Did you get sick after a vaccine? Then maybe you should consider an immune illness due to intoxication to aluminium.
It is called Macrophagic Myofasciitis and often confused with Chronique Fatigue Syndrome.
The symptoms are muscle pain (95%), fatigue, post-exertional malaise, joint pain (50-60%) and febrile syndrome (30%). It can only be diagnosed through muscle biopsy.
Most manufacturers of vaccines add aluminium to vaccines to enhance their action. The WHO already warned the doses are however far too high and the information leaflets too vague about the composition.
Many doctors have no clue about the toxic doses of vaccines.
Dr Jean Pilette studied closely the composition and calculated that babies get up to 170 times the allowed toxic doses in his blood serum several times a year.
If you got a few vaccines, subcutaneous nodules can form. Micro-analysis has shown the presence of aluminium in the macrophages of these nodules.
What else contains a lot of aluminium?
- gastric reflux medication
- baby milk (especially based on soya)
- tap water (it is used to clean dirty water)
- pesticides
- vaginal showers
- black tea
- melted cheese products
- food additives E173, E521, E522, E523, E554, E555, E556, E559
- aluminium frying pan
- percolator
- deodorant
- industrial work
Aluminium is an iron widely present in nature and often used by man. It is however very toxic for the nervous system because it passes easily through the brain blood barrier. Then it can access delicate parts of the deep brain.
Aluminium has also a negative influence on the Krebs cycle. This cycle is essential in the wellbeing and health of every individual. When the Krebs cycle is interrupted, the human system goes down. The engine of your cells brake down, they are poisoned.
Macrophagic Myofasciitis is considered a rare disease. Chances your doctor has never heard about it.
Sources:
http://www.orpha.net/data/patho/GB/uk-myofa.pdf
http://www.ncbi.nlm.nih.gov/pubmed/12797472
http://brain.oxfordjournals.org/content/124/5/974.full
http://onlinelibrary.wiley.com/doi/10.1046/j.1432-1033.2000.01328.x/full
The most important function of mitochondria is the oxidation of substrates to produce bioenergy. Several lines of evidence indicate that mitochondria from neurons affected by degenerative disorders related to aging exhibit aberrant oxidation processes [16]. Furthermore, it is worth mentioning that there is a strict correlation between Krebs cycle and glycolysis. In this connection it has been demonstrated that Al is a strong inhibitor of some enzymes of the glycolysis pathway [17–19] as well as glucokinase and phosphofructokinase [20]. All these elements reinforce the possibility that Al could interfere the bioenergetic pathways in mitochondria.
...
In addition, it has been demonstrated that aluminum alters the homeostasis of intracellular calcium in mitochondria, a phenomenon linked to initiation of apoptotic cell death; this observation provides support for the potential detrimental effects of this metal ion on this organelle [53].
woensdag 22 juni 2011
Agammaglobulinemia makes you susceptible to chronic enteroviral infections of CNS
http://www.ncbi.nlm.nih.gov/pubmed/3296100?dopt=Abstract
Chronic enteroviral meningoencephalitis in agammaglobulinemic patients.
McKinney RE Jr, Katz SL, Wilfert CM.
Rev Infect Dis. 1987 Mar-Apr;9(2):334-56.
Abstract
Patients with agammaglobulinemia are particularly susceptible to chronic enteroviral infections of the central nervous system. Data on 42 patients were obtained by literature review, communications with other physicians, and personal experiences. Thirty-eight patients had congenital immunodeficiencies, most frequently X-linked agammaglobulinemia. Most patients who could be assessed were receiving maintenance therapy with intramuscular gamma-globulin before their enteroviral infection. Seven patients had not been recognized as hypogammaglobulinemic before the onset of infection. The commonest pathogens were echoviruses (37 of 41 cases), especially type 11 (11 cases). Thus far, four patients have had sequential or simultaneous infections with a second enteroviral serotype. Other features of the disease have included weakness, lethargy or coma, headaches, hearing loss, seizures, ataxia, and paresthesias. Some patients have also had nonneurologic manifestations of chronic enteroviral infection, including fever, the dermatomyositis-like syndrome, edema, rashes, and hepatitis. Treatment has consisted primarily of antibody administration, either in intravenous immunoglobulin preparations or in immune plasma. Twelve patients have received intraventricular immunoglobulin through reservoir devices; six of these 12 have improved substantially, as judged by clinical criteria.
PMID: 3296100 [PubMed - indexed for MEDLINE]
Sources:
http://www.ncbi.nlm.nih.gov/pubmed/3296100?dopt=Abstract
http://www.jacionline.org/article/S0091-6749(01)70038-3/abstract
Chronic enteroviral meningoencephalitis in agammaglobulinemic patients.
McKinney RE Jr, Katz SL, Wilfert CM.
Rev Infect Dis. 1987 Mar-Apr;9(2):334-56.
