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Lack of Detection of XMRV in Seminal Plasma from HIV-1 Infected Men in The Netherland

Bob

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I think it is important to look at gay men and HIV positive people so this type of study is important. Maybe it's possible it's not in semen and that's why we havent heard about an epidemic of CFS in gay men? I understand some of the points people here have been making, but doesn't this address one of the biggest questions surrounding XMRV/CFS - if it is sexually transmissible via semen then why didn't CFS show up first or still mostly in gay male populations?
You make some very interesting points here Megan... I've been wondering why we haven't heard about any outbreaks in the gay population like there was for HIV, and yet there has been talk about ME running in families from people like Judy Mikovits, Byron Hyde and Malcolm Hooper.

I do note from the methodology section of the paper it sounds like they did use the Lombardi test as they have referenced it and stated they used Lombardi primers (at least for the first part of the PCR). It sounds to me like it was a nested PCR on the GAG part of XMRV, though its not clear if the second round of the PCR was the same as what Lombardi used?
I think that if you look at the statistics, then they show that this study wasn't a particularly serious study because of the numbers involved...
54 samples were tested, but none of these patients were diagnosed as having CFS. Therefore we'd expect about 4% of the samples to be XMRV positive (4% of 54 = 2.2). But they were not using the most sensitive tests in this study (I believe that testing for antibodies is the most sensitive test that the WPI use), so they might expect to find XMRV in 3% of the samples (3% of 54 = 1.6) (i.e. they would expect to find one positive sample). But the number of samples tested was so small that, statistically speaking, you might not expect to find any XMRV even if it was detectable at 1.6% in the wider HIV+ patient population. And if you add on top of that the fact that some of the patients in the study were taking anti-retrovirals, some of which have been shown to be active against XMRV, then you'd expect to find even fewer XMRV+ samples (i.e. fewer than 1.6 XMRV+ samples), just as the study only detected HIV in 5% of samples from the heterosexual HIV+ patients.
And XMRV might not be very prevalent in the HIV patient population because, as V99 said:
It may be that HIV patients who get XMRV die quicker?
I wonder too if the WPI have looked at these groups or looked at semen. Hard to believe they haven't! Would be interesting to hear from them on this.
There is so much to learn about XMRV, and so many different tissues to look at... I guess it all comes down to resources and priorities.
 

Cort

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Actually there have been quite a few identical twin studies in CFS. (I was actually a part of one.) Several have taken advantage of a big twin database in Sweden. I don't recall any of these stating that CFS ran in families. I think that would have really made news.

Chronic fatigue in a population sample: definitions and heterogeneity.
Sullivan PF, Pedersen NL, Jacks A, Evengrd B.
Psychol Med. 2005 Sep;35(9):1337-48.
PMID: 16168156 [PubMed - indexed for MEDLINE]
Related citations
10.
Twin analyses of chronic fatigue in a Swedish national sample.
Sullivan PF, Evengrd B, Jacks A, Pedersen NL.
Psychol Med. 2005 Sep;35(9):1327-36.
PMID: 16168155 [PubMed - indexed for MEDLINE]
Related citations
11.
The epidemiology of chronic fatigue in the Swedish Twin Registry.
Evengrd B, Jacks A, Pedersen NL, Sullivan PF.
Psychol Med. 2005 Sep;35(9):1317-26.
PMID: 16168154 [PubMed - indexed for MEDLINE]
Related citations

A population-based twin study of functional somatic syndromes.
Kato K, Sullivan PF, Evengrd B, Pedersen NL.
Psychol Med. 2009 Mar;39(3):497-505. Epub 2008 Jun 26.
PMID: 18578896 [PubMed - indexed for MEDLINE]
Related citations


In any case, it was clear from the beginning that AIDS was a transmissable disease; they were able to create networks of sexual partners long before HIV was identified. That's never been true with ME/CFS. If it had been that clear I imagine researchers would have focused on pathogens until they finally came up with one.

