XMRV and MS - articles or research references

anncavan

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Wondering if anyone can point me in the direction of articles and/or research that mention the connection between XMRV and MS. I reached out to an MS blogger I regularly read, telling him about Dr. Mikovits' upcoming presentation in Santa Rosa (the title references MS). He'd never heard of XMRV, and asked if I could send more info. I looked for articles and couldn't find any, yet I know claims have been made connecting the two.

Also, anyone recommend an article that could serve as an XMRV 101 to give to him, as well as for me to give to family?

Thanks!
 

Jemal

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As far as I know, there is no published research on the connection between XMRV and CFS. The Whittemore Peterson Institute claims it is finding it in large percentages in people with atypical MS however. They make a statement about it on this page:

We have detected the retroviral infection XMRV in greater than 95% of the more than 200 ME/CFS, Fibromylagia, Atypical MS patients tested.
http://www.wpinstitute.org/xmrv/index.html
 

anciendaze

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The main problem here is that nobody has a good way to distinguish atypical MS from CFS. Both are considered 'diagnoses of exclusion'. The difference appears to be that if you are sure it is organic you call it MS, if you are not sure, you call it CFS. How anybody can be sure without reliable biomarkers is an exercise left for the student. I note in passing that MS patients can even exhibit PEM, cognitive deficits and mood swings.

Generally, this is an example of diagnostic fragmentation. Anything with strong biomarkers falls in a separate category. Whether you are diagnosed as ill with ME/CFS, Lyme disease or a somatization disorder depends less on you than on the doctor making the diagnosis. This immensely complicates the problem of solving a medical mystery.
 

Mark

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Both answers above are spot on I think. The only real difference I can see to draw a line between MS and ME is you can get the MS diagnosis if they find the white spots on your MRI scan, indicating damage to the myelin sheath. Beyond that, they don't seem to know very much about it at all - but that's proven, observable, and reliable enough to get them recognition. That seems to be the only thing that finally took MS out of the wastebasket we're in, and into the world of big bucks research and social and political support. And MS sufferers, historically, were treated absolutely appallingly, in ways that have parallels to our own situation.

Oh, and another old theme I'd forgotten about: the epidemiology of MS is also highly suggestive: extremely geographical, and also, very much on the rise - in an atypical form that now disproportionately affects women - since the 80s...view all the facts and graphs in the light of the hypothesis of XMRV infection at a younger age, and the numbers and dates come out just right (you have to think it through and add about 20 years at some point, as I recall, with the realisation that original infection could precede onset by many years). The geographical distribution stuff is also incredibly tantalising, and well worth a look for anybody wondering about that issue: there's a genetics vs sunlight controversy to explain that, but few people seem to have been focused on flora/fauna distribution, like strains of mice and conditions for organisms like mold...

Seeing my mate who has MS has really helped me understand how similar the conditions are, in so many ways. And also to realise that so many of the tough and depressing issues we tend to think of as unique to us, due to our isolation and alienation, are actually common to any chronic ideopathic illness - and some of them really are unique to our situation. I'm still a little jealous of the perks you can get if you have those little white spots though...

Sorry, I'm not answering the question I suppose. But I'm pretty sure there's nothing more than a couple of comments by Dr Mikovits...ah, now there was Dr Mikovits' small study of family clusters - that may have included some atypical MS patients...perhaps somebody can track down the link to that?
 

Enid

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Enjoyed your information and discussion here - thank you - because at the time of my onset 11 years ago I was helping a family with their Mum (a form of dementia). Her daughter went down with full blown MS at the same time I slowly deteriotated into ME. (brain MRI scans high spots but not MS according to my Neurologist). Just strange that we both acquired related illnesses at the same time. In close contact so any virals could easily have been transmitted.
 

Jemal

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My first health issues appeared when I was seeing a woman with MS, more than 10 years ago. We'll see if there's a connection...
 

shannah

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Both answers above are spot on I think. The only real difference I can see to draw a line between MS and ME is you can get the MS diagnosis if they find the white spots on your MRI scan, indicating damage to the myelin sheath. Beyond that, they don't seem to know very much about it at all - but that's proven, observable, and reliable enough to get them recognition. That seems to be the only thing that finally took MS out of the wastebasket we're in, and into the world of big bucks research and social and political support. And MS sufferers, historically, were treated absolutely appallingly, in ways that have parallels to our own situation.