Abstract
Patients with agammaglobulinemia are particularly susceptible to chronic enteroviral infections of the central nervous system. Data on 42 patients were obtained by literature review, communications with other physicians, and personal experiences. Thirty-eight patients had congenital immunodeficiencies, most frequently X-linked agammaglobulinemia. Most patients who could be assessed were receiving maintenance therapy with intramuscular gamma-globulin before their enteroviral infection. Seven patients had not been recognized as hypogammaglobulinemic before the onset of infection. The commonest pathogens were echoviruses (37 of 41 cases), especially type 11 (11 cases). Thus far, four patients have had sequential or simultaneous infections with a second enteroviral serotype. Other features of the disease have included weakness, lethargy or coma, headaches, hearing loss, seizures, ataxia, and paresthesias. Some patients have also had nonneurologic manifestations of chronic enteroviral infection, including fever, the dermatomyositis-like syndrome, edema, rashes, and hepatitis. Treatment has consisted primarily of antibody administration, either in intravenous immunoglobulin preparations or in immune plasma. Twelve patients have received intraventricular immunoglobulin through reservoir devices; six of these 12 have improved substantially, as judged by clinical criteria.
PMID: 3296100 [PubMed - indexed for MEDLINE]
Sources:
http://www.ncbi.nlm.nih.gov/pubmed/3296100?dopt=Abstract
http://www.jacionline.org/article/S0091-6749(01)70038-3/abstract
donderdag 16 juni 2011
De link tussen genen, gluten, pijn en verstoorde stress-response
Heb je je ooit afgevraagd waarom sommige mensen goed reageren op Low Dose Naltrexone (LDN)?
Het antwoord is heel eenvoudig. LDN stimuleert je lichaam om meer mu opioide receptoren (MOR) te maken op de b-endorfine in je lichaam.
MOR zijn verantwoordelijk voor het opsporen van kanker cellen in je lichaam, maar ook om de pijn, verslavingen zoals koffie, nicotine, alcohol, drugs, games, ... onder controle te houden. Als je er geen (meer) hebt, zit je in de problemen. Studies hebben aangetoond dat MOR ook de reactie op stress (cortisol = immuniteit) in uw lichaam bemiddelen. Het wordt nog interessanter!
Wat is het probleem als je ME/CVS hebt? Veel mensen hebben een genetische verschil op de MOR receptor genaamd de A118G. Het is een gemeenschappelijk polymorfisme wat veel mensen hebben.
Wetenschappers ontdekten dat mensen met de A118G variant verschillend reageren op het geneesmiddel metyrapon. Hun ACTH hormoon steeg meer dan mensen zonder allel variant, maar hadden op het einde een beduidend lager ACTH-niveau. Dit betekent een grotere remming door de MOR op de hypothalamus-hypofyse-sites!
Metyrapon wordt vaak gebruikt om de controleren of u last heeft bijnier insuffiëntie. Het blokkeert de cortisol-synthese met als gevolg dat CRH en ACTH (hormonen) niveaus moeten stijgen als een reactie op de dalende cortisol niveaus.
Nu heb je het bewijs dat Low Dose Naltrexone ook uw cortisol regelt en dus je immuunsysteem.
Het stimuleert immers de aanmaak van nieuwe MOR, hoe meer hoe beter je lichaam zal functioneren.
Wat is de link met gluten? Opiaten doden MOR. Wordt u geplaagd door chronische pijn en ziekte? Misschien is het tijd om te overwegen om uw medicatie te veranderen. Stoppen met alle opiaten en dat omvat ook die in je eten: gluten, melk, soja en spinazie. Dit zijn natuurlijke opiaten en hebben hetzelfde effect op je gezondheid als pijnstillers.
(Een alternatief voor opiaten pijnstillers kunnen zijn Topamax of Normast.)
Veel van de chronisch zieke patiënten hebben problemen met een enzym genaamd DPP IV. Dit enzym verteert als het ware opiaten. Als om welke reden het enzym niet werkt naar behoren, worden de opgestapelde opiaten giftig en breken ze de MOR af in je lichaam.
Ik vraag me af wat het statistisch toeval is van DPP IV deficiëntie en de A118G variant?
Wilt u meer informatie over Low Dose Naltrexone, bezoek de website:
http://opstaanmetmecvs.blogspot.com/p/low-dose-naltrexone.html
Bronnen:
http://onlinelibrary.wiley.com/doi/10.1111/j.1369-1600.2011.00313.x/abstract
http://www.ncbi.nlm.nih.gov/pubmed/12627468
http://www.snpedia.com/index.php/Rs1799971
Het antwoord is heel eenvoudig. LDN stimuleert je lichaam om meer mu opioide receptoren (MOR) te maken op de b-endorfine in je lichaam.
MOR zijn verantwoordelijk voor het opsporen van kanker cellen in je lichaam, maar ook om de pijn, verslavingen zoals koffie, nicotine, alcohol, drugs, games, ... onder controle te houden. Als je er geen (meer) hebt, zit je in de problemen. Studies hebben aangetoond dat MOR ook de reactie op stress (cortisol = immuniteit) in uw lichaam bemiddelen. Het wordt nog interessanter!
Wat is het probleem als je ME/CVS hebt? Veel mensen hebben een genetische verschil op de MOR receptor genaamd de A118G. Het is een gemeenschappelijk polymorfisme wat veel mensen hebben.
Wetenschappers ontdekten dat mensen met de A118G variant verschillend reageren op het geneesmiddel metyrapon. Hun ACTH hormoon steeg meer dan mensen zonder allel variant, maar hadden op het einde een beduidend lager ACTH-niveau. Dit betekent een grotere remming door de MOR op de hypothalamus-hypofyse-sites!
