A Comparison of Immune Functionality in Viral versus Non-Viral CFS Subtype

[lansbergen]

http://www.strose.edu/academics/aca...roscienceresearch/journalcontents/article3814

A Comparison of Immune Functionality in Viral versus Non-Viral CFS Subtypes

Nicole Porter1*, Athena Lerch1, Leonard A. Jason1, Matthew Sorenson1, Mary Ann Fletcher2, and Joshua Herrington1

1DePaul University and 2University of Miami

Participants with CFS were grouped into viral and non-viral onset fatigue categories and assessed for differential immunological marker expression. Peripheral Blood Mononuclear Cells were assessed for differential phenotypic expression of surface adherence glycoproteins on circulating lymphocytes. The flow cytometric analysis employed fluorescent monoclonal antibody labeling. The viral in comparison to the non-viral group demonstrated significant elevations in several Th1 type subsets including: the percentage and number of CD4+ cells, the percentage and number of CD2+CD26+ cells, the percentage and number of CD2+CD4+CD26+ cells, the percentage and number of CD4+ CD26+ cells, and the percentage of Th2 nave cells (CD4+ CD45RA+CD62L+). Of the remaining significant findings, the non viral group demonstrated significant elevations in comparison to the viral group for the following Th1 type subsets: the percentage of CD8+ cells, the percentage of T-cytotoxic suppressor cells (CD3+8+), and the percentage and number of Th1 memory cells (CD8+CD45RA-CD62L-). The viral group demonstrated a pattern of activation that differed from that of the group with a non-viral etiology, as evidenced by an elevated and out of range percentage and number of CD4+ cells, the percentage of CD2+CD26+, and the percentage of Th2 nave cells (CD4+CD45RA+CD62L+). Both groups demonstrated reduced and out of range Natural Killer Cell Cytotoxicity and percentage of B-1 cells (CD5+CD19). In addition, both groups demonstrated an elevated and out of range percentage of CD2+CD8+CD26+, percentage of the Th1 memory subset (CD4+CD45RA-CD62L-), the percentage of Th1 memory and nave cells (CD8+CD45RA-CD62L-, CD8+CD45RA+CD62L-), the percentage and number of Th2 memory cells (CD4+CD45RA-CD62L+), and the percentage of Th2 memory and nave cells (CD8+CD45RA-CD62L+, CD8+CD45RA+CD62L+). These findings imply that the homeostatic mechanism responsible for the regulation of the Th1 (cell mediated) and Th2 (humoral) immune responses is disturbed in CFS. The implications of these findings are discussed

 

[free at last]

Thank you for posting this

Wish i understood what all this means,. Im so very careful not to pick up viruses, from people, never going out during winter, and catching viruses from familily members, that one wonders how symptoms would flare. living a life like that. But this really grabbed my attention, ive noticed often during crashes that i get ( embarresing but here goes ) very bad breath, that seems to come from the stomach. and with genreal upstet stomach during this period. ( Times that i would often eat Raw garlic and salads ) this pattern has been consistent over the years. so reading this part suddenly made sense to me, in a situation with immune problems right from the begining
qoute
2005). Reductions in the CD5+CD19+ subset in both groups is also suggestive of compromised integrity of the stomach/ intestinal tract and increased susceptibility to bacterial infection, which may contribute to the maintenance of symptoms
MY god i always wondered why i had the stomach involvment, and very bad breath during times of crashes. in the abcence of viruses affecting my health, it seems bacteria in the stomach can also produce symptoms. so no matter how careful one becomes to avoid viruses, ( trust me im like howard huges ) bacteria in the stomach will still produce symptoms, when the immune system clears these bacteria, symptoms start to subside, and the bad breath dissapears. usually between 2 and 3 days. I also wonder that continued improvement over the years, may be possibly linked to my obsessive avoidence of viruses continually washing my hands,avoiding people ( crowds ect ) .But the maintence of symptoms can not ever be truely stopped because of the bacteria problem. I also feel sure the bacteria problem is producing less severe crashes, than those that happen from viruses. as evidenced by my history. im really not sure of any of this. ( some may say to me it doesnt work like that ) and if so. then sorry for babbling, but im hoping someone will say yes it makes sense. As surely it does for others here. ? anyone ?

