What is this page about?
ME / CEBVS→ PVFS→ CFIDS→ CFS→ SEID?
- ME - myalgic encephalomyelitis
- CEBVS - chronic Epstein-Barr virus syndrome
- PVFS - post-viral fatigue syndrome
- CFIDS - chronic fatigue immune dysfunction syndrome
- CFS - chronic fatigue syndrome
- SEID - systemic exertion intolerance disease
They keep using more and more vague wording to deny the root cause of this disease, immunosuppression with multiple, ongoing viral and bacterial opportunistic infections.
Index
PMID: 2824604
Phenotypic and functional deficiency of natural killer cells in patients with chronic fatigue syndrome.
When tested for cytotoxicity against a variety of different target cells, patients with CFS consistently demonstrated low levels of killing.
...
most patients remained unable to lyse Epstein-Barr virus-infected B cell targets.
http://pubmedhh.nlm.nih.gov/cgi-bin/abstract.cgi?id=2824604
Natural killer (NK)3 cells are large granular lymphocytes that appear to play a significant role in the host's defense against viral infection. We performed an extensive phenotypic and functional characterization of NK cells on 41 patients with the chronic fatigue syndrome (CFS), or "chronic active Epstein-Barr virus infection" syndrome, and on 23 age- and sex-matched asymptomatic control subjects in an attempt to further characterize this illness. These studies demonstrated that a majority of patients with CFS have low numbers of NKH1+T3- lymphocytes, a population that represents the great majority of NK cells in normal individuals. CFS patients had normal numbers of NKH1+T3+ lymphocytes, a population that represents a relatively small fraction of NK cells in normal individuals. When tested for cytotoxicity against a variety of different target cells, patients with CFS consistently demonstrated low levels of killing. After activation of cytolytic activity with recombinant interleukin 2, patients were able to display increased killing against K562 but most patients remained unable to lyse Epstein-Barr virus-infected B cell targets. Additional cytotoxicity experiments were carried out utilizing anti-T3 monoclonal antibody to block killing by NKH1+T3+ cells. These experiments indicated that the NK cell that appears to be responsible for much of the functional activity remaining in patients with CFS belongs to the NKH1+T3+ subset, which under normal circumstances represents only approximately 20% of the NK cell population.
n.pl lymphocytes that are part of innate immunity that kill foreign substances and abnormal tissues. Decreased number or activity has been linked to a number of diseases, including AIDS, cancer, chronic fatigue syndrome, immuno-deficiencies, and viral infections. See also innate immunity.
PMID: 8148445
Decreased natural killer cell activity is associated with severity of chronic fatigue immune dysfunction syndrome.
http://pubmedhh.nlm.nih.gov/cgi-bin/abstract.cgi?id=8148445
Author: Ojo-Amaize EA, Conley EJ, Peter JB.
Journal: Clin Infect Dis; 1994 Jan; 18 Suppl 1():S157-9. PubMed ID: 8148445.
Abstract:
Natural killer (NK) cell activity was measured blindly in vitro with blood specimens from 50 healthy individuals and 20 patients with clinically defined chronic fatigue immune dysfunction syndrome (CFIDS) who met the criteria established by the Centers for Disease Control and Prevention (Atlanta). In accordance with a group scoring system of 1-10 points, with 10 being the most severe clinical status, the patient population was stratified into three clinical groups: A (> 7 points), B (5-7 points), and C (< 5 points). NK cell activity was assessed by the number of lytic units (LU), which for the 50 healthy controls varied between 20 and 250 (50%, 20-50 LU; 32%, 51-100 LU; 6%, 101-130 LU; and 12%, > 150 LU). In none of the 20 patients with CFIDS was the NK cell activity > 100 LU. For group C, the 10 patients stratified as having the least severe clinical condition, the measure was 61.0 +/- 21.7 LU; for group B (more severe, n = 7), it was 18.3 +/- 7.3 LU; and for group A (most severe, n = 3), it was 8.0 +/- 5.3 LU. These data suggest a correlation between low levels of NK cell activity and severity of CFIDS, which, if it is confirmed by additional studies of larger groups, might be useful for subgrouping patients and monitoring therapy and/or the progression of CFIDS.
PMID: 20520837
Biomarkers in chronic fatigue syndrome: evaluation of natural killer cell function and dipeptidyl peptidase IV/CD26.
http://pubmedhh.nlm.nih.gov/cgi-bin/abstract.cgi?id=20520837
Title: biomarkers in chronic fatigue syndrome: evaluation of natural killer cell function and dipeptidyl peptidase IV/CD26.
Author: Fletcher MA, Zeng XR, Maher K, Levis S, Hurwitz B, Antoni M, Broderick G, Klimas NG.
Journal: PLoS One; 2010; 5(5):e10817. PubMed ID: 20520837.