I didn't say all family member don't ME/CFS; I, like others, have heard of families with this disorder. That does not seem to be a key aspect of this disorder, however, and I think if that was true, it would be featured prominently in the literature about the disease. I have never seen it there so, while it happens, I think it probably only happens relatively rarely. It might be a good poll question! I think I will do a poll on it. :)

The Dubbo studies showed that a number of pathogens can trigger CFS; XMRV may be in there and it may be somehow potentiating those pathogens but the studies showed that it was those pathogens that triggered the disorder. So, while in some cases it could be a pathogen sweeping across a community, in many cases it's not; its a common pathogen making people sick, a percentage of which come down with ME/CFS. Who knows? Maybe that percentage is people infected with XMRV?

I just think its going to be much more complicated that HIV to figure out.
 

Esther12

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CFS doesn't seem like a normal infectious disorder... but viruses are funky little things that can do all sorts of surprising things.

I'd heard it was generally unusual for partners to 'catch' CFS. CFS research is so compromised by quackery though that we can't really say much about prevalence/transmission/anything with any confidence.

This XMRV stuff is so confused at the moment. Hopefully we'll have a better idea of what's happening when the NIH paper is out.

ps: re those twin studies on chronic fatigue... I recently read one (the Kato one), and it had defined 'chronic fatigue' in a way which included 20 percent of the population for some of their results, and around 2.5 (with no examination) for it's most demanding. Irritatingly it was quite a good study, just of limited interest for us unless you're already confident CFS is just an exaggerated form of normal fatigue, with the same causes and risk factors.
 
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Cort

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Bob

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Maybe ME is infectious, but with a genetic element (i.e. a genetic susceptibility might be needed to actually get ill with ME). Or maybe there are two or more pathogens involved with ME, making the spread of the illness unusual and unpredictable. Or maybe just one pathogen is involved (e.g. XMRV), but it's route of transmission is an unusual, or unpredictable, one.

Even if XMRV does turn out to be the cause, there's still so much for us to find out.
 

dannybex

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CFS doesn't seem like a normal infectious disorder... but viruses are funky little things that can do all sorts of surprising things.
Plus, there are many other things besides viruses or bacterial infections which can contribute to a CFS/ME diagnosis: molds, heavy metals, pesticide exposures, chemicals in our food supplies, poor methylation/detoxification function, etc., etc..
 
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> I've been wondering why we haven't heard about any outbreaks in the gay population like there was for HIV

Some varmints transmit far better among gay men, for at least three reasons, as compared to straights. And some transmit worse among gay men. I would think that by far the most likely reason for this, in most parasite taxa in which it occurs, is that the taxon is adapted to infect and shed from the ah... yin-restricted anatomy into the yang... principle, ...and is less suited, or is totally unsuited, to infect and/or shed from the ahhh... got it?

To be well-adapted to both environments probably entails: more polypeptide sequence for the immune system to recognize and attack, and/or more virulence (which almost always harms the parasite as well as the host). So, just as in non-parasites, there is a trade-off to being a generalist (as opp to a specialist), though the reason is sort of different. Not that many parasite taxa, for example, are generalists in terms of host range, though Borrelia burgdorferi is one spectacular exception.
 

dannybex

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Speaking of parasites -- that's another possible trigger or contributing factor -- a parasite infection -- that is often overlooked when treating CFS/ME. Thanks Eric! :)
 
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In any case, it was clear from the beginning that AIDS was a transmissable disease; they were able to create networks of sexual partners long before HIV was identified. That's never been true with ME/CFS. If it had been that clear I imagine researchers would have focused on pathogens until they finally came up with one.
They could show how HIV had spread because they identified the retrovirus. In ME, since the beginning, they have been looking for the pathogen that caused the disease outbreaks. They just haven't found it yet.
 

leaves

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Cort,
I am XMRV + and although there is not a lot of CFS in the family, except for my grandmother, there ar e a LOT of very weird things, health wise going on. So I think that it can go all directions. Maybe also ask about Autism, lupus, asthma, different types of cancers etc in the poll? And then compare to reposnses of healthy controls...
 