... I'm still a little jealous of the perks you can get if you have those little white spots though...
The little white spots don't seem to automatically guarantee a diagnosis of MS. It seems to depend on other things like what neurologist you see and probably also what country you live in (and in some cases, possibly even totally non-related events such as the day of the week you attend your appointment - lol).

I have numerous white lesions. The original neurologist who read the MRI said it indicated demyelination and MS. The second neurologist said no MS because I wasn't in a wheelchair and questioned whether the MRI was done correctly. The third neurologist with a new updated MRI said although she had no idea what it was, she was 85% sure it wasn't MS because the lesions were "in the wong place".

The last two neurologists I might add, were both well recognized neurologists practising at separate specialized institutions in a large cosmospolitan centre. Pretty scary! So I qualified for no 'perks' like a scooter or wheelchair or anything else for that matter.

In another case, I met someone a few years ago who had several lesions but with a diagnosis of Lyme Disease, sought a different well respected top neurologist and was told his six white lesions were probably due to smoking!

After expending the non-existent energy to attend all of the appointments, travel, etc., etc., this is very disheartening and the consequent explanations I find to be really unbelievable!
 

lancelot

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The little white spots don't seem to automatically guarantee a diagnosis of MS. It seems to depend on other things like what neurologist you see and probably also what country you live in (and in some cases, possibly even totally non-related events such as the day of the week you attend your appointment - lol).

I have numerous white lesions. The original neurologist who read the MRI said it indicated demyelination and MS. The second neurologist said no MS because I wasn't in a wheelchair and questioned whether the MRI was done correctly. The third neurologist with a new updated MRI said although she had no idea what it was, she was 85% sure it wasn't MS because the lesions were "in the wong place".

The last two neurologists I might add, were both well recognized neurologists practising at separate specialized institutions in a large cosmospolitan centre. Pretty scary! So I qualified for no 'perks' like a scooter or wheelchair or anything else for that matter.

In another case, I met someone a few years ago who had several lesions but with a diagnosis of Lyme Disease, sought a different well respected top neurologist and was told his six white lesions were probably due to smoking!

After expending the non-existent energy to attend all of the appointments, travel, etc., etc., this is very disheartening and the consequent explanations I find to be really unbelievable!
From what i've read, some PWC have small white plaques that are transitory(temporary) and in small numbers while the lesions in MS are much larger, permanent and widespread in the brain and spinal cord. All neurologists should be competent at interpreting MS from a MRI, but they may be confused and unfamiliar with CFS lesions. I will be seeing a neurologist who specializes in CFS so i will report back.
 
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And was it Dr. Cheney who said that the MRIs (or was it some other type of brain scan like PET?) of CFS patients looked just like those of AIDS patients?
 

WillowJ

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Ann, I have not heard of any studies connecting XMRV to MS. However, there is a lot of discussion of endogenous (already incorporated into the genome) retroviruses in MS. Look for articles on MSRV, the MS-associated retrovirus. There are some disbelievers, of course.

There's also a Discover magazine article about endogenous retroviruses in psychiatric-classified diseases, which mentions MS.
http://discovermagazine.com/2010/jun/03-the-insanity-virus/article_view?b_start:int=0&-C=

Lancelot, who is the neurologist? I need to see one of those.
 

WillowJ

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Antony JM, Deslauriers AM, Bhat RK, Ellestad KK, Power C. "Human endogenous retroviruses and multiple sclerosis: Innocent bystanders or disease determinants?" Biochim Biophys Acta. 2011 Feb;1812(2):162-76. Epub 2010 Aug 6. PMID: 20696240

Perron H, Lang A. "The human endogenous retrovirus link between genes and environment in multiple sclerosis and in multifactorial diseases associating neuroinflammation." Clin Rev Allergy Immunol. 2010 Aug;39(1):51-61. Review. PMID: 19697163

Perron H, Bernard C, Bertrand JB, Lang AB, Popa I, Sanhadji K, Portoukalian J. "Endogenous retroviral genes, Herpesviruses and gender in Multiple Sclerosis." J Neurol Sci. 2009 Nov 15;286(1-2):65-72. Epub 2009 May 17. Review. PMID: 19447411

Saresella M, Rolland A, Marventano I, Cavarretta R, Caputo D, Marche P, Perron H, Clerici M. "Multiple sclerosis-associated retroviral agent (MSRV)-stimulated cytokine production in patients with relapsing-remitting multiple sclerosis." Mult Scler. 2009 Apr;15(4):443-7. Epub 2009 Feb 27. PMID: 19251836