Abstract:
BACKGROUND: Chronic Fatigue Syndrome (CFS) studies from our laboratory and others described decreased natural killer cell
cytotoxicity (NKCC) and elevated proportion of lymphocytes expressing the activation marker, dipeptidyl peptidase IV
(DPPIV) also known as CD26. However, neither these assays nor other laboratory tests are widely accepted for the
diagnosis or prognosis of CFS. This study sought to determine if NKCC or DPPIV/CD26 have diagnostic accuracy for CFS.
METHODS/RESULTS: Subjects included female and male CFS cases and healthy controls. NK cell function was measured with
a bioassay, using K562 cells and (51)Cr release. Lymphocyte associated DPPIV/CD26 was assayed by qualitative and
quantitative flow cytometry. Serum DPPIV/CD26 was measured by ELISA. Analysis by receiver operating characteristic
(ROC) curve assessed biomarker potential. Cytotoxic function of NK cells for 176 CFS subjects was significantly lower
than in the 230 controls. According to ROC analysis, NKCC was a good predictor of CFS status.
There was no significant difference in NK cell counts between cases and controls. Percent CD2+ lymphocytes
(T cells and NK cells) positive for DPPIV/C26 was elevated in CFS cases, but there was a decrease in the number
of molecules (rMol) of DPPIV/C26 expressed on T cells and NK cells and a decrease in the soluble form of the enzyme
in serum. Analyses by ROC curves indicated that all three measurements of DPPIV/CD26 demonstrated potential as
biomarkers for CFS. None of the DPPIV/C26 assays were significantly correlated with NKCC.
CONCLUSIONS: By ROC analysis, NKCC and three methods of measuring DPPIV/C26 examined in this study had potential as biomarkers for CFS.
Of these, NKCC, %CD2+CD26+ lymphocytes and rMol CD26/CD2+ lymphocyte, required flow cytometry, fresh blood
and access to a high complexity laboratory. Soluble DPPIV/C26 in serum is done with a standard ELISA assay,
or with other soluble factors in a multiplex type of ELISA. Dipeptidyl peptidase IV on lymphocytes or in serum
was not predictive of NKCC suggesting that these should be considered as non-redundant biomarkers. Abnormalities
in DPPIV/CD26 and in NK cell function have particular relevance to the possible role of infection in the initiation and/or the persistence of CFS.
PMID: 22229027
Fatigue in medical residents leads to reactivation of herpes virus latency.
http://pubmedhh.nlm.nih.gov/cgi-bin/abstract.cgi?id=22229027
Author: Uchakin PN, Parish DC, Dane FC, Uchakina ON, Scheetz AP, Agarwal NK, Smith BE.
Journal: Interdiscip Perspect Infect Dis; 2011; 2011():571340. PubMed ID: 22229027.
Abstract:
The main objective of this study was to detect fatigue-induced clinical symptoms of immune suppression in medical residents. Samples were collected from the subjects at rest, following the first night (low-stress), and the last night (high-stress) of night float. Computerized reaction tests, Epworth Sleepiness Scale, and Wellness Profile questionnaires were used to quantify fatigue level. DNA of human herpes viruses HSV-1, VZV, EBV, as well as cortisol and melatonin concentrations, were measured in saliva. Residents at the high-stress interval reported being sleepier compared to the rest interval. EBV DNA level increased significantly at both stress intervals, while VZV DNA level increased only at low-stress. DNA levels of HSV-1 decreased at low-stress but increased at high-stress. Combined assessment of the viral DNA showed significant effect of stress on herpes virus reactivation at both stress intervals. Cortisol concentrations at both stress intervals were significantly higher than those at rest.
| Fatigue in medical residents leads to reactivation of herpes virus latency. | pmid22229027 | EBV HSV-1 VZV |
PMC3464733
A study in 2002 Evidence for the Presence of Immune Dysfunction in Chronic Fatigue Syndrome contributed to removing the ID (Immune Dysfunction) from CFIDS. It claimed no consistent dysfunctional immune markers could be found. The problem with the study was that it included patients who had CFIDS a short time and patients who had the disease for many years. CFIDS progresses over the course of many years with the immune response weakening over time. This next study and at least 7 more invalidate the 2002 study. There are consistent decreased immune system markers in CFIDS for the first few years of the disease.
Longitudinal investigation of natural killer cells and cytokines in chronic fatigue syndrome/myalgic encephalomyelitis
A decrease in NK cytotoxic activity is thus a recurring finding in CFS/ME research [16,17,20-24] ... Despite these striking alterations there are no follow up studies reporting on the profiling of both NK cells subsets and activity during an extended course of CFS/ME.
This shows natural killer cell activity is low in the first 12 months of disease and that it is consistent. "A decrease in NK cytotoxic activity" and "decreases in immune function" means a weakened immune response. It means 'SUPPRESSION', not 'DYSREGULATION'. Dysregulation is a term they use to describe CFS now. They don't use the word dysfunction anymore. ( Remember, immune suppression makes any vaccine dangerous. It can exhaust a weak immune system further and it can also give you the very disease it is supposed to protect you from. The CDC and the rest of the industry does not want you to know you can experience a major vaccine injury if you have CFS. )
Seven studies on this webpage plus six more here (one here is Entry 2) makes 13 studies which reveal immune suppression in Chronic Fatigue Syndrome.