Metyrapon wordt vaak gebruikt om de controleren of u last heeft bijnier insuffiëntie. Het blokkeert de cortisol-synthese met als gevolg dat CRH en ACTH (hormonen) niveaus moeten stijgen als een reactie op de dalende cortisol niveaus.
Nu heb je het bewijs dat Low Dose Naltrexone ook uw cortisol regelt en dus je immuunsysteem.
Het stimuleert immers de aanmaak van nieuwe MOR, hoe meer hoe beter je lichaam zal functioneren.
Wat is de link met gluten? Opiaten doden MOR. Wordt u geplaagd door chronische pijn en ziekte? Misschien is het tijd om te overwegen om uw medicatie te veranderen. Stoppen met alle opiaten en dat omvat ook die in je eten: gluten, melk, soja en spinazie. Dit zijn natuurlijke opiaten en hebben hetzelfde effect op je gezondheid als pijnstillers.
(Een alternatief voor opiaten pijnstillers kunnen zijn Topamax of Normast.)
Veel van de chronisch zieke patiënten hebben problemen met een enzym genaamd DPP IV. Dit enzym verteert als het ware opiaten. Als om welke reden het enzym niet werkt naar behoren, worden de opgestapelde opiaten giftig en breken ze de MOR af in je lichaam.
Ik vraag me af wat het statistisch toeval is van DPP IV deficiëntie en de A118G variant?
Wilt u meer informatie over Low Dose Naltrexone, bezoek de website:
http://opstaanmetmecvs.blogspot.com/p/low-dose-naltrexone.html
Bronnen:
http://onlinelibrary.wiley.com/doi/10.1111/j.1369-1600.2011.00313.x/abstract
http://www.ncbi.nlm.nih.gov/pubmed/12627468
http://www.snpedia.com/index.php/Rs1799971
The link between genes, gluten, pain and altered stressresponse
Have you ever wondered why some people react well on Low Dose Naltrexone (LDN)?
The answer is very simple. LDN stimulates your body to create more mu opioide receptors (MOR) on the b-endorphines in your body.
MOR are responsible for detecting cancer cells in your body but also to control pain , addictions to coffee, nicotine, alcohol, drugs, games, ... If you don't have them (anymore), you are in trouble. Studies have demonstrated that MOR also mediates the stress response (cortisol = immunity) in your body. It becomes even more interesting!
What is the problem when you have ME/CFS? A lot of people have a genetic difference called the A118G. It is a common polymorphism so many people have it.
Scientists discovered that people with the A118G variant react differently to the drug metyrapone. Their ACTH hormone rised more than people with no allele variant but had a resultant significantly lower ACTH level. This implies a greater inhibition through the MOR at the hypothalamic–pituitary sites!
Metyrapone is often used to the check if you suffer adrenal insuffiency. It blocks cortisol synthesis and as a result CRH and ACTH levels should rise as a response to the falling cortisol levels.
Now you have the proof that Low Dose Naltrexone also regulates your cortisol and therefore your immune system.
What is the link with gluten? Opiates kill MOR. Do you suffer chronic pain and illness? Maybe it's time to consider to change your medication. Stop all opiates and that includes those in your food: gluten, milk, soya and spinach. These are natural opiates and have the same effect on your health as painkillers.
(An alternative for opiate painkillers could be Topamax or Normast.)
A lot of chronic ill patients have problems with an enzym called DPP IV which is supposed to digest opiates. If for some reason the enzym does not work as it should in your body, opiates become toxic. They will kill MOR.
I wonder what the statistical coincidence is of DPP IV deficiency and the A118G variant?
Would you like more info on Low Dose Naltrexone, visit the webpage:
http://opstaanmetmecvs.blogspot.com/p/low-dose-naltrexone.html
Sources:
http://onlinelibrary.wiley.com/doi/10.1111/j.1369-1600.2011.00313.x/abstract
http://www.ncbi.nlm.nih.gov/pubmed/12627468
http://www.snpedia.com/index.php/Rs1799971
The answer is very simple. LDN stimulates your body to create more mu opioide receptors (MOR) on the b-endorphines in your body.
MOR are responsible for detecting cancer cells in your body but also to control pain , addictions to coffee, nicotine, alcohol, drugs, games, ... If you don't have them (anymore), you are in trouble. Studies have demonstrated that MOR also mediates the stress response (cortisol = immunity) in your body. It becomes even more interesting!
What is the problem when you have ME/CFS? A lot of people have a genetic difference called the A118G. It is a common polymorphism so many people have it.
Scientists discovered that people with the A118G variant react differently to the drug metyrapone. Their ACTH hormone rised more than people with no allele variant but had a resultant significantly lower ACTH level. This implies a greater inhibition through the MOR at the hypothalamic–pituitary sites!
Metyrapone is often used to the check if you suffer adrenal insuffiency. It blocks cortisol synthesis and as a result CRH and ACTH levels should rise as a response to the falling cortisol levels.
Now you have the proof that Low Dose Naltrexone also regulates your cortisol and therefore your immune system.
What is the link with gluten? Opiates kill MOR. Do you suffer chronic pain and illness? Maybe it's time to consider to change your medication. Stop all opiates and that includes those in your food: gluten, milk, soya and spinach. These are natural opiates and have the same effect on your health as painkillers.
(An alternative for opiate painkillers could be Topamax or Normast.)