Ruprecht K, Gronen F, Sauter M, Best B, Rieckmann P, Mueller-Lantzsch N. "Lack of immune responses against multiple sclerosis-associated retrovirus/human endogenous retrovirus W in patients with multiple sclerosis." J Neurovirol. 2008 Apr;14(2):143-51. PMID: 18444086
 

lancelot

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Lancelot, who is the neurologist? I need to see one of those.
A neurologist named Dr James Lin from monterey park, ca. i know nothing about him but he was highly recommended to me by my kind hearted PCP(who initially referred me to dr chia, but i declined later to see) and separately recommended by my mom's endocrinologist(who refuses to see CFS patients because it is too complicated). i had basically given up on doctors when most(5) just made me much much worse with the drugs, herbs, and all other conventional and alt treatments. but i realize now, i will never get well from this DD and stay disabled forever if i don't get some kind of specialized medical care or alternate diagnosis. i've been holding off on seeing him till after the lipkin, BWG, and singh studies come out, but i can't wait another 4-6months w/o a guaranteed consensus on this matter or government approved blood test.

As far as retroviruses goes, they have produced worldwide pandemics, but believe it or not they have also helped to evolve intelligent humans from other primates and mammals. Our dna is composed of about 11% endogenous retroviruses who were all once exogenous. those that helped mankind was passed on by our genes. those that killed us were never passed on. you can see humans contain a massive amount of endogenous retroviruses compared to primates, mammals, insects or any other living thing on earth. retroviruses actually helped humans evolve intelligence and away from other primates/mammals. you can see the need for endogenouse retroviruses whenever humans or other mammals are pregnant, ERV's are turned on to replicate in huge number in the placenta to help the fetus. Without ERV's in the placenta, the fetus will not be viable nor complete. so don't think all ERV's are bad when replicating in us. it's much more likely it is helpful in some way or it wouldn't have been passed on in our genes. make sense? it's not likely we will pass on HIV or HTLV to our siblings right? Why would we be passing on ERV's that cause a large amount of diseases like MS or Schizophrenia? It doesn't convey an advantage but rather an end to that human family, genome, or population. We should be worrying more about pathogenic exogenous retroviruses here and now.
 

WillowJ

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Lancelot, thanks so much for the name. I'm sorry about your doctor situation. I can relate. 12 years and not much help (and a lot of being ignored and patronized and some active scorn, but some sympathetic but can't suggest anything docs, too), although I now have a very kind and--even better--curious research pulmonologist who wants to know why I cannot tolerate activity. The first doctor I've met who does not test and diagnose by checklist. I quite love him. He knew nothing of ME/CFS prior to meeting me, but he took my research papers and read them.

that's why I put "junk" DNA in quotes, because some of the sequences have positive uses, and because it's an outdated idea that these are benign doing nothing, just taking up space (the origin of the term "junk DNA").

but you have to follow the science, not the model. Evolutionary model suggests ERV's should all be beneficial, but if science is able to demonstrate that some of them aren't, it's the model that needs to change.
 

lancelot

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Lancelot, thanks so much for the name. I'm sorry about your doctor situation. I can relate. 12 years and not much help (and a lot of being ignored and patronized and some active scorn, but some sympathetic but can't suggest anything docs, too), although I now have a very kind and--even better--curious research pulmonologist who wants to know why I cannot tolerate activity. The first doctor I've met who does not test and diagnose by checklist. I quite love him. He knew nothing of ME/CFS prior to meeting me, but he took my research papers and read them.

that's why I put "junk" DNA in quotes, because some of the sequences have positive uses, and because it's an outdated idea that these are benign doing nothing, just taking up space (the origin of the term "junk DNA").

but you have to follow the science, not the model. Evolutionary model suggests ERV's should all be beneficial, but if science is able to demonstrate that some of them aren't, it's the model that needs to change.
Holy moly 12 years! i feel for you. let me ask you, does it get easier to accept this disease as time goes by? If i knew that after 3 years of disabling CFS that i would be living with it for at least 12 years with no guarantee of being cured beyond that, i'd rather not live this torturous life anymore. I think most of us choose to live knowing that we will be well oneday. It's like we are POW's waiting to be saved oneday. F this disease!