The evidence is overwhelming. The CDC continues to deny the existence of immune suppression with ongoing infection in CF(ID)S even though multiple studies reveal it.
PMID: 24454857
Deficient EBV-specific B- and T-cell response in patients with chronic fatigue syndrome.
http://pubmedhh.nlm.nih.gov/cgi-bin/abstract.cgi?id=24454857
Author: Loebel M, Strohschein K, Giannini C, Koelsch U, Bauer S, Doebis C, Thomas S, Unterwalder N, von Baehr V, Reinke P, Knops M, Hanitsch LG, Meisel C, Volk HD, Scheibenbogen C.
Journal: PLoS One; 2014; 9(1):e85387. PubMed ID: 24454857.
Abstract:
Epstein-Barr virus (EBV) has long been discussed as a possible cause or trigger of Chronic Fatigue Syndrome (CFS). In a subset of patients the disease starts with infectious mononucleosis and both enhanced and diminished EBV-specific antibody titers have been reported. In this study, we comprehensively analyzed the EBV-specific memory B- and T-cell response in patients with CFS. While we observed no difference in viral capsid antigen (VCA)-IgG antibodies, EBV nuclear antigen (EBNA)-IgG titers were low or absent in 10% of CFS patients. Remarkably, when analyzing the EBV-specific memory B-cell reservoir in vitro a diminished or absent number of EBNA-1- and VCA-antibody secreting cells was found in up to 76% of patients. Moreover, the ex vivo EBV-induced secretion of TNF-α and IFN-γ was significantly lower in patients. Multicolor flow cytometry revealed that the frequencies of EBNA-1-specific triple TNF-α/IFN-γ/IL-2 producing CD4(+) and CD8(+) T-cell subsets were significantly diminished whereas no difference could be detected for HCMV-specific T-cell responses. When comparing EBV load in blood immune cells, we found more frequently EBER-DNA but not BZLF-1 RNA in CFS patients compared to healthy controls suggesting more frequent latent replication. Taken together, our findings give evidence for a deficient EBV-specific B- and T-cell memory response in CFS patients and suggest an impaired ability to control early steps of EBV reactivation. In addition the diminished EBV response might be suitable to develop diagnostic marker in CFS.
PMCID: PMC4465185
Distinct plasma immune signatures in ME/CFS are present early in the course of illness.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465185/
Authors: Mady Hornig, José G. Montoya, Nancy G. Klimas, Susan Levine, Donna Felsenstein, Lucinda Bateman, Daniel L. Peterson, C. Gunnar Gottschalk, Andrew F. Schultz, Xiaoyu Che, Meredith L. Eddy, Anthony L. Komaroff, and W. Ian Lipkin
Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is an unexplained incapacitating illness that may affect up to 4 million people in the United States alone.
There are no validated laboratory tests for diagnosis or management despite global efforts to find biomarkers of disease. We considered the possibility that inability
to identify such biomarkers reflected variations in diagnostic criteria and laboratory methods as well as the timing of sample collection during the course of the illness.
Accordingly, we leveraged two large, multicenter cohort studies of ME/CFS to assess the relationship of immune signatures with diagnosis, illness duration, and other clinical variables.
Controls were frequency-matched on key variables known to affect immune status, including season of sampling and geographic site, in addition to age and sex. We report here
distinct alterations in plasma immune signatures early in the course of ME/CFS (n = 52) relative to healthy controls (n = 348) that are not present in subjects with longer
duration of illness (n = 246). Analyses based on disease duration revealed that early ME/CFS cases had a prominent activation of both pro- and anti-inflammatory cytokines
as well as dissociation of intercytokine regulatory networks. We found a stronger correlation of cytokine alterations with illness duration than with measures of illness severity,
suggesting that the immunopathology of ME/CFS is not static. These findings have critical implications for discovery of interventional strategies and early diagnosis of ME/CFS.
Conclusion
These diagnoses exist for so-called "post" infectious syndromes
- post ebola syndrome
- post hepatitis syndrome
- post-infectious fatigue syndrome
- post-infectious glomerulonephritis with nephrotic syndrome
- post-infectious Irritable Bowel Syndrome
- post-malaria neurological syndrome
- post polio syndrome
- post Q-fever fatigue syndrome
- post sepsis syndrome
- post-streptococcal uveitis syndrome
- post treatment lyme disease syndrome
- post viral fatigue syndrome
These diagnosis add up to millions of people.
There is a vast amount of good research supporting the existence of immune suppression with active opportunistic infections. This evidence is ignored by those with authority in the medical system.
CFS patients are very disabled and can barely function. Rather than helping CFS patients, the current medical system is actually putting effort into denying them proper healthcare with
ongoing efforts to perpetuate a psychiatric definition of this disease. Their psychiatric interpretations are not evidence-based. They are scientifically invalid statements which contradict the
valid scientific evidence.
Action Points...