that were interrogated, the methods used and the limitations to the approaches that were chosen.

We conclude that there is considerable evidence that prior outbreaks of ME/CFS were caused by one or more enterovirus groups. Furthermore, we find that the methods used in prior studies were inadequate to rule out the presence of chronic enteroviral infections in individuals with ME/CFS.

Given the possibility that such infections could be contributing to morbidity and preventing recovery, further studies of appropriate biological samples with the latest molecular methods are urgently needed.

Excerpts from Discussion:

Many ME/CFS patients in a variety of studies indicate a viral-like illness immediately preceded their ME/CFS symptoms. However, surveys also indicate that patients ascribe their onset to a variety of other reasons, including emotional stress, life events, recent travel, accidents, toxic substances, or mold. However, some of these events and exposures could merely be coincidental and actually be due to an enteroviral infection that was unnoticed or very mild, given that many enteroviral infections are asymptomatic.

The COVID19 pandemic has made it obvious that persistent symptoms can arise from mild or asymptomatic infections. Were the existence of SARS CoV-2 not known, many of the individuals with long-lasting symptoms of COVID 19 might readily have ascribed their mysterious illness to some other factor than viral infection.

It is evident that more research must be conducted in order to determine whether or not the majority of pre-2020 ME/CFS cases have arisen from EV infection. At the time of this writing, there have been a number of anecdotal reports of individuals experiencing remission of long-term COVID19 symptoms after receiving anti-SARS COV2 vaccines. Such a therapy will not be possible for any ME/CFS patients whose illness is due to chronic infection unless the persistent virus is identified.

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NICE delays Roundtable – no invite for WAMES!

NICE ME/CFS guideline publication delay drags on…


Another delay in the revision process to the ME/CFS guideline was announced on 10th September:

Updated: 10th September, to change the month of the meeting from September to October.

A NICE spokesperson said: “In order for the meeting to be as effective as possible it is important to fully understand the issue and concerns that all groups attending the meeting wish to raise. We also recognise the difficulty that holding the meeting at short notice created for some attendees who would have been unable to make the original date.”

As of the 16th September there has still been no public announcement of the date and list of attendees. Some stakeholder groups have admitted to being invited, but although WAMES received an acknowledgement to our email, we did not receive an invitation. Because we still have not been told the purpose and agenda for the meeting we cannot tell what the impact will be of excluding the Welsh patient community from the table.

What do we think we know?

@NICE.comms on twitter are reported to have said that the date of 17th October has been set for the Roundtable, with Prof Dame Carol Black as the chair. Forward-ME and Science4ME are two of the groups who have been invited.

Journalist Tom Chivers at The Post says he was told by ‘two people with some knowledge of the internal workings of both NICE and the Royal Colleges’ that the issue is that:

‘NICE created a new definition of the disease when producing the new guidelines…  the new definition inevitably rendered all the evidence on GET low-quality.’

‘My understanding now is that the Royal Colleges were nervous that they were essentially being forbidden from offering GET, even though clinicians found that it was helpful for many patients.’

The sticking point would appear to be that patients without exercise intolerance and Post-Exertional Malaise (or Post-Exertional Symptom Exacerbation) are now excluded from the diagnosis of ME/CFS. Doctors, researchers and patient advocates in the global ME community will be well equipped to argue the necessity of keeping the two patient groups separate. Few would be upset to relinquish the term Chronic Fatigue Syndrome (CFS/ME) and hand it over to those patients it would describe better!

And what about the guideline?

Barrister with ME, Valerie Elliot Smith has leaked the ME/CFS guideline on her blog.  She believes:

‘There is a strong argument that this process is now not just “flawed” but has become “fatally flawed” ie. irretrievable. This has been brought about as a direct result of NICE’s extraordinary actions and its failure to provide adequate justification, explanation or information regarding its next steps.

It cannot now be argued that NICE is acting in good faith or with any degree of independence.’