That whole "junk" dna is outdated and not accepted by most scientist now. Some may think it as junk because evolution works in terms of millions of years not a human lifetime. did you know that an exogenous pathogenic retrovirus infection always produces recombinants with endogenous retroviruses(i got this off Dr R's TWIV interview with dr Goff who studies XMRV and other retroviruses)? so in fact if endogenous retroviruses are replicating to cause disease it is because of its recombination with a pathogenic exogenous retrovirus like HIV, HTLV and XMRV. That's why i'm still saying that it is exogenous retroviruses that is still responsible for large numbers of diseases rather than endogenous retroviruses being solely responsible for a disease affecting large numbers. i just can't see large numbers of disease causing genes being passed on from generation after generation to where we are now as modern humans. almost all human diseases now are due to exogenous events.

nice talking to you. take care, my brain is worn out for tonight. :sofa:
 

WillowJ

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Holy moly 12 years! i feel for you. let me ask you, does it get easier to accept this disease as time goes by? If i knew that after 3 years of disabling CFS that i would be living with it for at least 12 years with no guarantee of being cured beyond that, i'd rather not live this torturous life anymore. I think most of us choose to live knowing that we will be well oneday. It's like we are POW's waiting to be saved oneday. F this disease!

That whole "junk" dna is outdated and not accepted by most scientist now. Some may think it as junk because evolution works in terms of millions of years not a human lifetime. did you know that an exogenous pathogenic retrovirus infection always produces recombinants with endogenous retroviruses(i got this off Dr R's TWIV interview with dr Goff who studies XMRV and other retroviruses)? so in fact if endogenous retroviruses are replicating to cause disease it is because of its recombination with a pathogenic exogenous retrovirus like HIV, HTLV and XMRV. That's why i'm still saying that it is exogenous retroviruses that is still responsible for large numbers of diseases rather than endogenous retroviruses being solely responsible for a disease affecting large numbers. i just can't see large numbers of disease causing genes being passed on from generation after generation to where we are now as modern humans. almost all human diseases now are due to exogenous events.

nice talking to you. take care, my brain is worn out for tonight. :sofa:
I had a reply and it went away, poof! no reason? brain fog, not sure if I can repeat...

Thanks for the sympathy. I'd said some other stuff but can't find those words now just want to put up a link again. Laurel says it so much prettier (thanks to the Patient Advocate and PR for directing me to her blog):
Undoubtedly, this is not the road I chose or would have ever wanted for myself, and there is nothing in this world I wouldn't do to change it. And it is true that my dreams, my ambitions, my education, my career and all my hopes and goals have, thus far, gone by the wayside. And that, in any circumstance, is indeed a tragedy. But my life, with all its struggles, loss, pain, limits and difficulties, is still a life. It still has value. It still has joy and love and dreams and meaning and hope.
her post was very encouraging to me.

ya, I had put "junk DNA" in tickle marks to show it wasn't right, 'cause cannot remember proper term from genetics class... and thanks for sharing about exogenous and endogenous viruses recombining, that was very interesting and I hadn't looked the video (tend to have technical issues wtih videos).

nice talking to you, too, lancelot :)

have a nice rest and when you come back (or if someone else knows)... do you know if there are any exogenous retroviruses published as found in association with the ERV diseases, particularly MS since that was Ann's question
 

Enid

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WillowJ - thank you very much for your info on the present state/findings in MS research - "innocent bystanders or disease determinants" sounds very familiar for we MEers. Though my brain scans (high spots) were given the all clear for ME (Kings College) the doubts were quite evident in the expression of my own Neurologist here. And as all the symptoms of ME appeared (we know so well) I think it all became too confusing for him so with his apologies I was left. Can't help thinking of the similarities. (Correction - all clear for MS).
 

Enid

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Lancelot - if you are up to it, looking forward to your notes after your specialist Neurologist visit - sort of what are the high spots, and why such mental and physical decline (plus all the other nasties) over years. Hope he will be able to assist you too in getting better.
 

Recovery Soon

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I'm still a little jealous of the perks you can get if you have those little white spots though...
My brother has MS. His episodes are intense (such as waking up one morning without eyesight in one eye- which luckily returned 9 months later), but not chronically unremitting, such as what I face with CFS. So, while, I would never be jealous of his attention, there is a certain irony about all the well wishing he receives, and accolades about his bravery, while I'm standing next to him hiding a disease that excludes me from the most basic of behaviors, such as exercising, vacationing, drinking, etc. that are completely available to and routine for him. I have to kind of shake my head and smile. Luckily, because of his intuitive/compassionate nature, the irony is not lost on him.