A lot of chronic ill patients have problems with an enzym called DPP IV which is supposed to digest opiates. If for some reason the enzym does not work as it should in your body, opiates become toxic. They will kill MOR.
I wonder what the statistical coincidence is of DPP IV deficiency and the A118G variant?
Would you like more info on Low Dose Naltrexone, visit the webpage:
http://opstaanmetmecvs.blogspot.com/p/low-dose-naltrexone.html
Sources:
http://onlinelibrary.wiley.com/doi/10.1111/j.1369-1600.2011.00313.x/abstract
http://www.ncbi.nlm.nih.gov/pubmed/12627468
http://www.snpedia.com/index.php/Rs1799971
zondag 12 juni 2011
Dr Judy Mikovits on XMRV
Dr Judy Mikovits on XMRV
XMRV symposium, June 9, 2011, Leuven, Belgium (part 2)
Do XMRV and HGRV (Human Gamma Retro Viruses) play a role in ME/CFS?
Definition: heterogenous [ˌhɛtəˈrɒdʒɪnəs]
adj
(Life Sciences & Allied Applications / Biology) Biology Med not originating within the body; of foreign origin
What do we know about XMRV?
The sequences originally identified in prostate cancer with the HPC1/RNase L gene are allelic variations, especially the R462Q single nucleotide polymorphism.
Integration in situ hybridization in unmanipulated human tissue and antibody responses demonstrate that
XMRV is a human infection although closely related to Xeno, Poly and MLV's.
XMRV is not an endogenous retrovirus in human.
How it got into humans is unclear.
Definition: endogenous /en·dog·e·nous/ (en-doj´ĕ-nus) produced within or caused by factors within the organism
It needs all of your cells to make more virions (virus particles) so it can multiply itself.
Virions have a complex structure and consist of an envelope, a nucleocapsid, and a nucleoid. Virions are spherical to pleomorphic measuring 90-100 nm in diameter[4] or 137 nm[3]. This is very small!
Dr Mikovits went through slides to explain the following studies:
The studies speak for themselves, you can find them here
1. Detection of an infectious retrovirus XMRV, in blood cells of patients of patients with chronic fatigue syndrome
2. Cell-free transmission of XMRV and MRV from PRC negative CFS patients plasma to LNCaP cells
In a study reported in 2009, DNA from peripheral blood mononuclear cells (PBMCs) of CFS patients and healthy controls from the US were tested for the presence of XMRV sequences. XMRV sequences were found in 68 out of 101 CFS patients (67%), as compared to 8 of 218 (3.7%) healthy US controls.
Viral gene sequences identified in CFS patients clustered with sequences from PC, and both sequences were virtually identical. Further investigation using activated CFS patient PBMC co-cultured with susceptible PC cells (LNCaP) showed that virus could be transmitted by cells and supernatant, as indicated by protein expression and transmission electron microscopy, suggesting that the virus being detected by protein expression was infectious.
Virus could also be transmitted in LNCaP cells from 10/12 CFS patient plasma samples. These studies suggested that both cell associated and cell-free transmission of XMRV is possible. Finally, antibodies to XMRV were detected in 9/18 CFS patients using a test based on the envelope of a closely related virus, spleen focus forming virus (SFFV).
Source: http://webcache.googleusercontent.com/search?q=cache:MBxg88Hnw9UJ:forums.phoenixrising.me/archive/index.php/t-8823.html+Cell-free+transmission+of+XMRV+and+MRV+from+PRC+negative+CFS+patients+plasma+to+LNCaP+cells&cd=4&hl=nl&ct=clnk&gl=be&source=www.google.be
3. Detection of MLV-related virus gene sequences in blood of patients with chronic fatigue syndrome and healthy blood donors
Study: http://thirdreviewer.com/2010/pnas-dump-file/detection-of-mlv-related-virus-gene-sequences-in-blood-of-patients-with-chronic-fatigue-syndrome-and-healthy-blood-donors/
Why do some groups fail to detect XMRV?
Variantions in XMRV sequences and low levels of replication of the virus in the blood are the main reasons why some groups fail to detect XMRV.
Clues to pathogenesis?
Hormones + Inflammation => Increase of replication of XMRV
XMRV is responsive to cortisol because stress is often onset to disease.
Stress can be a car accident, an operation, illness, ...
Question of the public: Is cortisol supplementation of hormone therapy detrimental?
Answer of Dr Mikovits: "Everything should be in balance and that includes cortisol."
A footprint of infection?
Can one recognize XMRV infection in the blood? Does it leave a footprint?
Dysregulated cytokine/chemokine production is detected in plasma from ME/CFS patients. It is a typical inflammatory signature of XMRV/MRV infection.
The Random Forest (RF) analysis reveals the inflammatory footprint
http://www.ncbi.nlm.nih.gov/pubmed/21576403
Full study here:
http://merutt.files.wordpress.com/2011/05/mikovits_lombardi-publikasjon-mai2001.pdf
Increased in ME/CFS and XMRV patients
CD3+
CD56+
NKT population
Of the CD19+ B cells, the % of CD20+, CD23+ are increased in XMRV patients.
Study: http://www.retrovirology.com/content/8/S1/A230
XMRV sequences in B cells from infected individuals have G to A changes.
Sequence data indicate there are different strains of XMRV/HGRV that can infect humans.
