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One more reason to suspect viruses in CFS

Discussion in 'Other Health News and Research' started by guest, Jul 25, 2010.

  1. guest

    guest Guest

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    HIV attacks the gastrointestinal tract.

    It really shocked when I read what influence HIV has on the gastrointestinal tract of humans. When not treated, this leads from diarrhea to pancreatic dysfunction and as a consequence to malabsorption and weight loss which in the end make it much riskier to die from a normal infection because the body has no more means to fight it off.
    What really gives me hope is that HAART (highly active anti-retroviral therapy) normalizes everything. All the HIV patients who have extreme gastrointestinal problems (including increased intestinal permeability) improve on treatment till the gastrointestinal tract normalizes completely (!). I cannot say for sure of course but to me it looks much like we suffer from a viral disease! So if XMRV or other viruses are the cause of CFS this would perfectly fit into the picture since many of us have gastrointestinal problems.

    Prof De Meirleir is using a test called "Immunobilan" which checks for IgAs and IgMs directed at intestinal bacteria. Positive results indicate a translocation of bacteria. The following study shows that this is also a problem with HIV:


    Exposure to HIV-1 directly impairs mucosal epithelial barrier integrity allowing microbial translocation.

    Collectively, our data shows that mucosal epithelial cells respond directly to envelope glycoprotein of HIV-1 by upregulating inflammatory cytokines that lead to impairment of barrier functions. The increased permeability could be responsible for small but significant crossing of mucosal epithelium by virus and bacteria present in the lumen of mucosa. This mechanism could be particularly relevant to mucosal transmission of HIV-1 as well as immune activation seen in HIV-1 infected individuals.
    PMID: 20386714


    Here are some more conclusions:

    CONCLUSIONS: Suppressive HAART abrogates HIV-induced intestinal barrier defect and villous atrophy. The HIV-induced barrier defect is due to altered tight junction protein composition and elevated epithelial apoptoses. Mucosal cytokines are mediators of the HIV-induced mucosal barrier defect and villous atrophy.
    PMID: 18936106


    The digestive-absorptive functions are impaired, with steatorrhea, nutrient malabsorption, and increased permeability occurring in 20-70% of children.
    PMID: 15612836


    CONCLUSIONS: Cell-cell interaction of HIV-infected macrophages with PBMC leads to a release of cytokines sufficient to alter intestinal epithelial barrier function. The main effect was mediated by TNFalpha inducing a leak-flux which may contribute to the diarrhoea by HIV per se (HIV-enteropathy).
    PMID: 11953464


    CONCLUSION: Because systemic exposure of oral ganciclovir (Valcyte) is enhanced in AIDS patients with diarrhea and wasting syndrome, oral ganciclovir therapy may benefit these patients.
    PMID: 11015151


    BACKGROUND: Impaired intestinal function could account for diarrhoea and weight loss, which are common features of advanced human immunodeficiency virus (HIV) infection.
    CONCLUSIONS: These findings suggest a loss of intestinal functional absorptive surface as HIV disease progresses. This process may be present at the early stage of infection. Impaired intestinal permeability is observed later in AIDS patients when digestive signs are present, particularly diarrhoea.
    PMID: 10048729


    Weight loss, the gut and the inflammatory response in aids patients.
    Stein TP, Koerner B, Schluter MD, Leskiw MJ, Gaprindachvilli T, Richards EW, Cope FO, Condolucci D.
    Department of Surgery, University of Medicine and Dentistry of New Jersey, School of Osteopathic Medicine, Stratford 08084, USA.
    Abstract
    The objective of this study was to test the hypothesis that the integrity of the large bowel wall in AIDS patients is compromised in a manner that favours the chronic translocation of bacteria and/or products of bacterial metabolism into the bloodstream. When such translocation occurs, it induces a characteristic stress/inflammatory response in the body. Urinary butyrate, a unique product of colonic microbial metabolism, was used to assess gut wall permeability. Excretion of the pro-inflammatory cytokine IL-6 in the urine was used as a marker for the stress/inflammatory response. Four groups of subjects were studied, controls (n = 12), HIV + (n = 35) and AIDS patients with (n = 14) and without (n = 17) weight loss. Results: measurable amounts of interleukin 6 (IL-6) and butyrate were found in the urine of all subjects. There were no significant differences in IL-6 excretion between the controls (0.68 +/- 0.64 pg/ml), asymptomatic HIV + subjects (0.59 +/- 0.37 pg/ml) and AIDS patients without weight loss (1.18 +/- 0.33 pg/ml) but IL-6 levels were significantly higher in the AIDS group with weight loss (4.02 +/- 1.26 pg/ml, P < 0.05). A similar pattern of results was found with interleukin 1 receptor antagonist (IL-1ra). Like IL-6 and (IL-1ra), urinary butyrate levels were increased in the AIDS patients with weight loss (2.83 +/- 0.67 mumol/l) relative to the controls (1.31 +/- 0.13 mumol/l, P < 0.05), with the HIV + patients (1.65 +/- 0.18 mumol/l) and AIDS patients without weight loss (1.90 +/- 0.22 mumol/l) falling in between. The data are consistent with a low, but chronic rate of bacteria and/or bacterial products seeping across a compromised colonic wall causing a chronic low stress response in AIDS patients.
    PMID: 9071566


    CONCLUSIONS: Patients with AIDS and diarrhea have altered intestinal permeability. The decreased absorption of mannitol suggests that the functional absorptive surface of the intestine decreases as HIV disease progresses.
    PMID: 8198098


