Discussion in 'Phoenix Rising Articles' started by Phoenix Rising Team, May 24, 2010.
If they have active EBV infection by definition they cant be CFS patients
Active epstein barr infection is an exclusion factor under fukuda. Chronic epstein barr infection is largely asymptomatic.there are only two kinds of epstein Barr infection acute and chronic .
Epstein-Barr virus syndrome
In the early 1980s, patients with symptoms including fatigue, muscle pain, and depression were often diagnosed with chronic Epstein-Barr virus syndrome or chronic mononucleosis syndrome. [ 1 ] These patients had symptoms that suggested infection, such as low-grade fever, recurrent sore throat, and tender lymph nodes. Epstein-Barr virus (EBV), which causes acute mononucleosis, was considered a likely source. But researchers could not isolate EBV as the cause of the syndrome and, as yet, have not definitively identified any other infectious agents.
Nonpermissive Infection - Certain host cells may lack essential factors for viral replication or may repress certain viral functions. Such cells are called nonpermissive cells and do not support viral replication
Essentially this means that in some cells the virus enters the cell and cant make new particles and reproduce
Speaking only as someone who's had chronic Lyme + bartonella, babesiosis, both kinds of ehrlichiosis & viral reactivations of CMV & EBV, the following concerned me: "There were 106 CFS patients who had negative IgM and IgG serum antibody titers to B. burgdorferi by Western blot and ELISA test, with antistreptolysin 0 titers ,400 units, and negative serum IgM and IgG antibody titers to B. microti and A. phagocytophila. These patients were categorized as Group A CFS."
So if you made no antibodies against borrelia (as those w/HLA DR1 may not), or against b.microti (again some produce no antibodies, plus other strains exist such as b.duncani, etc) you were put into a CFS group? No PCR or culture done for borrelia, no FISH for babesia of any kind?
"An additional 36 CFS patients had elevated serum antibody titers to B. burgdorferi, B. microti, A. phagocytophila, or antistreptolysin 0 . 400, and comprised Group B CFS."
What am I missing or otherwise not understanding? This is why it's so important to understand study design - in order to determine confidence level in the results... I'm not criticizing Lerner - just trying to understand logic in inclusion criteria...
btw, in addition to antibiotics & antiparasitics, I also took Valtrex during my treatment & both the EBV & CMV calmed back down nicely (tho I can occasionally feel EBV acting up).
There are cells which are non permissive for EBV which are mainly epithelial.There are only two kinds of EBV infection .They are active and Latent.Active is an exclusion criteria and latent is mostly asymptomatic.
Re: why common latent infections reactivate in us (from Chia)"...during and after an initial infection, viruses often hide in our bodies by manipulating our Immune Systems and vulnerable cells. Research has demonstarted the presence of stable viral Genome on cells long after the initial infection - but the "True Viral Particle" is difficult to isolate. Once viral persistence is established and protected by our own cells, the Immune Response can only react to these Viral Particles with futility causing continuing or cyclical symptoms of me/cfs (virus "hide and seek"!)
(Also, Herpes 1&2, Chickenpox, EBV, CMV and HHV-6 are known to survive in our bodies - sometimes DESPITE a good immune response...as they don't kill their cell hosts. Our own cells actually protect them from the attack of the "Immune Response".
Ex: from the start of a virus infection, the Immune System fails to kill off the infected cells. Afterwards, the Immune Systems efforts are useless in destroying the virus and unintentionally continuing the flu-like symptoms. Periodically, the virus load in the cells will decrease as a resut of the immune response...you feel better for a few days or so, since the immune response subsides. Then, the virus grows back (like garden weeds) and the immune system reacts again. Since many infections behave this way, AV treatment should be/may need to be taken for years. (When you keep getting sick this may not be a new infection, but a relapse of the same infection when the th2 immune response is shifted to the th1 direction. Virus infecton is fought with the th2 response...the th1 side is sifted downward and the virus survives the immune attack and persists in the body.") Right? Makes perfect sense to me! ha! does this answer the question...or did I lose the question in looking for the answer? j
A nonpermissive infection seems to be a middle-ground between latent and active. Anyway, even a latent herpes infection can alter gene expression, and these are smart viruses. CMV is the largest virus known, producing 230 viral proteins. If that is a nonpermissive infection then it is partly active and some of those proteins are probably being produced. Also, again, it alters immune genes and down-regulates immune response even when latent.
Personally I think there has to be some genetic or pre-existing co-infection vulnerability in the CFS population if Learner is right, otherwise everyone carrying these viruses in latent form would get sick.
I'm curious. I this the good news you said a few days ago that was coming this week, or do we have something else good to look forward to?
There have been several rumors back-channel and to be honest it is hard to know right now exactly when we will see the reports, if not this week then hopefully at least over the next one or two.
The Learner study is certainly good news for people who test positive on the indicated herpes tests.
This study looked at activity of HCMV during the latent stage. Just an interesting point of reference, if Learner if finding nonpermissive infections (or theorizes that is what he sees), then that goes beyond the latent stage. But what strikes me from this study (below) is that if one herpes virus in LATENT stage can manipulate the immune system to allow it to persist, then is that like opening a door to other infections? What else will that immune manipulation allow to proliferate?