I have numerous white lesions. The original neurologist who read the MRI said it indicated demyelination and MS. The second neurologist said no MS because I wasn't in a wheelchair and questioned whether the MRI was done correctly. The third neurologist with a new updated MRI said although she had no idea what it was, she was 85% sure it wasn't MS because the lesions were "in the wong place".
The second neurologist is a moron. Everyone knows you don't need to be wheelchair bound to have MS. That's like saying you need to be dead to have cancer. I'm not sure which MRI you had done, but the proper way is have MRI with Contrast- that's the standard.

I'm seeing a world class neurologist now and having an MRI done- with a battery of other testing, lasting over a month (nerve testing in upper and lower extremities, cognitive functioning test- called Neurotrax), sleep test, and some other exam called ANSAR, which I'm not really sure about yet.

I think this thorough examination, in congress with a highly competent neurologist should should paint a clear picture of something. I'm curious to see if there are lesions, in any location.

BTW- I understand that lesions in certain areas (that are not thought to be associated with MS, ARE associated with CFS. Does anyone know about this???

If so, where are they located in the brain- I'd like to point this out to the neurologist in the event they find such lesions on my scan.
 

Enid

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Recovery Soon - looking forward (if/when up to it) results of your visit. Knowledgeable Neurologists virtually non existant here. Only info from my Neurologist - abnormalties - "patchy high signal changes in the brain" (scan of whole spine normal) and weak anti-smooth muscle antibody etc. Someone may have more specifics for you. Must say at the time barely able to think or walk and feelings about to pass out (twice lost consciousness).
 

WillowJ

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yes, Recovery, there are lesions specific to ME. Small spots on frontal lobes, I think.

Lange G, DeLuca J, Maldjian JA, Lee H, Tiersky LA, Natelson BH. "Brain MRI abnormalities exist in a subset of patients with chronic fatigue syndrome." J Neurol Sci. 1999 Dec 1;171(1):3-7. PMID: 10567042
The CFS-No Psych group showed a significantly larger number of brain abnormalities on T2 weighted images than the CFS-Psych and HC groups. Cerebral changes in the CFS-No Psych group consisted mostly of small, punctate, subcortical white matter hyperintensities, found predominantly in the frontal lobes. No significant difference was found when both CFS groups were combined and compared to the HC group. The use of stratification techniques is an important strategy in understanding the pathophysiology of CFS. This frontal lobe pathology could explain the more severe cognitive impairment previously reported in this subset of CFS patients.
Cook DB, Lange G, DeLuca J, Natelson BH. "Relationship of brain MRI abnormalities and physical functional status in chronic fatigue syndrome." Int J Neurosci. 2001 Mar;107(1-2):1-6. PMID: 11328679
These results demonstrate that the presence of brain abnormalities in CFS are significantly related to subjective reports of physical function and that CFS subjects with MRI brain abnormalities report being more physically impaired than those patients without brain abnormalities.
Dickinson CJ. "Chronic fatigue syndrome--aetiological aspects." Eur J Clin Invest. 1997 Apr;27(4):257-67. Review. PMID: 9134372
Studies by modern imaging techniques have not been entirely consistent, but many magnetic resonance imaging (MRI) studies already suggest that small discrete patchy brain stem and subcortical lesions can often be seen in CFS. Regional blood flow studies by single photon-emission computerized tomography (SPECT) have been more consistent. They have revealed blood flow reductions in many regions, especially in the hind brain. Similar lesions have been reported after poliomyelitis and in multiple sclerosis--in both of which conditions chronic fatigue is characteristically present. In the well-known post-polio fatigue syndrome, lesions predominate in the RAS of the brain stem. If similar underlying lesions in the RAS can eventually be identified in CFS, the therapeutic target for CFS would be better defined than it is at present. A number of logical approaches to treatment can already be envisaged.
[this from St. Barts ?! evidently that is not solely a bastion of ignorance]