She is concerned that the lengthy delay to revising and publishing the guideline has meant many more patients have been subjected to harm by allowing the current (2007) guideline to stand and that people need to know that there is evidence to explain why this is so.

Many in the ME community however would prefer that the guideline is published quickly, accepted, and more research urgently embarked upon to find diagnostic tests to distinguish patients with PEM and those without, so that it is clear which treatments suit which patients. We wait a bit longer to see if those invited to the Roundtable can persuade NICE or if we are plunged into a decade of legal wrangles!

In the meantime if you choose not to download the embargoed guideline, journalist Steve Topple has analysed the leaked final guideline and has listed the key differences to the draft.

What does the ME community say about the Roundtable Announcements?

See our collection of links

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Genetic research: Fine mapping of the major histocompatibility complex (MHC) in ME/CFS

Fine mapping of the major histocompatibility complex (MHC) in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) suggests involvement of both HLA class I and class II loci, by Riad Hajdarevic, Asgeir Lande, Ingrid Rekeland, Anne Rydland, Elin B Strand, Daisy D Sosa, Lisa E Creary, Olav Mella, Torstein Egeland, Ola D Saugstad, Øystein Fluge, Benedicte A Lie, Marte K Viken in Brain Behav Immun. 2021 Aug 14;S0889-1591(21)00509-2 [doi: 10.1016/j.bbi.2021.08.219]



  • By far the largest genetic study in ME/CFS.
  • Multi-level HLA and SNP analysis.
  • Independent HLA class I and II associations.
  • Positive association of HLA-DQB1 amino acid residue 57D.


The etiology of Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS) is unknown, but involvement of the immune system is one of the proposed underlying mechanisms. Human leukocyte antigen (HLA) associations are hallmarks of immune-mediated and autoimmune diseases.

We have previously performed high resolution HLA genotyping and detected associations between ME/CFS and certain HLA class I and class II alleles. However, the HLA complex harbors numerous genes of immunological importance, and there is extensive and complex linkage disequilibrium across the region.

In the current study, we aimed to fine map the association signals in the HLA complex by genotyping five additional classical HLA loci and 5,342 SNPs in 427 Norwegian ME/CFS patients, diagnosed according to the Canadian Consensus Criteria, and 480 healthy Norwegian controls.

Crystallographic structure of HLA-DQA1 (cyan) complexed with HLA-DQB1 (green) & HCRT (magenta) based on PDB: 1uvq​.

SNP association analysis revealed two distinct and independent association signals (p≤0.001) tagged by rs4711249 in the HLA class I region and rs9275582 in the HLA class II region. Furthermore, the primary association signal in the HLA class II region was located within the HLA-DQ gene region, most likely due to HLA-DQB1, particularly the amino acid position 57 (aspartic acid/alanine) in the peptide binding groove, or an intergenic SNP upstream of HLA-DQB1.

In the HLA class I region, the putative causal locus might map outside the classical HLA genes as the association signal spans several genes (DDR1, GTF2H4, VARS2, SFTA2 and DPCR1) with expression levels influenced by the ME/CFS associated SNP genotype.

Taken together, our results implicate the involvement of the MHC, and in particular the HLA-DQB1 gene, in ME/CFS. These findings should be replicated in larger cohorts, particularly to verify the putative involvement of HLA-DQB1, a gene important for antigen-presentation to T cells and known to harbor alleles providing the largest risk for well-established autoimmune diseases.


Riad Hajdarevic says:

Hello I am the first author of the studies. I want to bring some clarity to the paper to you guys.

Our study was trying to see the involvement of HLA genes in ME/CFS. We observed some genetic changes (SNPs) to be associated with ME/CFS across the immunologically important HLA genes.

The patients we analyzed were diagnosed according to the CCC. As you know the CCC are more stringent than the Fukuda or similar criteria. Our patient population was 427 Norwegian ME/CFS patients. This is the largest ME/CFS cohort diagnosed according to the CCC however we need much more (up to 10 x) to definitely make a correlation between our findings and ME/CFS.

