Help, still confused about the # of healthy positives, please explain

[leaves]

The healthy controls were tested for antibody and came up negative.

Yes but as the post of busybee suggested, this happened Also to cfs patients that were in fact infected with xmrv

 

[acer2000]

Yeah and it appears they only tested 7 of the 218 controls for antibodies. (If the 7 they refer to were part of the original 218 controls - probably a safe assumption to make). Thats not a very big data set. I wonder if, after the paper was published, they went on to test the other 211 controls in that cohort and if the number went up. Also, did the controls who tested negative by antibody overlap with the 8 who tested positive by PCR? Or were they people who also tested negative by PCR?

NEED CHART

 

[busybee]

I understood George to mean the XMRV positive controls (from the PCR) were not included in the test for antibodies.

IE the control group were either positive XMRV using PCR or not at all.

Bx

 

[kurt]

I'm the opposite. I don't want to believe that ME/CFS is caused by a retrovirus. Unfortunately up till now I haven't seen any convincing evidence to the contrary.

The evidence we have is interesting, but far from conclusive. Until there are multiple replication and validation studies and a scientific consensus emerges we will not really know. WPI will not have the last word on XMRV, that is the job of outside researchers, and even Mikovitz repeats that this is only a hypothesis, and XMRV might be a passenger virus.

The healthy controls were tested for antibody and came up negative.

Where is that stated? I have looked for that and can not find a statement that controls were tested for MuLV antibody.

 

[usedtobeperkytina]

I think that even if the virus is found more in healthy people, and I actually suspect it is, the difference in the ability to find it, as evidenced by the 67% contrast to 4%, might reflect that CFS is caused by the virus.

Remember, HTLV (don't remember the number) can be in many people and only cause illness in very few.

The amount of the activity of the virus might make it more detectable and the level of illness might also match the amount of activity. So therefore, even if it is in 50% of healthy people, it can still be causing CFS.

Tina

 

[kurt]

I think that even if the virus is found more in healthy people, and I actually suspect it is, the difference in the ability to find it, as evidenced by the 67% contrast to 4%, might reflect that CFS is caused by the virus.

Remember, HTLV (don't remember the number) can be in many people and only cause illness in very few.

The amount of the activity of the virus might make it more detectable and the level of illness might also match the amount of activity. So therefore, even if it is in 50% of healthy people, it can still be causing CFS.

Tina

Certainly, this is possible. However, even if XMRV is in 100% of PWC, it can also still be a passenger virus, present due to a weak NK function. My point is just that we do not know at this time. The evidence does not yet support one conclusion over another, this is still a hypothesis.

There must be something wrong with the immune system to explain the problems managing viral load. And maybe a retrovirus, either a HERV or a novel retrovirus. WPI could be right about XMRV, but I think they made their case too assertively. Think about this, XMRV does not cause CFS in prostate cancer. And in other diseases a weak NK function (such as sJRA) does not cause CFS. This is a pretty complex illness, involving more than just a bad NK function.

 

[Julia Rachel]

Hi Leaves:
Honestly, after talking to many people across the U.S. and Abroad...I don't think there is enough information to determine any % of sick or infected at this point. We are at "C" on the A-Z Scale. More testing, more research and more studies need to occur before any solid information is disseminated. It is my impression of the translation, that in a healthy control group, 3.7% of the healthy folks have XMRV and 96.3% DO NOT HAVE THIS. So No....not everyone has a retro-virus, not at least anyway!
Blessings,
Julia

 

[usedtobeperkytina]

I agree there is another factor, besides just the virus. Mikovitz said the "turn on" triggers cause XMRV to replicate, and if it happens enough, whether in one incident or multiple ones over many years, at some point, XMRV wins over the immune system, causing the illness (theory).

So that would explain why some people have the virus, but no illness. And this is still logical if someone has low NK cells for another reason, but no CFS. And it fits with XMRV being in prostate cancer cells, but no CFS. Isn't this like HIV, where viral load is the measuring rod to determine if someone is about to come down with AIDS?

Kurt, I am going to plead ignorance here. I don't understand how a retrovirus can be a passenger virus. I mean, it does replicate, it does infect, it does kill immune system cells (which is what is part of CFS), and it is found much more in CFS than healthy controls. Now, I know this has to be verified, but so far, WPI research stands without legitimate challenge. (IC don't count, their study was nothing like WPI's.) Now, do passenger retroviruses occur in diseased people more than healthy controls and not contribute to the disease? I mean, I guess I can understand other viruses acting like that, such as herpes, etc. And I know some retroviruses are benign and endogenous. But do they occur at a higher level in disease people?