Schwartz RB, Garada BM, Komaroff AL, Tice HM, Gleit M, Jolesz FA, Holman BL. "Detection of intracranial abnormalities in patients with chronic fatigue syndrome: comparison of MR imaging and SPECT." AJR Am J Roentgenol. 1994 Apr;162(4):935-41. PMID: 8141020
SUBJECTS AND METHODS: Sixteen patients who fulfilled the Centers for Disease Control, British, and/or Australian criteria for chronic fatigue syndrome had MR and SPECT examinations within a 10-week period.
RESULTS: MR abnormalities consisted of foci of T2-bright signal in the periventricular and subcortical white matter and in the centrum semiovale; there were 2.06 foci per patient, vs 0.80 foci per control subject. MR abnormalities were present in eight (50%) of 16 patients, compared with three (20%) of 15 age-matched control subjects. Neither of these differences reached significance, although the power of the study to detect differences between groups was small. Patients with chronic fatigue syndrome had significantly more defects throughout the cerebral cortex on SPECT scans than did normal subjects (7.31 vs 0.43 defects per subject, p < .001). SPECT abnormalities were present in 13 (81%) of 16 patients, vs three (21%) of 14 control subjects (p < .01). SPECT scans showed significantly more abnormalities than did MR scans in patients with chronic fatigue syndrome (p < .025). In the few patients who had repeat SPECT and MR studies, the number of SPECT abnormalities appeared to correlate with clinical status, whereas MR changes were irreversible.

CONCLUSION: SPECT abnormalities occur more frequently and in greater numbers than MR abnormalities do in patients with chronic fatigue syndrome. SPECT may prove to be useful in following the clinical progress of patients with this syndrome.


Of course, there's the classic one (abstract doesn't say what kind of MRI findings, but maybe it's in the library)

Buchwald D, Cheney PR, Peterson DL, Henry B, Wormsley SB, Geiger A, Ablashi DV, Salahuddin SZ, Saxinger C, Biddle R, et al. "A chronic illness characterized by fatigue, neurologic and immunologic disorders, and active human herpesvirus type 6 infection." Ann Intern Med. 1992 Jan 15;116(2):103-13. PMID: 1309285
CONCLUSIONS: Neurologic symptoms, MRI findings, and lymphocyte phenotyping studies suggest that the patients may have been experiencing a chronic, immunologically mediated inflammatory process of the central nervous system. The active replication of HHV-6 most likely represents reactivation of latent infection, perhaps due to immunologic dysfunction. Our study did not directly address whether HHV-6, a lymphotropic and gliotropic virus, plays a role in producing the symptoms or the immunologic and neurologic dysfunction seen in this illness. Whether the findings in our patients, who came from a relatively small geographic area, will be generalizable to other patients with a similar syndrome remains to be seen.
here's one using the name:

Daugherty SA, Henry BE, Peterson DL, Swarts RL, Bastien S, Thomas RS. "Chronic fatigue syndrome in northern Nevada." Rev Infect Dis. 1991 Jan-Feb;13 Suppl 1:S39-44. PMID: 1850542
Abstract

The clinical and laboratory findings from studies of patients with chronic fatigue syndrome (CFS) from northern Nevada are summarized. Physicians caring for these patients have estimated that greater than 400 patients with CFS from northern Nevada and nearby communities in California were identified between 1984 and 1988. As a result of these studies, a cluster of clinical and laboratory features associated with the illness in moderately to severely affected patients has been identified: profound fatigue of prolonged duration; cervical lymphadenopathy; recurrent sore throat and/or symptoms of influenza; loss of cognitive function manifested by loss of memory and loss of ability to concentrate; myalgia; impairment of fine motor skills; abnormal findings on magnetic resonance imaging brain scan; depressed level of antibody to Epstein-Barr virus (EBV) nuclear antigen; elevated level of antibody to EBV early antigen restricted component; elevated ratio of CD4 helper to CD8 suppressor cells; and strong evidence of association of this syndrome with infection with human herpesvirus 6. More-serious and longer-lasting neurologic impairments, including seizures, psychosis, and dementia, have also been observed in some of these patients.



Natelson BH, Cohen JM, Brassloff I, Lee HJ. "A controlled study of brain magnetic resonance imaging in patients with the chronic fatigue syndrome." J Neurol Sci. 1993 Dec 15;120(2):213-7. PMID: 8138812
Two neuroradiologists compared the brain MR scans of 52 patients with the CDC criteria for the chronic fatigue syndrome (CFS) with those of 52 age and sex matched controls who had undergone imaging because of histories of head trauma or headache. CFS patients had significantly more abnormal scans than controls--27% vs 2%. Abnormalities seen were foci of increased white matter T2 signal in 9 CFS patients and one control and ventricular or sulcal enlargement in 5 CFS patients. Follow up of patients with subcortical signal hyperintensities revealed 3 who had symptoms suggestive of other known medical causes of what appeared to be CFS.