I guess she meant a change at the level of nucleotides:
Description of nucleotides at DNA level follows the recommendations of the IUPAC-IUBMB. Nucleotides are designated by the bases, in upper case, A (adenine), C (cytosine), G (guanine), T (thymidine), including those for uncertain nucleotides like Y (pYrimidine) and R (puRine).
Nucleotides are molecules that, when joined together, make up the structural units of RNA and DNA. In addition, nucleotides play central roles in metabolism.
More info at: http://en.wikipedia.org/wiki/Nucleotide
The last study she discussed was about an antiviral defense protein APOBEC3G that attacks viral RNA and changes is sequence.
Cell lines expressing APOBEC3G result in greatly reduced titer (x100) when infected with virus than cell lines that do not express A...
It has been well described in the study of Groom et al.,
http://www.pnas.org/content/early/2010/02/24/0913650107.full.pdf
XMRV symposium, June 9, 2011, Leuven, Belgium (part 2)
Do XMRV and HGRV (Human Gamma Retro Viruses) play a role in ME/CFS?
- diagnosis of exclusion
- > 6 months with no other explanation
- heterogenous
- including multiple immune and inflammatory abnormalities
- anti viral (RNase L) dysfunction
- low natural killer cells and functions
- they kill:
- tumor cells
- viral cells
- innate immune activation
- > number of activated T cells
- increased production of inflammation cytokines/chemokines
- chronic active infections - inflammatory syndromes
Definition: heterogenous [ˌhɛtəˈrɒdʒɪnəs]
adj
(Life Sciences & Allied Applications / Biology) Biology Med not originating within the body; of foreign origin
What do we know about XMRV?
The sequences originally identified in prostate cancer with the HPC1/RNase L gene are allelic variations, especially the R462Q single nucleotide polymorphism.
Integration in situ hybridization in unmanipulated human tissue and antibody responses demonstrate that
XMRV is a human infection although closely related to Xeno, Poly and MLV's.
XMRV is not an endogenous retrovirus in human.
How it got into humans is unclear.
Definition: endogenous /en·dog·e·nous/ (en-doj´ĕ-nus) produced within or caused by factors within the organism
It needs all of your cells to make more virions (virus particles) so it can multiply itself.
Virions have a complex structure and consist of an envelope, a nucleocapsid, and a nucleoid. Virions are spherical to pleomorphic measuring 90-100 nm in diameter[4] or 137 nm[3]. This is very small!
Dr Mikovits went through slides to explain the following studies:
The studies speak for themselves, you can find them here
1. Detection of an infectious retrovirus XMRV, in blood cells of patients of patients with chronic fatigue syndrome
2. Cell-free transmission of XMRV and MRV from PRC negative CFS patients plasma to LNCaP cells
In a study reported in 2009, DNA from peripheral blood mononuclear cells (PBMCs) of CFS patients and healthy controls from the US were tested for the presence of XMRV sequences. XMRV sequences were found in 68 out of 101 CFS patients (67%), as compared to 8 of 218 (3.7%) healthy US controls.
Viral gene sequences identified in CFS patients clustered with sequences from PC, and both sequences were virtually identical. Further investigation using activated CFS patient PBMC co-cultured with susceptible PC cells (LNCaP) showed that virus could be transmitted by cells and supernatant, as indicated by protein expression and transmission electron microscopy, suggesting that the virus being detected by protein expression was infectious.
Virus could also be transmitted in LNCaP cells from 10/12 CFS patient plasma samples. These studies suggested that both cell associated and cell-free transmission of XMRV is possible. Finally, antibodies to XMRV were detected in 9/18 CFS patients using a test based on the envelope of a closely related virus, spleen focus forming virus (SFFV).
Source: http://webcache.googleusercontent.com/search?q=cache:MBxg88Hnw9UJ:forums.phoenixrising.me/archive/index.php/t-8823.html+Cell-free+transmission+of+XMRV+and+MRV+from+PRC+negative+CFS+patients+plasma+to+LNCaP+cells&cd=4&hl=nl&ct=clnk&gl=be&source=www.google.be
3. Detection of MLV-related virus gene sequences in blood of patients with chronic fatigue syndrome and healthy blood donors
Study: http://thirdreviewer.com/2010/pnas-dump-file/detection-of-mlv-related-virus-gene-sequences-in-blood-of-patients-with-chronic-fatigue-syndrome-and-healthy-blood-donors/
Why do some groups fail to detect XMRV?
Variantions in XMRV sequences and low levels of replication of the virus in the blood are the main reasons why some groups fail to detect XMRV.
Clues to pathogenesis?
Hormones + Inflammation => Increase of replication of XMRV
XMRV is responsive to cortisol because stress is often onset to disease.
Stress can be a car accident, an operation, illness, ...
Question of the public: Is cortisol supplementation of hormone therapy detrimental?
Answer of Dr Mikovits: "Everything should be in balance and that includes cortisol."
A footprint of infection?
Can one recognize XMRV infection in the blood? Does it leave a footprint?
Dysregulated cytokine/chemokine production is detected in plasma from ME/CFS patients. It is a typical inflammatory signature of XMRV/MRV infection.
The Random Forest (RF) analysis reveals the inflammatory footprint
http://www.ncbi.nlm.nih.gov/pubmed/21576403
Full study here:
http://merutt.files.wordpress.com/2011/05/mikovits_lombardi-publikasjon-mai2001.pdf
Increased in ME/CFS and XMRV patients
CD3+
CD56+
NKT population
Of the CD19+ B cells, the % of CD20+, CD23+ are increased in XMRV patients.