I think retroviruses are different in the way they go into the cells and become part of the DNA. And, benign endogenous viruses are not infectious, are they?

So are you saying there is a defect that makes someone more susceptible to infection when exposed to XMRV? And the defect is CFS, so the XMRV is opportunistic. Well, then why do 3.7% of healthy controls have XMRV?

I just think the evidence is really falling in line that XMRV is very similar to HIV. But, difference being it can go dormant and be turned on. The way you can have it, but not show symptoms, the way it attacks immune system, the way that you can gradually get sick or suddenly get sick was explained in the Jan. 22 meeting and fits with ultimate downfall when the viral load gets high enough.

This just seems to be such a repeat of HIV.

Tina

 

[garcia]

However, even if XMRV is in 100% of PWC, it can also still be a passenger virus, present due to a weak NK function. My point is just that we do not know at this time. The evidence does not yet support one conclusion over another, this is still a hypothesis.

I disagree. If it is in 100% of PWC and a lot less than 100% of healthy people, and it's an exogenous retrovirus then it's almost certainly causal. As Judy Mikovits said in her talk:

Retroviruses don't infect people differently (Q&A session 31:45)

I agree it's still a hypothesis, but in science everything is a hypothesis, a best-guess based on current knowledge waiting to be falsified.

 

[garcia]

Yeah and it appears they only tested 7 of the 218 controls for antibodies.

Asus, do you have a source for this - that it was only 7 of the controls they tested for antibodies?

(If the 7 they refer to were part of the original 218 controls - probably a safe assumption to make). Thats not a very big data set. I wonder if, after the paper was published, they went on to test the other 211 controls in that cohort and if the number went up. Also, did the controls who tested negative by antibody overlap with the 8 who tested positive by PCR? Or were they people who also tested negative by PCR?

NEED CHART

I'm guessing they only tested the control PCR-negatives for antibodies as in the people with CFS.

 

[usedtobeperkytina]

And all human infectious retroviruses discovered so far cause disease.

 

[garcia]

Where is that stated? I have looked for that and can not find a statement that controls were tested for MuLV antibody.

You are right. My apologies. I re-watched the whole lecture. At 37:00 Judy Mikovits talks about testing antibodies on healthy controls, but she is talking about antibodies used to detect viral proteins not endogenously produced antibodies.

 

[acer2000]

We next investigated whether XMRV stimulates an immune response in CFS patients. For this purpose, we developed a flow cytometry assay that allowed us to detect antibodies to XMRV Env by exploiting its close homology to SFFV Env (16). Plasma from 9 out of 18 CFS patients infected with XMRV reacted with a mouse B cell line expressing recombinant SFFV Env (BaF3ER-SFFV-Env) but not to SFFV Env negative control cells (BaF3ER), analogous to the binding of the SFFV Env mAb to these cells (Fig. 4D and S6A). In contrast, plasma from seven healthy donors did not react (Fig. 4D and fig. S6A). Furthermore, all nine positive plasma samples from CFS patients but none of the plasma samples from healthy donors blocked the binding of the SFFV Env mAb to SFFV Env on the cell surface (fig. S6B). These results are consistent with the hypothesis that CFS patients mount a specific immune response to XMRV.

This is quoted from the actual paper, second page, right coloumn about half way down. What I read from that is, of 18 CFS patients "infected with XMRV" (which I took to mean PCR positive by their first method - 67/101) nine of them showed an antibody response when their plasma was put in a test tube with a mouse B cell line expressing what appears to be a protien that they think is similar to XMRV env. ie the human plasma contained antibodies that already knew about XMRV env (or close enough). They say "the plasma from 7 healthy donors did not react". I am not clear which 7 healthy donors they are talking about. I guess you can assume they are 7 of the 218 controls and that they are not part of the 3.7% controls that tested positive (but were not sick).

I guess my point is that it could be more clear.

 

[leaves]

Right! But these healthy donors were tested only through pcr. AND some cfsers with positive xmrv through pcr still tested negative with the antibody test. As we know now pcr is not a reliable method to identify xmrv. I myself tested negative for pcr but positive for culture. My point is that infected people may still be negative for pcr and antibodies I.e. The healthy people may all be xmrv infected. Hmmm I hope this explanation will be ruled out in the near future.