 

[George]

Great find Lansbergen! I was surprised to see the nod to the Reeves criteria but they look like they had a good group of patients to work with. I really think that when it comes down to it, it's all about the inflammation.

 

[Snow Leopard]

This is exactly the same type of probing for subtypes that should have been done 20 years ago.

 

[OverTheHills]

Now that we have a proven difference between patients with viral & non-viral onset and ME vs ME + fibromyalgia (the graphs looked different on the Light presentation) whose job is it to influence researchers to use these subsets in future research? Is it the iacfs/me???? I don't think we need to look to the CDC to do anything useful.

OTH

 

[Glynis Steele]

Hi Free,

This may not be relevant, but (and I'm sorry for this ) I tend to babble out d-lactic acid to anyone whose symptoms "might" match. If you click on my profile, you can view my posts. Dla lasts about 72 hours, which is 3 days, when carb intake is suspended. Dla is being investigated as a research study in CFS patients. Please feel free to write, if you want more info, or read my post's, where I have written and sent links regarding dla. It is usually seen in short bowel patients, but just yesterday I managed to snaffle a case study on a boy with an intact bowel, but with a known carb malabsorption problem who developed dla. I spoke to a gentleman from ME Research UK about the XMRV link to CFS and he told me that the inflammatory markers they had found could just as easily come from a bacterial source - all that was confirmed was that CFS patients had inflammatory markers.

Paul Gooley a biochemist is following up on the CFS/DLA study, but I don't know how far the study has progressed. Dla does not show up in routine blood testing, and needs a specific d-lactate assay kit bought in, to test for. I think it can be tested for in urine, but don't know how this works. Dla should not be found in a healthy human, or in minute amounts 0.0-0.25 being normal.

I have found 2 posts which state the CFS patient had tested positive for dla, one stated her level was 2.4, which is way too high, and would cause dla symptoms, which are very similar to CFS symptoms, somnolence, change in gait, feeling of being drunk and othe symptoms.

Hope this helps.

Glynis

 

[Glynis Steele]

Oh, and you might want to check out the Dr Logan interview's on The Gut section. I know high lactate levels have been discussed as part of CFS, and I know L-lactate and D-lactate cross-inhibit each other's metabolism, so high l-lactate might mean that d-lactate will not be metabolized, leading to state where there is raised d-lactate, if that makes sense.

Glynis

 

[Sasha]

I've always been surprised by studies not stratifying by acute viral onset vs not. It has always seemed such an obviously potentially important distinction.

 

[Berthe]

Hi Lansbergen, perhaps you can explain me something.
Viral and non-viral onset of fatigue. Do they mean people with the virus and people without the virus? Or do they mean the division between the cause of the fatigue. I personally think that people who carry the virus can also experience an onset of the virus through different causes. Perhaps an accident, a stroke, a trauma or sugery. Biomedically it's plausible that the virus activates after very stressful events. Can you help me out here?

Love,
Berthe

http://www.onwilliglichaam.blogspot.com

 

[lansbergen]

Hi Lansbergen, perhaps you can explain me something.
Viral and non-viral onset of fatigue. Do they mean people with the virus and people without the virus? Or do they mean the division between the cause of the fatigue. I personally think that people who carry the virus can also experience an onset of the virus through different causes. Perhaps an accident, a stroke, a trauma or sugery. Biomedically it's plausible that the virus activates after very stressful events. Can you help me out here? Love, Berthe

Quote from the paper.

Participants were assigned to either the viral or non-viral onset subgroups based on self reported illness phenotypes, or indication that their CFS onset occurred due to a viral illness.

No mention of XMRV/MLV.

