Montoya was at this before as far as I remember, didn't seem to make a difference then and I would not be optimistic at all this time.
The whole CMRC is a farce, if they remove Day 2 then maybe it would be a positive but until then I fail to get excited about this conference.
Maybe you weren't concentrating hard enough?
Or not even at the conference?
I though he gave an outstanding presentation to the Newcastle conference about both his immune function research and the clinical trials involving valganciclovir
Jose also came to the Workshop on Neuropathogy and made a very useful contribution, including collaboration with our UK post-mortem research group
CS
Main conference report:
http://www.meassociation.org.uk/2015/10/global-mecfs-research-22-october-2015/
Summary of his presentation
Professor Jose Montoya, Stanford University, USA, opened the first plenary session on neuropathology with an outstanding presentation that commenced with a one-minute silent tribute to his close colleague and friend Dr Martin Lerner, who had recently died. Martin Lerner had worked with Professor Montoya on a number of research studies, including the use of antiviral treatment.
Professor Montoya also referred positively to the impact of the Institute of Medicine (IoM) report and is a supporter of the new IoM diagnostic definition for ME/CFS (or systemic exertion intolerance disease/SEID as is being recommended in the report) because he believes that clinicians need a simple and accurate way of making a diagnosis.
He believes that the new IoM definition, which emphasises post-exertional malaise and orthostatic intolerance, is preferable to the options – eg Canadian, Fukuda – that are currently available. Work from the Stanford group indicates that there is a strong (90%) concordance between Canadian, Fukuda and IoM definitions.
He then said that people with ME/CFS had been ignored and humiliated by the very people who were supposed to be helping them – the medical profession. In his own words….
“I have a wish and a dream that medical and scientific research societies in the US apologise to their ME/CFS patients”.
Turning to treatment, Professor Montoya described how the publication of a flawed clinical trial involving acyclovir back in 1988 had led to the view that ME/CFS was not caused by EBV infection and that antiviral drugs do not have any role in the treatment of ME/CFS.
Despite this, he has been involved in a number of the clinical trials that have assessed the efficacy and safety of the antiviral drug valganciclovir.
This is a treatment option – involving a lower dose than is normally used in other situations and over a prolonged period of time, at least 6 months, possibly much longer – that he now uses for some ME/CFS patients with considerable success.
In addition to antiviral activity and reduction of latent HHV-6 replication, he believes that this drug may have immunomodulatory effects in ME/CFS as well (as it can decrease the level of white blood cells called monocytes and reduce microglia activation in mice).
[CS note: During the discussion that followed I pointed out that here in the UK antiviral treatment is not recommended by NICE – so antiviral drugs are seldom used in ME/CFS and very little interest has been shown in further research or clinical trials involving antiviral treatment. The ME Assoxciation has met with Roche, the pharmaceutical company that makes this drug, but we did not have any success in trying to set up a UK clinical trial. We clearly need an independent randomiaed placebo-controlled trial to assess the value of valganciclovir in ME/CFS.]
Professor Montoya then described some of the other research that his multidisciplinary group at Stanford are carrying out on a large group of ME/CFS patients, along with healthy controls, with the help of a $5 million anonymous donation. In particular:
• Immune function studies that are looking at the response to infection with various organisms. In particular, the role of immune system chemicals called cytokines, how the cytokine pattern changes over time (less or more than 3 years – the Hornig/Lipkin study), as well as daily fluctuations in cytokines relating to activity levels. To do so they can measure over 50 individual cytokines and have access to a cohort of around 200 ME/CFS patients and 400 controls. Proposed research at Stanford will also involve a detailed study of the role of NK cell status and function in ME/CFS.
• Virology studies examining the role of latent herpes viruses including EBV and HHV-6 and how low NK function may be maintaining HHV-6 activation in ME/CFS. Professor Montoya also referred to research involving Torque viruses. CS note: Torque teno virus is considered to be a relatively new global marker of immune function and the more immunosuppression occurs, the higher the level of torque viruses. Professor Montoya pointed out that torque viruses have been found to be lower in ME/CFS – adding further support to the role of immune system activation in ME/CFS.
• Neuroimaging studies looking at both grey and white matter in the brain – one of which has used diffusion tensor imaging, an MRI based technique that can visualize location, orientation and anisotropy of white matter tracts in the brain. This study has recently been published and described a very significant structural abnormality involving the right arcuate fasciculus. This structure contains fibres which connect different areas of the brain. The fibres are thicker in ME/CFS than in healthy controls and the inference is that nerve fibre transmission is therefore affected. The abnormality could turn out to be a diagnostic marker for ME/CFS.
• Genetic studies examining HLA characteristics in ME/CFS and a genetic predisposition to ME/CFS
Key references:
Immunology: cytokine status and illness duration
www.ncbi.nlm.nih.gov/pubmed/26079000
Neuroimaging: right arcuate fasciculus abnormality
http://pubs.rsna.org/doi/abs/10.1148/radiol.14141079
Valganciclovir clinical trials:
Kogelnick 2006:
www.ncbi.nlm.nih.gov/pubmed/17276366
Lerner et al, 2002:
www.ncbi.nlm.nih.gov/pubmed/12582420
Lerner et al: 2004:
www.ncbi.nlm.nih.gov/pubmed/12582420
Montoya et al 2013:
www.ncbi.nlm.nih.gov/pubmed/23959519
In this trial Montoya et al randomized (2:1) 30 ME/CFS patients with elevated IgG antibody titres against HHV-6 and EBV to receive valganciclovir (VGCV) or placebo for 6 months in a double-blind, placebo-controlled trial.
Statistically significant differences between groups were observed in mental fatigue sub-scores and cognitive function.
The VGCV patients experienced improvements within the first three months and maintained that benefit for the remaining 9 months.
In the VGCV arm monocyte counts decreased, neutrophil counts increased, and cytokines were more likely to evolve towards a Th-1 profile.]
Watt et al, 2012
www.ncbi.nlm.nih.gov/pubmed/23080504
Valganciclovir reduces inflammation in HIV:
http://hivandhepatitis.com/recent/2011/0426_2011_c.html
All patients treated with valganciclovir had undetectable CMV viral load after 8 weeks of treatment, while 44% of those in the placebo group still had detectable CMV.
In addition, valganciclovir-treated participants had significantly greater reductions in CD8 T-cell activation (defined as CD38+HLA-DR+ marker profile) compared with placebo recipients at weeks 8 and 12 — a reduction of about 20%.
Patients in the valganciclovir arm also had reduced levels of high-sensitivity C-reactive protein (CRP), a blood biomarker of inflammation.]
Virology: Torque viruses:
http://jid.oxfordjournals.org/content/early/2014/05/05/infdis.jiu210.full<
YouTube video of opening remarks from Professor Stephen Holgate and presentation from Professor Jose Montoya:
www.youtube.com/watch?v=69Jz43kSQX0
Ends