    These data indicate that abnormal permeability and reduced intestinal absorption capacity are common in HIV patients, occur at all stages of HIV disease, especially in the presence of diarrhoea, and, with the exception of lactulose permeation, are relatively similar to the alterations seen in coeliac disease.
    PMID: 8362208


    Altered small-intestinal permeability is associated with symptomatic diarrhoea in human immunodeficiency virus infection in both Caucasian and African patients.
    PMID: 1655333


    Our results suggest that severe diarrhea may be uncommon in children with HIV infection receiving antimicrobial prophylaxis, but that the intestinal function is frequently, and often markedly, impaired.
    PMID: 1865278
     
  2. muffin

    muffin Senior Member

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    Yup, GI issues are a biggie with CFIDS people. Thought I was going to die from the spasms, etc. in the first few years. I got on Doxy for 6 months and that did clear up a lot of the 15 times a day to the powder room issue - Mycoplasma prob. was the issue there.

    Also, the very simple fact that many of us got sick after a virus is another really basic tell tale sign that this is a viral-based disease (or a big subset of it anyway). I knew after my husband and I got that virus and he recovered and I got sicker and sicker that there had to be at least one virus if not many more in my body and my body was fighting like crazy to get rid of them all. I had nightsweats that were like the AIDS people nightsweats -soaking wet body, bedsheets, clothing, etc. and then freezing afterwards. Morning wakeup temperatures between 85 degrees and 101 degrees and it varied from day to day. I usually ran a temp of about 100, not quite a full fever. That was more than enough evidence for me that I had some sort of viral implication and so I never kissed my baby niece on the face, never shared food/utensils/toothbrushes, etc. I still don't put my face near other's faces and I don't kiss people on the mouth or near their face. I KNEW I had something and was not going to give it to someone else - esp. my family due to the genetics that I and others believed way back 15 years ago.

    So, no one can tell me that viruses are not a big part of this disease. No one. The CDC and the UK can take their GET and CBT and put it where the sun don't shine.
     
  3. guest

    guest Guest

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    I agree completely.
     
  4. voner

    voner Senior Member

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    diesel & anyone else interested:

    here is a post over at the ProHealth site of an abstract by Dr. Kenny De Meirleir concerning the gut & XMRV & HIV similarities.. :

    http://www.prohealth.com/library/showarticle.cfm?libid=15624

    Is the mechanism of systemic immune activation in XMRV-positive CFS patients similar to that observed in HIV? Source: 1st International XMRV Workshop Abstract Book, Sep 2010


    here is a scary, but worth looking at, poster about HIV & the gut (17th Conference on Retroviruses and Opportunistic Infections):

    retroconference.org/2010/PDFs/303.pdf

    [I]Plasma Levels of Soluble CD14 Predict Mortality in HIV Infection[/I]

    Background:

    HIV infection causes increased intestinal permeability, microbial translocation and chronic systemic immune activation. In order to define the long- term consequences of this process, we investigated the relationship of baseline biomarkers of microbial translocation with all-cause mortality.
    Methods: In the Strategies for Management of Antiretroviral Therapy (SMART) trial, patients with CD4+ T cell counts >350/mm3 were randomized to a viral suppression arm with continuous antiretroviral therapy (VS) or a drug conservation arm (DC) with episodic antiretroviral therapy (ART) based on CD4+ T cell count. Using stored baseline plasma specimens, a nested case-control study was performed for 74 of the 85 patients who died and had available plasma and 128 controls matched on age, country, sex, and enrollment date. Five biomarkers were studied: soluble CD14 (sCD14), endotoxin core antibody (EndoCAb), and intestinal fatty acid binding protein (I-FABP) were assessed by ELISA; lipopolysaccharide (LPS) by the limulus amebocyte lysate assay; and 16S ribosomal DNA (16S rDNA) by quantitative PCR. The association of each biomarker with mortality was assessed using conditional logistic regression by categorizing biomarkers into quartiles. Odds ratios (ORs) with 95% confidence intervals (CI) and p-values of each of the top three quartiles versus the lowest quartile were calculated.

    Results: Patients in the highest quartile of LPS bioactivity, with sCD14 levels >2.71x106 pg/ml, had an OR of death of 6.0 versus the lowest quartile with levels <2.01x106 pg/ml. Several adjustments performed for baseline covariates, including previously identified risk factors for death; CD4+ T cell count and HIV viral load; and interleukin-6, high sensitivity C-reactive protein, serum amyloid A, and D-dimer, did not substantially alter the associations. The association of sCD14 with death was similar for the DC and VS groups (ORs were 3.7 and 2.0, respectively; P=0.43 for the difference). Other markers were not significantly associated with death, although there was a trend towards increased mortality in patients with higher I-FABP levels (OR=1.9, 95% CI: 0.9-3.8, P=0.09).

    Conclusions: Among patients with HIV infection, greater monocyte responsiveness to LPS, exhibited by high sCD14 levels, is associated with all-cause mortality, but other biomarkers of microbial translocation are not related to all-cause mortality.


    comments? (the BOLD is put in by me!)

    also - sure wasn't much XMRV/MLV action at 17th (2010) Conference on Retroviruses and Opportunistic Infections!
     
  5. guest

    guest Guest

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    Thanks, Voner. Very interesting. It fits into the picture.
     

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