 

[free at last]

Hi Free,

This may not be relevant, but (and I'm sorry for this ) I tend to babble out d-lactic acid to anyone whose symptoms "might" match. If you click on my profile, you can view my posts. Dla lasts about 72 hours, which is 3 days, when carb intake is suspended. Dla is being investigated as a research study in CFS patients. Please feel free to write, if you want more info, or read my post's, where I have written and sent links regarding dla. It is usually seen in short bowel patients, but just yesterday I managed to snaffle a case study on a boy with an intact bowel, but with a known carb malabsorption problem who developed dla. I spoke to a gentleman from ME Research UK about the XMRV link to CFS and he told me that the inflammatory markers they had found could just as easily come from a bacterial source - all that was confirmed was that CFS patients had inflammatory markers.

Paul Gooley a biochemist is following up on the CFS/DLA study, but I don't know how far the study has progressed. Dla does not show up in routine blood testing, and needs a specific d-lactate assay kit bought in, to test for. I think it can be tested for in urine, but don't know how this works. Dla should not be found in a healthy human, or in minute amounts 0.0-0.25 being normal.

I have found 2 posts which state the CFS patient had tested positive for dla, one stated her level was 2.4, which is way too high, and would cause dla symptoms, which are very similar to CFS symptoms, somnolence, change in gait, feeling of being drunk and othe symptoms.


Hope this helps.
Glynis

Hi Glynis many thanks for taking the trouble to explain this, I have always had stomach involment, but its something ive tended to ignore. reason being, is the illness clearly started with frequent viral onset, and i know the immune system was heavily involved. So i tended to ignore this side of the picture. I have been looking at some of your links, and a lot does add up, many of the symptoms do. However im wondering about specific causes for conditions of fermentation and bacteria growth, other than short bowel. As a model i have been thinking about HIV paitents, and the possibilltie that the immune system, also could to a degree regulate fermentation in high carb diets. Im wondering if dysregulation of the immune system like in HIV or XNRV could cause similair problems of fermentation with bacterial growth to occur. i may google HIV gut fermentation bacterial overgrowth ( or something similair ) and see what i learn. A lot just seems to make sense in the abcesnse of virall illness, bacterial toxin and acid effects could really take over where viral symptoms leave off. so again im very interested in learning more about all this. Thank you for your information. there really could be a lot more to what your saying than a lot of people might accept. And i think a lot ( symptoms included ) does seem to fit quite well. if i learn anything about gut fermentation bacterial growth in HIV patients ( as a model for xmrv ) then ill post up. Interesting for all of us i hope. Which is one reason why sometimes it is worth mentioning our conditions, to compare knowledge to learn more.

 

[free at last]

Using HIV as a model for xmrv is obviously on shakey ground, but still possibly enlightening.

as maybe shown here
qoute

The etiology of malnutrition in HIV-1 individuals is multifactorial; however, the causal factors can be categorized as: change in food intake, malabsorption and metabolic alterations (4, 18, 47). These factors, therefore, can contribute to changes in the normal intestinal bacterial flora, since the gastrointestinal tract is one of the biggest targets of diseases related to HIV-1 infection, favoring the occurrence of diarrhea and malabsorption (21, 49).

the full link is here if anyone is interested, i will add more if i find out anything interesting
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1678-91992007000200003

 

[Glynis Steele]

Hi Free at last,

Wow, I have often wondered myself if a viral problem could dis-regulate normal bacterial flora, so I find this very exciting! Thank you for so much for posting. My daughter has autistic trait's (without an autism diagnosis, long story ) and though her problems started way before her MMR, probably shortly after birth, I believe that for some autistic children, having the MMR may have kicked off a change in their gut flora. I believe CFS and autism are closely connected, they both respond to certain dietary changes such as gluten free, casein free, low carb, low oxolate, soya free. Maybe the gut changes occur as a consequence of a virus, in both CFS and autism.

Thanks again for the post, I look forward to seeing if you find out anything else, and I'll let you know if I do!

Best Wishes

Glynis

 

[Dolphin]

FWIW, for those calling for stratification/subgrouping:

Stratification using biological factors should be performed in more CFS studies.

Kindlon T.

Psychol Med. 2010 Feb;40(2):352. Epub 2009 Oct 12.