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The Dubbo studies showed that a number of pathogens can trigger CFS; XMRV may be in there and it may be somehow potentiating those pathogens but the studies showed that it was those pathogens that triggered the disorder. So, while in some cases it could be a pathogen sweeping across a community, in many cases it's not; its a common pathogen making people sick, a percentage of which come down with ME/CFS. Who knows? Maybe that percentage is people infected with XMRV?
All that study showed was that people developed CFS after they had a virus. There is no explanation of how those viruses may cause some patients to develop the disease, and others to not. There are over 70 recorded outbreaks of ME.
 

Cort

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They could show how HIV had spread because they identified the retrovirus. In ME, since the beginning, they have been looking for the pathogen that caused the disease outbreaks. They just haven't found it yet.
That's almost an oxymoron - they knew how HIV was spread because they found it.

Actually they knew it was spread by sexual contact long before they identified the pathogen. They were able, as I remember, to draw big networks of patients. They were even able, as I remember, to isolate 'patient zero' or whatever - the person or small group of persons who introduced it into the community - altho there is some controversy over the idea.

http://en.wikipedia.org/wiki/Ga%C3%ABtan_Dugas

That has not been true in CFS.

I just did see a post,though, where a study lenny jason did found increased incidence of ME/CFS in blood relatives - it was not huge but it was there. Strangely enough diabetes was hugely increased in CFS patients blood relatives. FM was as well - not nearly as much as diabetes but more than CFS. It contradicted the findings of an earlier study by his group so its still not really clear. It does suggest increased incidence though. More work is clearly needed.
 

Cort

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Cort,
I am XMRV + and although there is not a lot of CFS in the family, except for my grandmother, there ar e a LOT of very weird things, health wise going on. So I think that it can go all directions. Maybe also ask about Autism, lupus, asthma, different types of cancers etc in the poll? And then compare to reposnses of healthy controls...
That's a good idea. I'll bet you are right. We hope to do that in the Patient Data Repository. My mother died of an autoimmune disease. She had a relative with a severe case of MCS. My twin, however, is disgustingly healthy - as is the rest of my family. :)
 
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No, they suspect it was, just as they have always suspect ME to be infectious.

To trace it, people would have had to be showing symptoms, not everyone was, so they suspected AIDS was infectious.

With ME they have also been able to show in outbreaks the path from one person to the next. Again, sexual transmission is not the be all and end all of infection.
 

Cort

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All that study showed was that people developed CFS after they had a virus. There is no explanation of how those viruses may cause some patients to develop the disease, and others to not.
That is the central question, though, isn't it? Wouldn't CFS be solved if they had answered how the viruses caused CFS ?????. I think the study did enough on its own without answering the central question facing researchers in this disorder.
 
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The disease is probably due to infection by an unknown agent or group of related agents.
1959: E D Acheson. "The Clinical Syndrome Variously Called Benign Myalgic Encephalomyelitis, Iceland Disease and Epidemic Neuromyasthenia" in the American Journal of Medicine.

ME has always been suspected to be caused by an infectious agent.

I'm not sure what the point of your last post was?
 
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Every attempt was made to correlate this epidemic with the previous outbreaks in the various hospitals of the group, but no success was achieved. Such pathological examinations as were carried out showed the same negative results as in previous epidemics.
The occurrence of sporadic cases unassociated with the bulk of cases in the limited sphere of the hospital epidemic was a feature of the outbreak in the previous year and, in fact, of outbreaks described in other countries.
'AN OUTBREAK OF ACUTE INFECTIVE ENCEPHALOMYELITIS IN A RESIDENTIAL ROME FOR NURSES IN 1956' GEFFEN & TRACY, BMJ, Ocr. 19 1957
 