Study: http://www.retrovirology.com/content/8/S1/A230
XMRV sequences in B cells from infected individuals have G to A changes.
Sequence data indicate there are different strains of XMRV/HGRV that can infect humans.
I guess she meant a change at the level of nucleotides:
Description of nucleotides at DNA level follows the recommendations of the IUPAC-IUBMB. Nucleotides are designated by the bases, in upper case, A (adenine), C (cytosine), G (guanine), T (thymidine), including those for uncertain nucleotides like Y (pYrimidine) and R (puRine).
Nucleotides are molecules that, when joined together, make up the structural units of RNA and DNA. In addition, nucleotides play central roles in metabolism.
More info at: http://en.wikipedia.org/wiki/Nucleotide
The last study she discussed was about an antiviral defense protein APOBEC3G that attacks viral RNA and changes is sequence.
Cell lines expressing APOBEC3G result in greatly reduced titer (x100) when infected with virus than cell lines that do not express A...
It has been well described in the study of Groom et al.,
http://www.pnas.org/content/early/2010/02/24/0913650107.full.pdf
vrijdag 10 juni 2011
Dr Frank Ruscetti on XMRV
XMRV symposium, June 9, 2011, Leuven, Belgium (part 1)
Dr Frank Ruscetti was introduced as the father of retroviruses and kicked off the symposium about XMRV.
Today we have three known retroviruses and XMRV turns out to be 'atrocious'. It appears to be involved in prostate cancer by men, the second most common cancer in men. He asked with a smile if we knew what the first was? ... Marriage.
How did they make the link between prostate cancer and XMRV?
Research in the area of genetic susceptibility to prostate cancer has revealed two potential genes but he essentially spoke about RNaseL:
RNase L turns out to be a candidate prostate cancer gene on chromosome 1q24-25 (HPC1)
=> XMRV is a human retrovirus and is similar to HIV and HTLV-1. It was first identified by Dr. Robert Silverman, in prostate cancer tissue of men with a specific genetic defect in their antiviral defense pathway. (http://www.wpinstitute.com/)
The first studies of RNase L in individuals with CFS were initiated because the clinical symptoms associated with CFS could often be explained by a persistent viral infection or immune suppression, particularly in those patients who experience acute onset. Viral infection of cells results in the production and secretion of cytokines, including the interferons. Interferons control the way cells respond to a virus through a group of inter-related enzymes that comprise an antiviral defense pathway. This pathway is known as the 2',5'-oligoadenylate synthetase/RNase L pathway.
Antiviral pathway abnormalities
The status of the RNase L pathway is measured in humans by sampling peripheral blood mononuclear cells (lymphocytes). RNase L is the key enzyme of the antiviral pathway, and it is designed to degrade viral RNA. While RNase L is found in nearly all mammalian cells, it has to be "turned on" by a small molecule, 2-5A.
Binding of 2-5A to RNase L changes the enzyme from its inactive (latent) state to its active state.
Source: http://www.cfids.org/archives/2000rr/2000-rr1-article01.asp
Is prostate cancer an infectious disease?
Variants in:
- RNase L
- MSR1 (variants of the macrophage scavenger receptor 1 (MSR1) gene)
- and TLR4 (toll-like receptor 4 is a key innate immunity receptor that initiates an inflammatory response primarily against gram-negative bacteria)
associated with risk
- for infections in mammals
- prostate cancer in humans
XMRV is related to MLV
In mice, MLV and related viruses cause:
- immune defiency
- neurodegenerative diseases
- cancer
His conclusion:
XMRV must be heterogenous.
Definition: heterogenous [ˌhɛtəˈrɒdʒɪnəs]
adj
(Life Sciences & Allied Applications / Biology) Biology Med not originating within the body; of foreign origin
He emphasized that XMRV was detected in stroma (human fluid) not tumor cells. Men who stimulated their prostate contained more viral antibodies to ENV (envelop or the cover of the virus) and infectious XMRV in their bodily fluids than men who didn't.
It seems important not to stress the tissue where XMRV is hiding?
http://www.nature.com/nrurol/journal/v7/n7/fig_tab/nrurol.2010.77_T2.html
Conclusion: This is impossible to be explained by contamination.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739868/
XMRV is present in malignant prostatic epithelium and is associated with prostate cancer, especially high-grade tumors
He explained how he found antibodies with the help of his wife Dr Sandra Ruscetti, Head of the Retroviral Pathogenesis Section, Laboratory of Cancer Prevention. She never throws anything away, that's the reason why he's still married to her ...
Why does he think the negative studies are negative?
HTLV is asymptomatic in majority of individuals.
How is XMRV identified?
Dr Ruscetti mentioned an interesting quote from Dr Judy Mikovits: "In chronic diseases viruses seldom come alone, and in ME/CFS many viruses may be implicated."
He referred to the article "War and Peace between microbes" if you like more information about it.