 

[garcia]

My point is that infected people may still be negative for pcr and antibodies I.e. The healthy people may all be xmrv infected. Hmmm I hope this explanation will be ruled out in the near future.

They have tested (a different set of) controls for viral proteins and 0 out of 70 have come up positive so far (Judy Mikovits Prohealth talk 37:00).

You are right though, healthy controls need to have these other tests done on them to rule out the possibility they are carrying the virus.

The good news is this should be pretty straight-forward to do.

 

[George]

Tail wags and big grins.

Good morning everybody, I've had a nasty of some sort and just been lurking for the last couple of weeks. I think the news about Dr. Reeves being reassigned to a more appropriate division just fixed me right up though. (big grins) I find myself feeling better today!
Reading through this thread I though I'd put my two cents in for what it's worth.

I think we may be beating a dead horse with the Science Study. That poor study was designed to do one thing which is to show that XMRV was infectious. That's it! The fact that the paper happened to use the patient cohort that is most affected by this retrovirus is more coincident, divine providence, serendipity, blind luck or what ever you might want to call it than anything else.

The Science study was about lighting a fire under the Retroviral research community that this virus was a threat. It was designed to create a sensation and avalanche of interest a Tsunami, a tidal wave within the research community. And it's done a great job of that and we are incredibly luck to be in the center of that storm.

What the Science paper is not however, is all the things that we would LIKE it to be. (big grins) The first three months I pored over that paper line by line. I was obsessed. Finally at some point I'm not sure when, I realized that it just didn't contain the answers, just questions for other researchers to answer.

I've seen the criticism's of the paper on this and other boards, why didn't they do the study blind, why didn't they use a larger group here or more there or run this this way. (grins) Because they couldn't, Because one paper can't be everything to everybody, no matter how much we want it to be. We have suffered so long and are so desperate and hungry for answers that we keeping beating the only thing we have to beat, the one Science study. (smilies)

So Leaves my answer to your question on what is the prevalence of XMRV in the healthy population is . . . Nobody really knows. . .yet (big grins and a tail wag)

I think Aftermath said it best -hang in there guys, it's coming-

 

[Hysterical Woman]

Hi George,

Good assessment. Love the comment about hang in there, it's coming. Also, wasn't it Dr. Coffin who said it was an excellent first paper?

So many of as are beyond desperate. I am closing in on two decades of this illness and others out there have been much longer with it! We want our lives back (regardless of what some psychiatrists say). I personally (and suspect all of you) do not have a fear of exercise, my life was very nice before, thank you very much. I have searched every inch of my psyche and for the life of me, I can't find the tiniest bit of evidence that I "get something" from this illness.

In the meantime, I am incredibly grateful to this list for the sharing of information, support, smiles, and doggie wags and grins.

Take care,

HW

 

[leaves]

I totally agree with this assesment. Please note that my post was NOT intended to criticise the paper. It was a genuine question for information asked to prevent myself from getting carried away. All your replies have been very useful; know I know that conform my suspicion the causality is not sufficiently proven for me to wholeheartedly accept the xmrv hypothsis. Thanks all.

 

[usedtobeperkytina]

Agreed, although I would say it not only was to show infectious nature, but "connection" with CFS patients. Which means it is possible it has a role in the pathogenesis of the illness.

Mikovitz said they had to reword it three times to get it approval, the part about role in pathogenesis. They ended with the word "significant".

And to me, that is why I trust this study so. Three labs and strongest scrutiny by Science editors and reviewers. (Take that Reeves and IC).

Many theories come from this study, which leads to studies needed to find whether the theories are true. One is the percentage in population. As Mikovitz said, it can be regional. The other retrovirus she knows well (not HIV) is regional. The question, in today's travel over borders, why would a retrovirus be more common in certain areas? One answer could be that an environmental factor activates the virus in certain geographical areas, and a virus is more likely to be transmitted in the active stage. I think it was one of the HTLV viruses she was showing is much more common, or was it the illness caused by that virus, in Japan.

The fact that the WPI brings up more questions than answers is why the research community is so interested. There is much more to discover, including how much it is in the healthy population.

I know many are just wanting treatment now. But I for one am glad to ride this ride. I think it is like getting many, many, many, many gifts instead of just one big one.

Tina

 

[julius]

posted by George
"Reading through this thread I though I'd put my two cents in for what it's worth. "

Well, it's worth 2.17 cents Canadian.


But it's worth a whole lot more to me.

Welcome back...good boy....and this time....sit and stay.