So far, no clinical implications can be made from this. However, it is indicative that those genetic changes (SNPs) influenced gene expression of some relevant genes for the observed ME/CFS clinical picture. Likewise, it seems (from this statistically limited data set) that some of those changes correlate with response to cyclophosphamide treatment in patients with ME/CFS. You have heard, I assume, about our collaborator’s study from Bergen where they reported improved symptoms for some ME/CFS patients taking the drug.

I just have to emphasize that we need much more research with much, much more patients diagnosed with the CCC to make any deeper assumptions.
If you have any extra questions please let me know I am glad to explain the findings in detail to anyone who wants to know the details.

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Research: A map of metabolic phenotypes in patients with ME/CFS

A map of metabolic phenotypes in patients with myalgic encephalomyelitis/ chronic fatigue syndrome by Fredrik Hoel, August Hoel, Ina Kn Pettersen, Ingrid G Rekeland, Kristin Risa, Kine Alme, Kari Sørland, Alexander Fosså, Katarina Lien, Ingrid Herder, Hanne L Thürmer, Merete E Gotaas, Christoph Schäfer, Rolf K Berge, Kristian Sommerfelt, Hans-Peter Marti, Olav Dahl, Olav Mella, Øystein Fluge, Karl J Tronstad in JCI Insight 2021;6(16):e149217 []


Research abstract:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disease usually presenting after infection. Emerging evidence supports that energy metabolism is affected in ME/CFS, but a unifying metabolic phenotype has not been firmly established.

Energy metabolism is the general process by which living cells acquire and use the energy needed to stay alive, to grow, and to reproduce.  Da Poian et al

We performed global metabolomics, lipidomics, and hormone measurements, and we used exploratory data analyses to compare serum from 83 patients with ME/CFS and 35 healthy controls.

Some changes were common in the patient group, and these were compatible with effects of elevated energy strain and altered utilization of fatty acids and amino acids as catabolic fuels. In addition, a set of heterogeneous effects reflected specific changes in 3 subsets of patients, and 2 of these expressed characteristic contexts of deregulated energy metabolism. The biological relevance of these metabolic phenotypes (metabotypes) was supported by clinical data and independent blood analyses.

Metabolic phenotypes are the products of interactions among a variety of factors-dietary, other lifestyle/environmental, gut microbial and genetic.             Holmes et al

In summary, we report a map of common and context-dependent metabolic changes in ME/CFS, and some of them presented possible associations with clinical patient profiles. We suggest that elevated energy strain may result from exertion-triggered tissue hypoxia and lead to systemic metabolic adaptation and compensation. Through various mechanisms, such metabolic dysfunction represents a likely mediator of key symptoms in ME/CFS and possibly a target for supportive intervention.


Science Norway: ME/CFS may be linked to failure in energy supply to the cells

ME Association blog: Research SummaryA map of metabolic phenotypes in patients with myalgic encephalomyelitis/chronic fatigue syndrome 

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UK Gov CFS research funding – Q&A in parliament

UK Parliament Written Question & Answers: CFS

1. Question from Alex Norrie MP, Labour, Nottingham North

To ask the Secretary of State for Health and Social Care, how much Government funding has been provided to ME research in each of the last three years. [UIN 38397, tabled on 22 July 2021]

Answer from Edward Argar MP, Minister of State (Department of Health and Social Care)

The following table shows the funding for research into myalgic encephalomyelitis through the National Institute for Health Research and UK Research and Innovation in the last three years.

Financial Year   Pounds
2018-19                   862,212
2019-20                   691,516
2020-21                   907,848

[Source: UK House of Commons, September 6, 2021]

2. Question from Janet Daby MP, Labour, Lewisham East

To ask the Secretary of State for Health and Social Care, whether he has made a recent assessment of the potential merits of increasing funding for research into ME and Chronic Fatigue Syndrome.  [UIN 41247, tabled on 18 August 2021]

Answer from Edward Argar MP, Minister of State (Department of Health and Social Care)

The Government invests in health research through the National Institute for Health Research (NIHR) and the Medical Research Council (MRC), through UK Research and Innovation. The NIHR and MRC both welcome high-quality applications for research into all aspects of myalgic encephalomyelitis (ME), otherwise known as chronic fatigue syndrome (CFS).

