Intended for healthcare professionals

Rapid response to:


Pressure grows on Lancet to review “flawed” PACE trial

BMJ 2018; 362 doi: (Published 22 August 2018) Cite this as: BMJ 2018;362:k3621

Rapid Response:

We can specifically treat several infective CFS/ME subtypes

Now that the biopsychosocial treatments, cognitive behavioural therapy (CBT) and graded exercise therapy (GET), are correctly recognised to be ineffective and even harmful (in the case of GET), it seems appropriate to reconsider what we can offer CFS/ME patients in terms of real benefit.

We can identify some disease subtypes for which effective treatments already exist. Psychological stress has been shown to weaken cellular immunity leading to reactivation of endogenous Epstein-Barr virus (EBV) with expression of EBV dUTPase which creates a pro-inflammatory state which if prolonged can lead to development of CFS/ME (1,2). Clinical benefit in EBV-induced CFS/ME patients has been achieved using valganciclovir (3). We can identify this important and treatable CFS/ME subtype (up to 50% CFS/ME patients) by detection of antibodies to EBV dUTPase and DNApol (4) and/or by detection of the EBV induced gene 2 (EBI2), which is upregulated in peripheral blood mononuclear cells (PMBC) (5).

Parvovirus B19 has also been shown to trigger CFS/ME. B19-CFS/ME maybe identified by a characteristic viral illness at the onset of CFS/ME with serum anti-B19 IgM positivity, and persisting B19 DNA positivity. B19-CFS/ME has been cured in several cases using intravenous immunoglobulin (IVIG), the specific treatment for parvovirus B19 (6).

Acute Q-fever may also trigger CFS/ME and Q-CFS/ME has been shown to respond to tetracyclines (7). These approaches actually work and their widespread implementation, along with other more general supportive treatments, would be a respectful clinical service to CFS/ME patients.

1. Glaser R, et al. Psychoneuroendocrinology 1994;19:765-72.
2. Padgett DA, et al. J Med Virol 2004;74:442-8.
3. Montoya JG, et al. J Med Virol 2013;85:2101-9.
4. Lerner AM, et al. PLoS One 2012;7:e47891.
5. Kerr JR, et al. J Infect Dis 2008;197:1171-84.
6. Kerr JR, et al. Clin Infect Dis 2003;36:e100–6.
7. Arashima Y, et al. Intern Med 2004;43:49–54.


Competing interests: No competing interests

29 August 2018
Jonathan R Kerr
Consultant in Microbiology
West Suffolk Hospital Foundation Trust
Hardwick Lane, Bury St Edmunds, Suffolk IP33 2QZ