Summary
HIV-1 disrupts the homeostatic equilibrium between the host and coinfecting microbes, facilitating reactivation of persistent viruses and invasion by new viruses. These viruses usually accelerate HIV disease but occasionally create conditions detrimental for HIV-1. Understanding these phenomena may lead to anti-HIV-1 strategies that specifically target interactions between HIV-1 and coinfecting viruses.
http://www.cell.com/cell-host-microbe/abstract/S1931-3128(09)00354-0
Where are we now? Is there contamination?
http://www.retrovirology.com/content/7/1/112
The question remains:
1. the virus has spread through several labs as a cell lab contaminant
or
2. people are contaminated with a virus that originated from cancer research
or
... there is no contamination.
Dr Frank Ruscetti was introduced as the father of retroviruses and kicked off the symposium about XMRV.
Today we have three known retroviruses and XMRV turns out to be 'atrocious'. It appears to be involved in prostate cancer by men, the second most common cancer in men. He asked with a smile if we knew what the first was? ... Marriage.
How did they make the link between prostate cancer and XMRV?
Research in the area of genetic susceptibility to prostate cancer has revealed two potential genes but he essentially spoke about RNaseL:
RNase L turns out to be a candidate prostate cancer gene on chromosome 1q24-25 (HPC1)
=> XMRV is a human retrovirus and is similar to HIV and HTLV-1. It was first identified by Dr. Robert Silverman, in prostate cancer tissue of men with a specific genetic defect in their antiviral defense pathway. (http://www.wpinstitute.com/)
What is the link with ME/CFS?
RNase L is one promising marker that is consistent with an activated immune system in CFS. The first studies of RNase L in individuals with CFS were initiated because the clinical symptoms associated with CFS could often be explained by a persistent viral infection or immune suppression, particularly in those patients who experience acute onset. Viral infection of cells results in the production and secretion of cytokines, including the interferons. Interferons control the way cells respond to a virus through a group of inter-related enzymes that comprise an antiviral defense pathway. This pathway is known as the 2',5'-oligoadenylate synthetase/RNase L pathway.
Antiviral pathway abnormalities
The status of the RNase L pathway is measured in humans by sampling peripheral blood mononuclear cells (lymphocytes). RNase L is the key enzyme of the antiviral pathway, and it is designed to degrade viral RNA. While RNase L is found in nearly all mammalian cells, it has to be "turned on" by a small molecule, 2-5A.
Binding of 2-5A to RNase L changes the enzyme from its inactive (latent) state to its active state.
Source: http://www.cfids.org/archives/2000rr/2000-rr1-article01.asp
Is prostate cancer an infectious disease?
Variants in:
- RNase L
- MSR1 (variants of the macrophage scavenger receptor 1 (MSR1) gene)
- and TLR4 (toll-like receptor 4 is a key innate immunity receptor that initiates an inflammatory response primarily against gram-negative bacteria)
associated with risk
- for infections in mammals
- prostate cancer in humans
In mice, MLV and related viruses cause:
- immune defiency
- neurodegenerative diseases
- cancer
His conclusion:
XMRV must be heterogenous.
Definition: heterogenous [ˌhɛtəˈrɒdʒɪnəs]
adj
(Life Sciences & Allied Applications / Biology) Biology Med not originating within the body; of foreign origin
He emphasized that XMRV was detected in stroma (human fluid) not tumor cells. Men who stimulated their prostate contained more viral antibodies to ENV (envelop or the cover of the virus) and infectious XMRV in their bodily fluids than men who didn't.
It seems important not to stress the tissue where XMRV is hiding?
http://www.nature.com/nrurol/journal/v7/n7/fig_tab/nrurol.2010.77_T2.html
Conclusion: This is impossible to be explained by contamination.
Image: http://vipdx.com/faqs/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739868/
XMRV is present in malignant prostatic epithelium and is associated with prostate cancer, especially high-grade tumors
He explained how he found antibodies with the help of his wife Dr Sandra Ruscetti, Head of the Retroviral Pathogenesis Section, Laboratory of Cancer Prevention. She never throws anything away, that's the reason why he's still married to her ...
Why does he think the negative studies are negative?
- XMRV is not truly associated with human disease;
- The technique: everything is in the details;
- unrecognized sequence details
- geographical distribution (cfr HTLV)
- Primates don't necessarily develop human diseases (cfr HIV)
HTLV is asymptomatic in majority of individuals.
- 5-8% lifetime risk
- evidence for geographical distribution like Japan
- adult T-cell leukemia
- clonal malignancy of CD and T cells
- long latency
- immune deficiency
- TAX and HBZ needed for transformation
- inflammatory syndromes
How is XMRV identified?
- antibody detection
- PCR for viral genes
- FISH (Fluorescence in situ hybridization)
- integration into human tissue
Dr Ruscetti mentioned an interesting quote from Dr Judy Mikovits: "In chronic diseases viruses seldom come alone, and in ME/CFS many viruses may be implicated."
He referred to the article "War and Peace between microbes" if you like more information about it.
Summary
HIV-1 disrupts the homeostatic equilibrium between the host and coinfecting microbes, facilitating reactivation of persistent viruses and invasion by new viruses. These viruses usually accelerate HIV disease but occasionally create conditions detrimental for HIV-1. Understanding these phenomena may lead to anti-HIV-1 strategies that specifically target interactions between HIV-1 and coinfecting viruses.
http://www.cell.com/cell-host-microbe/abstract/S1931-3128(09)00354-0
Where are we now? Is there contamination?
http://www.retrovirology.com/content/7/1/112
The question remains:
1. the virus has spread through several labs as a cell lab contaminant
or
2. people are contaminated with a virus that originated from cancer research
or
... there is no contamination.
donderdag 9 juni 2011
Wat veranderde er?