No assessment has been made of the merits of increasing funding for research into ME/CFS. While it is not usual practice for the NIHR and MRC to ring-fence funds for particular topics or conditions, the MRC has had a cross-board highlight notice on CFS/ME open since 2003.

[Source: UK House of Commons, September 6, 2021]

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NICE – ME community response to ‘Roundtable’ announcement

The ME community responds to NICE ‘Roundtable’ announcement


NICE made an announcement about ‘next steps’ following the ‘pause’ in publication– a roundtable discussion between stakeholders in September.

WAMES responded by writing to NICE expressing our commitment to the publication of the ME/CFS guideline, our willingness to join the Roundtable & the urgent need for transparency surrounding the process.


ME community responses:

Trial By Error: An updated letter to the NICE Chief Executive about the unpublished ME/CFS Guideline: Virology blog  15 Sep 2021

Signed by more than 150 experts and more than 100 UK and international charities, support groups and other relevant organizations, including WAMES.

The leak of NICE’s finalised ME guidelines exposes the ‘psych lobby’ scandal: The Canary  14 Sep 2021

Abuse of process & abuse of power: a NICE publication (with file download): Valerie Eliot Smith  13 Sep 2021

Ron Davis issues a statement on the NICE guidelines: Open Medicine Foundation, 7 Sep 2021

Medical advice must follow the evidence and not personal beliefs or political positions. If doctors treating ME/CFS patients do not agree with evidence based guidelines, they should not be treating these patients. This is why we have guidelines.

NICE Guidelines development debacle – and so it continues. Comment: A continuing saga of ineptitude: Invest in ME, 4 Sep 2021

Statements about ME/CFS from New Zealand Academics: Prof Warren Tate & Dr Lynette Hodges  2 Sep 2021


Legal opinion and legal advice: the “paused” NICE guideline for “ME/CFS”: Valerie Elliot-Smith  1 Sep 2021

Trial By Error: A Letter Urging NICE to Publish ME/CFS Guideline Without Delay: Virology blog   1 Sep 2021

Prof Tuller sent a letter to the CE of NICE signed by an international collection of 107 clinicians & researchers urging NICE to publish the guideline. He also told her about the new US guideline.  5 medics from Wales also signed, some from the long COVID community.

Forward-ME Statement concerning NICE Sept 2021 meeting: MERUK  30 Aug

Letter sent…to NICE about the ‘pause’ and roundtable meeting: S4ME  30 Aug

Public letter to DHSC, MRHA, HoC, NICE: call for a medial regulatory agency: Doctors with ME  29 Aug 2021

Physios for ME response to delayed NICE Guidelines: Physios for ME  29 Aug 2021

As stakeholders we had already taken part in the lengthy and in-depth consultation process and we find it difficult to understand what more can be discussed given the finalised guidelines were based on a robust analysis of the current evidence base.

NICE announces roundtable event to ensure implementation of ME/CFS guideline: #MEAction, 27 Aug

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Research: The SARS-CoV-2 receptor ACE2 in ME/CFS

The SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2) in  Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: a meta-analysis of public DNA methylation and gene expression data, by João Malato, Franziska Sotzny, Sandra Bauer, Helma Freitag, André Fonseca, Anna D Grabowska, Luís Graça, Clara Cordeiro, Luís Nacul, Eliana M Lacerda, Jesus Castro-Marrero, Carmen Scheibenbogen, Francisco Westermeier, Nuno Sepúlveda in Heliyon 2021 Jul 29;7(8):e07665 [doi: 10.1016/j.heliyon.2021.e07665]


Research abstract: 


People with myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS) often report a high frequency of viral infections and flu-like symptoms during their disease course. Since this reporting is in line with different immunological abnormalities and altered gene expression profiles observed in the disease, we aimed to explore whether the expression of the human angiotensin-converting enzyme-2 (ACE2), the major cell entry receptor for SARS-CoV-2, is also altered in this neglected clinical population. In particular, a low expression of ACE2 is usually indicative of a high risk of developing COVID-19.

