CFS and Immune Suppression.
With Active Opportunistic Infections

 

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What is this page about?

ME / CEBVSPVFSCFIDSCFSSEID?

This disease has gone by many names.

  • 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.
 
O PMID: 2824604
CFS patients had low natural killer cell counts, also most CFS patients were unable to kill Epstein-Barr virus-infected B cells.

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.
— Caligiuri M1, Murray C, Buchwald D, Levine H, Cheney P, Peterson D, Komaroff AL, Ritz J. J Immunol. 1987 Nov 15;139(10):3306-13.

http://www.researchfraud.com//#pmid2824604
Downloaded From:
http://pubmedhh.nlm.nih.gov/cgi-bin/abstract.cgi?id=2824604

 

Title Phenotypic and functional deficiency of natural killer cells in patients with chronic fatigue syndrome.
Author: Caligiuri M, Murray C, Buchwald D, Levine H, Cheney P, Peterson D, Komaroff AL, Ritz J.
Journal: J Immunol; 1987 Nov 15; 139(10):3306-13.
PubMed ID: 2824604
Abstract:
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.

Mobile Desktop Retrieved on: 8/9/2016

NK cells 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.

natural killer cells. (n.d.) Jonas: Mosby's Dictionary of Complementary and Alternative Medicine. (2005). Retrieved June 25 2016 from http://medical-dictionary.thefreedictionary.com/natural+killer+cells
  O PMID: 8148445

Decreased natural killer cell activity is associated with severity of chronic fatigue immune dysfunction syndrome.

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.
http://www.researchfraud.com/cfs-immune-suppression/#pmid8148445
CFIDS CFS EBV
Downloaded From:
http://pubmedhh.nlm.nih.gov/cgi-bin/abstract.cgi?id=8148445
Title: Decreased natural killer cell activity is associated with severity of chronic fatigue immune dysfunction syndrome.
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.
Mobile Desktop Retrieved on: 05/01/2015
 
  O PMID: 20520837

Biomarkers in chronic fatigue syndrome: evaluation of natural killer cell function and dipeptidyl peptidase IV/CD26.

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.
Immunosuppression due to decreased natural killer call activity in CFS.
http://www.researchfraud.com/cfs-opportunistic-infections/#pmid20520837
biomarker CFS
Downloaded From:
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.

Mobile Desktop Retrieved on: 05/12/2015
 
  O PMID: 22229027

Fatigue in medical residents leads to reactivation of herpes virus latency.

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.
Immune suppression leading to reactivation of latent Epstein-Barr viral infections.
http://www.researchfraud.com/cfs-immune-suppression/#pmid22229027
EBV VZV HSV-1
Previously downloaded from:
http://pubmedhh.nlm.nih.gov/cgi-bin/abstract.cgi?id=22229027
Title: Fatigue in medical residents leads to reactivation of herpes virus latency.
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.
Mobile Desktop Retrieved on: June 28, 2015
 
  O 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

These results confirm decreases in immune function in CFS/ME patients, suggesting an increased susceptibility to viral and other infections.Furthermore, NK cytotoxic activity may be a suitable biomarker for diagnosing CFS/ME as it was consistently decreased during the course of the 12 months study.

 

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.

Studies which found a decrease in natural killer cell activity.
[ 16, 17, 20, 21, 22, 23 Entry 2, 24 ].
16.
Barker E, Fujimura SF, Fadem MB, Landay AL, Levy JA. Immunologic abnormalities associated with chronic fatigue syndrome. Clin Infect Dis. 1994;18(Suppl 1):S136–S141. [PubMed]
17.
Masuda A, Nozoe SI, Matsuyama T, Tanaka H. Psychobehavioral and immunological characteristics of adult people with chronic fatigue and patients with chronic fatigue syndrome. Psychosom Med. 1994;56:512–518. [PubMed]
20.
Brenu EW, Staines DR, Baskurt OK, Ashton KJ, Ramos SB, Christy RM, Marshall-Gradisnik SM. Immune and hemorheological changes in chronic fatigue syndrome. J Transl Med. 2010;8:1. [PMC free article] [PubMed]
21.
Klimas NG, Salvato FR, Morgan R, Fletcher MA. Immunologic abnormalities in chronic fatigue syndrome. J Clin Microbiol. 1990;28:1403–1410. [PMC free article] [PubMed]
22.
Fletcher MA, Zeng XR, Maher K, Levis S, Hurwitz B, Antoni M, Broderick G, Klimas NG. Biomarkers in chronic fatigue syndrome: evaluation of natural killer cell function and dipeptidyl peptidase IV/CD26. PLoS One. 2010;5:e10817. [PMC free article] [PubMed]
Entry (2)
Ojo-Amaize EA, Conley EJ, Peter JB. Decreased natural killer cell activity is associated with severity of chronic fatigue immune dysfunction syndrome. Clin Infect Dis. 1994;18(Suppl 1):S157–S159. [On This Page] [PubMed]
24.
Maher KJ, Klimas NG, Fletcher MA. Chronic fatigue syndrome is associated with diminished intracellular perforin. Clin Exp Immunol. 2005;142:505–511. [PMC free article] [PubMed]