De opkomst voor het XMRV-symposium in Brussel was bedroevend laag. Veel patienten blijken te ziek om zich te verplaatsen zelfs al kwamen topwetenschappers hun bevindingen over XMRV voorstellen.
De informatie was zeer degelijk. Vraagstukken, onderzoeksmethodes en conclusies werden gestructureerd gepresenteerd. Later poog ik een samenvatting te maken van de nota's.
Na afloop had ik de kans enkele woorden te wisselen met Dr Maureen Hanson en Dr Frank Ruscetti. Mijn vraag was welke informatie voor hen van belang is in het onderzoek. Ze waren redelijk unaniem.
"Wat veranderde er in je omgeving vlak voor jij ziek bent geworden?"
Heb je een huisdier gekregen?
Is er een nanny in huis gekomen?
Had je (wilde) muizen of andere knaagdieren in huis?
Heb je een vaccin gekregen?
Kreeg je een nieuwe vriend(in)?
Ben je verhuisd?
Ging je kind naar een andere kinderopvang?
Ben je naar een feest geweest?
Ben je op vakantie gegaan?
...
Denk er eens over na. We komen er later op terug.
De informatie was zeer degelijk. Vraagstukken, onderzoeksmethodes en conclusies werden gestructureerd gepresenteerd. Later poog ik een samenvatting te maken van de nota's.
Na afloop had ik de kans enkele woorden te wisselen met Dr Maureen Hanson en Dr Frank Ruscetti. Mijn vraag was welke informatie voor hen van belang is in het onderzoek. Ze waren redelijk unaniem.
"Wat veranderde er in je omgeving vlak voor jij ziek bent geworden?"
Heb je een huisdier gekregen?
Is er een nanny in huis gekomen?
Had je (wilde) muizen of andere knaagdieren in huis?
Heb je een vaccin gekregen?
Kreeg je een nieuwe vriend(in)?
Ben je verhuisd?
Ging je kind naar een andere kinderopvang?
Ben je naar een feest geweest?
Ben je op vakantie gegaan?
...
Denk er eens over na. We komen er later op terug.
vrijdag 3 juni 2011
donderdag 2 juni 2011
Dag 459 Twijfel
Ik probeer het weer eens zonder cortisone vandaag. De pijnlijke borstkast, keelpijn en 50 kilo onzichtbare kilo’s trekken me op de zetel. Angst voor de nevenwerkingen van dit straffe goedje doen me weer eens twijfelen.
Wat is wijsheid? Kiezen voor een pijnlijk leven vol uitputting en orgaanbeschadiging of eindelijk minder pijn en meer energie maar een paar jaar vroeger sterven met – een greep uit de mogelijkheden - kans op diabetes, botbreuken en 20 kilo extra?
Vanavond zal ik op mijn tandvlees zitten, megachagrijnig zijn en uiteindelijk een hekel aan alles en iedereen hebben. Dan zal ik weer snakken naar dat pilletje cortisone en begint de twijfel opnieuw.
Dag 458 Vooruitgang
Voor het eerst sinds lang voel ik me lekker. Mijn armen blijken weer functioneel, een niet te versmaden voordeel. De haardroger is geen marteltuig vandaag. Mijn ogen staan fris en helder. De huisarts is benieuwd naar de dosis hydrocortisone (20 mg ochtend en 10 mg namiddag) en DHEA (10mg).
Het blijkt een straffe hoeveelheid te zijn. Dat vermoedde ik al maar het werkt. Na een maand gebruik en 4 baxters (eiwitten, vitaminen en mineralen) in het dagziekenhuis gaat mijn gezondheid met sprongen vooruit. Vandaag voor het eerst sinds lang weer tot halfdrie ’s middags op de been kunnen blijven! Normaal gezien kom ik voor 16 uur mijn bed niet uit ... behalve om te eten.
De vlekken op mijn benen zijn inderdaad een vorm van vasculitis. Niet erg elegant maar het zou tijdelijk moeten zijn. Als ik de literatuur mag geloven, is het eigen aan systeemlupus. Dat heb je als ze je ziekte jarenlang negeren. Dan gaat alles flippen in je lijf. Aan wie mag ik de rekening presenteren? Aan de heren psychiaters van de referentiecentra?
Het blijkt een straffe hoeveelheid te zijn. Dat vermoedde ik al maar het werkt. Na een maand gebruik en 4 baxters (eiwitten, vitaminen en mineralen) in het dagziekenhuis gaat mijn gezondheid met sprongen vooruit. Vandaag voor het eerst sinds lang weer tot halfdrie ’s middags op de been kunnen blijven! Normaal gezien kom ik voor 16 uur mijn bed niet uit ... behalve om te eten.
De vlekken op mijn benen zijn inderdaad een vorm van vasculitis. Niet erg elegant maar het zou tijdelijk moeten zijn. Als ik de literatuur mag geloven, is het eigen aan systeemlupus. Dat heb je als ze je ziekte jarenlang negeren. Dan gaat alles flippen in je lijf. Aan wie mag ik de rekening presenteren? Aan de heren psychiaters van de referentiecentra?
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