We then performed a meta-analysis of public data on CpG DNA methylation and gene expression of this enzyme and its homologous ACE protein in peripheral blood mononuclear cells and related subsets. We found that patients with ME/CFS have decreased methylation levels of four CpG probes in the ACE locus (cg09920557, cg19802564, cg21094739, and cg10468385) and of another probe in the promoter region of the ACE2 gene (cg08559914). We also found a decreased expression of ACE2 but not of ACE in patients with ME/CFS when compared to healthy controls.

Accordingly, in newly collected data, we found evidence for a higher proportion of samples with an ACE2 expression below the limit of detection in patients with ME/CFS than in healthy controls.

Altogether, patients with ME/CFS could be at a higher COVID-19 risk when infected by SARS-CoV-2. To further support this conclusion, similar research should be conducted for other human cell entry receptors and other cell types, namely, those mainly targeted by the virus.


ME Association: Research Summary – Are people with ME/CFS at higher risk of complications from COVID infection?

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Treatment Research: Cortene’s InTime trial of CT38 results in sustained symptom improvement in ME/CFS

Acute Corticotropin-Releasing Factor Receptor Type 2 Agonism Results in Sustained Symptom Improvement in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, by Gerard Pereira, Hunter Gillies, Sanjay Chanda, Michael Corbett, Suzanne D. Vernon, Tina Milani and Lucinda Bateman in Front. Syst. Neurosci., 01 Sep 2021 []


Research abstract:


Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex multi-symptom disease with widespread evidence of disrupted systems. The authors hypothesize that it is caused by the upregulation of the corticotropin-releasing factor receptor type 2 (CRFR2) in the raphé nuclei and limbic system, which impairs the ability to maintain homeostasis. The authors propose utilizing agonist-mediated receptor endocytosis to downregulate CRFR2.

Materials and Methods:

This open-label trial tested the safety, tolerability and efficacy of an acute dose of CT38s (a short-lived, CRFR2-selective agonist, with no known off-target activity) in 14 ME/CFS patients. CT38s was subcutaneously-infused at one of four dose-levels (i.e., infusion rates of 0.01, 0.03, 0.06, and 0.20 μg/kg/h), for a maximum of 10.5 h. Effect was measured as the pre-/post-treatment change in the mean 28-day total daily symptom score (TDSS), which aggregated 13 individual patient-reported symptoms.


ME/CFS patients were significantly more sensitive to the transient hemodynamic effects of CRFR2 stimulation than healthy subjects in a prior trial, supporting the hypothesized CRFR2 upregulation. Adverse events were generally mild, resolved without intervention, and difficult to distinguish from ME/CFS symptoms, supporting a CRFR2 role in the disease. The acute dose of CT38s was associated with an improvement in mean TDSS that was sustained (over at least 28 days post-treatment) and correlated with both total exposure and pre-treatment symptom severity. At an infusion rate of 0.03 μg/kg/h, mean TDSS improved by −7.5 ± 1.9 (or −25.7%, p = 0.009), with all monitored symptoms improving.


The trial supports the hypothesis that CRFR2 is upregulated in ME/CFS, and that acute CRFR2 agonism may be a viable treatment approach warranting further study.


Biospace: Clinical trial provides preliminary evidence of a cure for myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) and Long Covid

Cortene believes the CRFR2 pathway is upregulated and therefore overactive, leading to the wide variety of symptoms in ME/CFS.  “The conventional approach would be to block the overactive pathway. Instead, our counterintuitive approach seeks to overstimulate CRFR2, causing it to downregulate, without the need for chronic treatment.”