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On the basis of case to case contact, attempts have been made to fix the incubation period of the disorder. In the Iceland6, Bethesda15, Royal Free Hospital27 and Punta Gorda16 outbreaks the evidence indicated an incubation period of less than one week, probably five to six days. In Los Angeles5 the information on this point is incomplete, but a few patients became ill four days after their first exposure, indicating the minimum incubation period. On the other hand, the Middlesex Hospital8 and Durban18 reports suggested a longer period of two to three weeks. An incubation period of fourteen days was present in the single case in which isolated contact occurred in the small second outbreak in the Royal Free Hospital in 195613.
Most curious of all the epidemiologic features is the apparent susceptibility of the nursing medical and ancillary processions. Seven of the fourteen outbreaks have occurred in the staffs of hospitals.
It is recognized that nurses through contact with patients have an increased risk of contracting certain infections. As far as this syndrome is concerned, however, there has been evidence that the nurses might have been infected by patients in only two outbreaks5,10. Thus in Los Angeles cases occurred both earlier and more commonly in those members of the hospital staff who were in close contact with patients with poliomyelitis who had been admitted from the city. On the other hand the clinical evidence suggests that the illness among the staff was different. In the Coventry
Hospital10, the disorder may have reached the staff by way of the patients. Galpine and Bradley32 were of the opinion that some of the cases admitted immediately prior to the outbreak in the staff in Coventry were not poliomyelitis but an illness identical with that which affected the staff. In the remaining five institutional outbreaks there is no evidence that nurses were infected by patients. Spread in the reverse direction (nurses to patients) has either been extremely uncommon12,15 or absent.
Observations concerning the possible mode of spread are available in nine outbreaks. In eight there is good reason to suppose that the agent responsible was not food- or water-borne. The distribution of cases did not correspond with any source of water or food. In the Iceland outbreak spread occurred along the main traffic route from Akureyri. Instances of spread by personal contact have been recorded8,13,27 and most authors agree that this is the probable means of dissemination. The best authenticated example is cited by Crowley27. A nurse who had attended the first and fourth girls to fall sick in the Royal Free Hospital epidemic became ill six days later. During the incubation period “she had accompanied a surgical case from ward to operating theatre, remained in attendance during the operation, and escorted the case to bed in a different ward. The patient,
the ward sister, the theatre sister, a medical officer, a medical student working in the theatre and the second ward sister all became ill within eight days.” In the Bethesda outbreak15 the discovery of a paracolon organism in the stools of a large proportion of the affected nurses and in a kitchen attendant focussed attention on the possibility of food- borne infection. However, only one doubtful case developed among the patients who were also supplied with food from the same source. The world-wide distribution of the outbreaks (Fig. 1) together with the marked differences in the types of community affected are points against either an insect vector or a toxic agent, both of which have been sought without success.
The Clinical Syndrome Variously Called Benign Myalgic Encephalomyelitis, Iceland Disease and Epidemic Neuromyasthenia, E.D. Acheson, 1959
 

lansbergen

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http://www.cell.com/abstract/S0092-8674(09)00783-1

Redefining Chronic Viral Infection

Herbert W. Virgin1, E. John Wherry2 and Rafi Ahmed3.

1 Department of Pathology and Immunology, Department of Molecular Microbiology, and the Midwest Regional Center for Excellence in Biodefense and Emerging Infectious Diseases, Washington University School of Medicine, St. Louis, MO 63110, USA
2 Immunology Program, The Wistar Institute, Philadelphia, PA 19104, USA
3 Emory Vaccine Center and Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322, USA

Summary

Viruses that cause chronic infection constitute a stable but little-recognized part of our metagenome: our virome. Ongoing immune responses hold these chronic viruses at bay while avoiding immunopathologic damage to persistently infected tissues. The immunologic imprint generated by these responses to our virome defines the normal immune system. The resulting dynamic but metastable equilibrium between the virome and the host can be dangerous, benign, or even symbiotic. These concepts require that we reformulate how we assign etiologies for diseases, especially those with a chronic inflammatory component, as well as how we design and interpret genome-wide association studies, and how we vaccinate to limit or control our virome.
 
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THere is a big difference between getting an infection and coming down with something and being an infectious disorder. If ME was an infectious disorder it would predominantly show up in the family members, sexual contacts of people ME patients were in contact with - depending on the route of transmission..
What evidence is there that it isn't commoner in sexual contects? I'm not aware of any. I saw something in Straus' book about it - while I didn't do the math, the sample size was pathetic.

Also, it is not absolutely necessary that CFS be more common in sexual contacts if it is caused by sexually-trasmitted XMRV. It is possible that everyone is exposed "equally" in a functional sense - that is, it is possible that everyone is exposed beyond the point of "saturation" - and only some people are suceptible.