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.
http://www.researchfraud.com/cfs-immune-suppression/#PMC3464733
biomarker ME CFS
 
  O PMID: 24454857

Deficient EBV-specific B- and T-cell response in patients with chronic fatigue syndrome.

...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.
They found that 76% of the 400+ study participants EBV-specific B- and T-cells couldn't "remember" the EBV antigens.
http://www.researchfraud.com/cfs-immune-suppression/#pmid24454857
biomarker EBV CFS
Previously downloaded from:
http://pubmedhh.nlm.nih.gov/cgi-bin/abstract.cgi?id=24454857
Title: Deficient EBV-specific B- and T-cell response in patients with chronic fatigue syndrome.
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.
Mobile Desktop Retrieved on: June 29, 2015
 
  O PMCID: PMC4465185

Distinct plasma immune signatures in ME/CFS are present early in the course of illness.

There is a greater activation of the immune response in ME/CFS patients early in the disease. Early disease here means less than 3 years. The level of most immune markers drops below the levels detected in healthy controls after 3 years of illness. The immune response becomes progressively weaker.
This is the first study to demonstrate altered plasma immune signatures early in the course of ME/CFS that are not present in subjects with longer duration of illness.... However, analyses that considered duration of illness revealed that early ME/CFS cases had a prominent activation of both pro- and anti-inflammatory cytokines...
http://www.researchfraud.com/cfs-immune-suppression/#PMC4465185
CFS
Previously downloaded from:
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.

Desktop Retrieved on: July 8, 2015
 
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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.


ResearchFraud.com Action Points... ResearchFraud.com

"The root cause of CFS is continuing active opportunistic infections with immune suppression."
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Definitions

  1. arthralgia
    ar·thral·gi·a (ahr-thral'jē-ă)
    Pain in a joint, especially noninflammatory.
    arthralgia. (n.d.) Medical Dictionary for the Health Professions and Nursing. (2012). Retrieved June 1 2016 from http://medical-dictionary.thefreedictionary.com/arthralgia
    pain in a joint, especially if the absence of inflammation makes the term arthritis inappropriate.
    intermittent or periodic arthralgia joint pain at intervals, usually accompanied by swelling (e.g. of the knee).
    arthralgia. (n.d.) Dictionary of Sport and Exercise Science and Medicine by Churchill Livingstone. (2008). Retrieved June 1 2016 from http://medical-dictionary.thefreedictionary.com/arthralgia
  2. biomarker
    /bio·mark·er/ (bi´o-mahr″ker)
    a biological molecule used as a marker for a substance or process of interest.
    biomarker. (n.d.) Dorland's Medical Dictionary for Health Consumers. (2007). Retrieved June 22 2016 from http://medical-dictionary.thefreedictionary.com/biomarker
  3. EBV   Epstein-Barr virus
    A virus in the herpes family that causes mononucleosis.
    Mentioned in: Chronic Fatigue Syndrome
    EBV. (n.d.) Gale Encyclopedia of Medicine. (2008). Retrieved June 22 2016 from http://medical-dictionary.thefreedictionary.com/EBV
  4. And others.