Health arising: The Cortene drug trial results for ME/CFS are in

Dr. Bateman indicated that many of the participants reported subtle but noticeable improvements of their symptoms over the 1-2 years following the trial.

In an interview, Cortene proposed that partial downregulation of the CRFR2 receptor had indeed occurred, and that further trials would determine if they could fully return it and the stress response system in ME/CFS to a healthy state.

Cortene hopes to embark on a 60-person $4 million trial next.

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Research: An alternative model of CBT for CFS/ME

‘A life I can cope with’. An alternative model of cognitive behavioural therapy (CBT) for CFS/ME, by Catherine Clark, Sue Holttum in Health Expectations 2021 [DOI: 10.1111/h ex.13326]


Research abstract:


This study aimed to explore the experience of cognitive behavioural therapy (CBT) aimed at better management of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME), rather than increasing activity.


This was a qualitative study using grounded theory analysis.


Semi-structured interviews were conducted with 13 adults who had engaged in CBT at a specialist CFS/ME service in which CBT is aimed at improved management of the condition.


A model was produced in which participants felt more able to cope with CFS/ME. Reduced fatigue did not seem to be a necessary precondition to managing. This has implications for CBT for CFS/ME.


Specialist CBT for CFS/ME may result in improved coping and reduced distress, independently of changes in fatigue.

I don’t think in any way it helped my ME, but it did help my mind. (Sarah)

I don’t want to say reduced the symptoms, but probably have slightly fewer relapses and maintain a slightly better level quality of life. (Susan)

I came away just with that re-focus on putting myself first and not being afraid to do that actually, it is okay to do that when you are not well. (Sarah)

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WAMES responds to NICE ’roundtable’ announcement

WAMES writes to NICE re ‘Roundtable event’


On 27th August, 10 days after publication of the ME/CFS guideline was ‘paused’, NICE made another announcement. Yet again this gave the bare minimum of information – their plan to invite stakeholders to a roundtable discussion in September ‘to better understand the issues raised and determine how it can gain support for the guideline to ensure effective implementation.

No information was given about the nature of the challenge or the people making the challenge, or the rules and regulations governing this unprecedented move.

In the media and on social media, the critics of the guideline have made it clear that:

  • they believe GET and CBT are the only valid evidence based interventions that can help patients
  • the PACE trial should be upgraded from low quality and that this could be done if the diagnostic criteria was widened.

NICE says they believe it is possible to reach an agreement. Whether that is realistic or wishful thinking remains to be seen.

It is now September, so WAMES has written to NICE to express our commitment to continuing to work towards publication of the guideline.


Dear Prof Leng, Mr Chrisp and Ms Stafford,

As a stakeholder in the ME/CFS NICE guideline revision process, and a charity working with the estimated 13,000 people with ME in Wales, we confirm our interest in being part of the Roundtable event. WAMES supports the publication of the guideline as soon as possible, as it was developed by following a search for best evidence and represents years of hard work and emotional investment from all involved.

We hope this will be an inclusive event with virtual participation from a wide range of stakeholders as we are concerned about the lack of transparency surrounding the challenge to the guideline and ‘pause’ in publication. This has severely damaged NICE’s credibility in the ME community and future openness will be critical in achieving ‘a guideline that will have the support of people living with ME/CFS’.

We therefore look forward to receiving the following in advance, so we have plenty of time to prepare:

  • Full details of the challenge to the publication of the guideline
  • Details of the procedure by which others can also challenge the publication of the guideline in its current form
  • Details of any expert witnesses that are being called or further evidence being gathered
  • A clear plan for the steps and timescale that will be followed until publication
  • Details of all stakeholders invited and the role they will play in this, both in person and via written submission
  • Details of any stakeholders who are not invited to the Roundtable and how they can contribute
  • The plan of action if agreement cannot be achieved
  • An assurance that ongoing delay to publication will be accompanied by a warning on the current guideline that GET can cause deterioration for people with PEM, thus preventing further harm.

Yours sincerely,

Jan Russell   Chair of WAMES

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