Then I must be misunderstanding the text of the Fukuda definition:
"Tests should be directed toward confirming or excluding other etiologic possibilities. Examples of specific tests that do not confirm or exclude the diagnosis of the chronic fatigue syndrome include serologic tests for Epstein-Barr virus, retroviruses, human herpesvirus 6, enteroviruses, and Candida albicans; tests of immunologic function, including cell population and function studies; and imaging studies, including magnetic resonance imaging scans and radionuclide scans (such as single-photon emission computed tomography and posi-tron emission tomography) of the head."
i,m afraid that you are epstein barr infection is a known medical cause for fatigue .
That is not true. Almost everyone with EBV is asymptomatic. That leaves two possible diagnoses, 1. infectious mononucleosis (glandular fever) or 2. CFS. There is no such diagnosis as "fatigue caused by chronic EBV."
Active epstein barr infection is a known cause of fatigue.Active epstein barr infection mirrors CFS but does not cause it
There are many good clues to that difference. Most CFS patients are pathological detoxifiers, for example. And we have a host of gene abnormalities including immune, adrenal, methylation, etc. Full genomic profiling is becoming less an less expensive, one company says they will have a $100 full genomic profile test by the end of the year. That is the entire human genome for a given patient. I think the answers are coming.
I think Gerwyn is talking about mono, which is not CFS, people get over mono. But a certain percent does go on to acquire CFS so even if not a cause it can be a trigger for CFS.
however, Learner looked at other herpes viruses as well, and at multiple herpes, co-infections, etc. His argument is not reliant only on EBV.
There is no such thing apart from mononucleosis/glandular fever, which is not what these patients had.
lucky for us...sickofcfs, we finally have some good docs who are trying to find the answer to that queston...and they will. (imo...it's genetic) and as long as nobody comes along to tell me that I DON't really have me/cfs...I'll be just fine. jackie
That didn't really address my question, but others have answered it.
We dont know what the patients had.Learner chose to measure IgG levels with all the viruses save EBV.He considered EBV to be active if IGm levels were raised
Patients were evaluated by EIPS with consensus of
physician and patient. An EIPS of 05 is diagnostic of CFS.
At EIPS values 610, patients no longer have CFS. An effect
size of 0.8 is significant. A CFS patient was considered a
responder to antiviral treatment if the change in EIPS effect
size was 1. A CFS patient was considered a nonresponder
to antiviral treatment if the effect size was ,1 (Figure 2).
someone was a responder if the change in the Eips scale was as little as one.The dianosis of CFS was based on the Eips scale value which was agreed with the patient less than 5 is cfs. More than 5 not CFS. I really dont see how things could be made more subjective.If they had a certain level of disability then they had CFS. That is not a diagnostic method that is used by anyone else that I have ever heard of.Coupled with the lack of a placebo where self limiting infections are involved and unequal numbers in group B(with much higher overt pathology) I,m not realy suprised that it took two years from initial presentation (2008) to publication.Jason told us that Fukuda itself is a highly unreliable tool for diagosing ME/cfs.In my view diagnosing ME,cfs in this manner adds a whole new dimension to this unreliability. I am also concerned that the study was published in a journal owned by one of the researchers.The peer review process of this journal is the subject of controversy to put it mildly.If people find antiviral therapy useful then i am really glad.There are however a number of reasons for that.
If the viruses in question are active(raised IgG) when normally latent then something has brought them out of latency.We dont know if the EBV was active because the IgG level was not measured.I agree that active viruses need to be treated as co pathogens and hopefully people will feel better as a result.That does not mean that these pathogens are in any way causative.the last data I read said that about 90% of Americans had been exposed to cyclomegalovirus.that makes the 4% of XMRV paltry in comparison.
indicates that you can have positive EBV, retroviral, HHV-6, enteroviral and Candida tests and still fit the definition of CFS - which is a good thing because a considerable portion of patients do have positive test results.
I don't understand the focus on diagnosis - there was little focus on diagnosis in this paper; the focus was on the average 2+ mean increased rate of progress according to the EPIS scale. The question of where Dr. Lerner places a diagnosis of CFS on his scale really has very little bearing on the outcome of the study.
I don't see how the criteria for who's a responder matters either. The responders made up 75% of the patients - it was a large group of people. What matters to me is that those people moved up the scale rather dramatically - they improved greatly.
I don't know if Dr. Lerner cares if EBV is 'active' in the sense that you mean. If he cared about that - if his years of studying these patients had indicated that traditional measures of EBV activity was the pertinent he would have measured it - but that's not what he found. He found other measures were important and those were the ones he used. The scientific community was all over 'active' EBV at one time - it doesn't appear to make a difference in CFS.
Most people have been exposed to EBV, HHV6 and CMV. The question here is do they have the kind of nonpermissive infection that Dr. Lerner has found in these patients and if they do - how important is it to their health.
You can also try a Google Site Search
Separate names with a comma.