     

    [L. et alii]
    et al. (n.d.) Medical Dictionary for the Health Professions and Nursing. (2012). Retrieved May 24 2016 from http://medical-dictionary.thefreedictionary.com/et+al
  5. lymphadenopathy
    [limfad′inop′əthē]
    any disorder characterized by a localized or generalized enlargement of the lymph nodes or lymph vessels.
    lymphadenopathy. (n.d.) Mosby's Medical Dictionary, 8th edition. (2009). Retrieved June 22 2016 from http://medical-dictionary.thefreedictionary.com/lymphadenopathy
  6. Muscular pain or tenderness, typically of a diffuse and/or nonspecific nature.
    Mentioned in: Chronic Fatigue Syndrome, Ross River Virus
    myalgia. (n.d.) Gale Encyclopedia of Medicine. (2008). Retrieved May 22 2016 from http://medical-dictionary.thefreedictionary.com/myalgia
  7. myogenic
    (mī'ō-jě-net'ik, -jen'ik)
    1. Originating in or starting from muscle.
    2. Relating to the origin of muscle cells or fibers.
    myogenic. (n.d.) Medical Dictionary for the Health Professions and Nursing. (2012). Retrieved June 22 2016 from http://medical-dictionary.thefreedictionary.com/myogenic
  8. NK cells 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.
    natural killer cells. (n.d.) Jonas: Mosby's Dictionary of Complementary and Alternative Medicine. (2005). Retrieved June 25 2016 from http://medical-dictionary.thefreedictionary.com/natural+killer+cells
  9. A condition affecting the nerves supplying the arms and legs. Typically, the feet and hands are involved first. If sensory nerves are involved, numbness, tingling, and pain are prominent, and if motor nerves are involved, the patient experiences weakness.
    neuropathy. (n.d.) Gale Encyclopedia of Medicine. (2008). Retrieved June 22 2016 from http://medical-dictionary.thefreedictionary.com/neuropathy
  10. Being attracted to, or having an affinity for, nerve tissue. Various toxic substances and some viruses are neurotropic.
    neurotropic. (n.d.) Collins Dictionary of Medicine. (2004, 2005). Retrieved June 22 2016 from http://medical-dictionary.thefreedictionary.com/neurotropic
  11. serologic
    (sē'rō-loj'ik)
    Etymology: L, serum, whey; Gk, logos,
    science pertaining to the branch of medicine concerned with the study of blood sera.
    serologic. (n.d.) Mosby's Medical Dictionary, 8th edition. (2009). Retrieved June 22 2016 from http://medical-dictionary.thefreedictionary.com/serologic
  12. titer
    /ti·ter/ (ti´ter)
    the quantity of a substance required to react with or to correspond to a given amount of another substance.
    titer. (n.d.) Dorland's Medical Dictionary for Health Consumers. (2007). Retrieved June 22 2016 from http://medical-dictionary.thefreedictionary.com/titer
  13. virology
    /vi·rol·o·gy/ (vi-rol´ah-je)
    the study of viruses and virus diseases.
    virology. (n.d.) Dorland's Medical Dictionary for Health Consumers. (2007). Retrieved June 22 2016 from http://medical-dictionary.thefreedictionary.com/virology

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References


  1. Caligiuri M, Murray C, Buchwald D, et al. Phenotypic and functional deficiency of natural killer cells in patients with chronic fatigue syndrome. J Immunol. 1987;139(10):3306-13.
    PMID: 2824604
  2. Ojo-amaize EA, Conley EJ, Peter JB. Decreased natural killer cell activity is associated with severity of chronic fatigue immune dysfunction syndrome. Clin Infect Dis. 1994;18 Suppl 1:S157-9.
    PMID: 8148445
  3. Fletcher MA, Zeng XR, Maher K, et al. Biomarkers in chronic fatigue syndrome: evaluation of natural killer cell function and dipeptidyl peptidase IV/CD26. PLoS ONE. 2010;5(5):e10817.
    PMID: 20520837
  4. Uchakin PN, Parish DC, Dane FC, et al. Fatigue in medical residents leads to reactivation of herpes virus latency. Interdiscip Perspect Infect Dis. 2011;2011:571340.
    PMID: 22229027
  5. Brenu EW, van Driel ML, Staines DR, et al. Immunological abnormalities as potential biomarkers in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis. Journal of Translational Medicine. 2011;9:81. doi:10.1186/1479-5876-9-81.
    PMC3464733
  6. Loebel M, Strohschein K, Giannini C, et al. Deficient EBV-specific B- and T-cell response in patients with chronic fatigue syndrome. PLoS ONE. 2014;9(1):e85387.
    PMID: 24454857
  7. Hornig M, Montoya JG, Klimas NG, et al. Distinct plasma immune signatures in ME/CFS are present early in the course of illness. Sci Adv. 2015;1(1)
    PMC4465185
  1. Click here to go to the
    study on this page.
  2. The study relies on invalid psychiatric conclusions.
    ( Lacks scientific validity. )
Last modified: 8/9/2016 7:00pm