Coxsackie & EBV in Muscles, and Coxsackie in Ticks – Good LORD!!

 

Br Med Bull. 1991 Oct;47(4):852-71.

Persistent virus infection of muscle in postviral fatigue syndrome.

Abstract

Nucleic acid was extracted from muscle biopsy samples from a series of highly selected patients suffering from chronic muscle fatiguability following a viral infection (Postviral Fatigue Syndrome: PVFS). Samples were examined for the presence of enteroviral RNA sequences or Epstein-Barr (EBV) virus DNA sequences by molecular hybridisation as these two agents have been implicated by retrospective serology in the aetiology of PVFS. We found enteroviral RNA in 24% of biopsy samples and EBV DNA in a further 9% of biopsy samples: no biopsy was positive for both enteroviral RNA and EBV DNA. In addition, in the case of enteroviruses we found that the persisting virus is defective in control of RNA replication as both strands of enteroviral RNA are present in similar amounts: this is unlike the asymmetric synthesis of genomic RNA seen in a productive, cytolytic enterovirus infection. The implications of these data in relation to mechanisms of viral persistence and muscle dysfunction are discussed.

https://www.ncbi.nlm.nih.gov/pubmed/1665379https://www.ncbi.nlm.nih.gov/pubmed/1665379

 

 

CROSS TOLERANCE means one immunosuppressing type antigen leads to immunosuppression against another type of antigen.  Like how shed blebs or OspA vaccination (TLR2/1) cause suppression against EBV (TLR7/9, as shown by Clifford Harding at Case Western Reserve, …and Nicole Baumgarth/Steve Barthold at UC Davis re influenza virus:

 

Clifford Harding on how fungal toxins like OspA turn off the immune response to viruses like EBV:

”Because IRAK1 is required for TLR7/9-induced IFN-I production, we propose that TLR2 signaling induces rapid depletion of IRAK1, which impairs IFN-I induction by TLR7/9. This novel mechanism, whereby TLR2 inhibits IFN-I induction by TLR7/9, may shape immune responses to microbes that express ligands for both TLR2 and TLR7/TLR9, or responses to bacteria/virus coinfection.”  https://www.ncbi.nlm.nih.gov/pubmed/22227568

 

An experiment injecting mycoplasma and live viruses together:

 

THE RELATIONSHIP OF EPERYTHROZOON COCCOIDES TO THE HEPATITIS VIRUS OF PRINCETON MICE    
“In Swiss mice, animals with high natural resistance to hepatitis virus, the pathogenicity of this agent was markedly enhanced by combined infection with eperythrozoa. Eperythrozoa were maintained throughout 18 successive passages in normal Princeton and Swiss weanlings with intact spleens. The combined infection of Princeton mice with eperythrozoa and the virus component of Gledhill, Dick, and Andrewes, which is nearly inactive when injected alone, resulted in acute hepatitis with fatal outcome.”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136329/?tool=pubmed

 
’Which is why Thimerosal is put in vaccines – to prevent fungi -, since the immunosuppression results in reactivated viruses and this is actually a well-known thing.

 

 

Where else do we see immunosuppression resulting in reactivate latent herpesviruses?

Stelara, Humira (“lymphoma” warnings, which means EBV) commercials, transplant victims. hospital sepsis victims, astronauts and medical school student due to their cortisol (stress !!) induced immunosuppression (Chronic Fatigue from reactivated Mono) and disruption of their sleep-wake cycle…

 

You see it and you hear about it every day.

 

Only one thing predictably happens in immunosuppression: EBV, et al, have a free for all.

 

And guess what, there is no vaccine against it, since such prevention would put BigPharma out of business, wouldn’t it.

 

 

 

See:

Mono: Symptoms, Diagnosis and Treatment Options – Sep, 2014

“People believe that it is common to have a chronic mono infection that can cause problems for years. This is really not the case,” said Hymes. EBV is a viral illness in the same family as herpes and varicella (chickenpox). Like those other members of the herpes virus family, the virus can stick around in your body, Hymes explained. However, the virus is dormant and only very rarely reactivates, usually in times of stress. “Chronic active Epstein-Barr infection is something we really only see in people with immune problems — transplant patients, HIV patients, or people born missing a part of their immune system or immune function,” said Hymes. Lab testing can detect chronic presence of the virus and can rule it out, so it is easily diagnosed.

 

“Some studies suggested that acute infectious mononucleosis and Epstein-Barr virus may permanently alter or impair the immune response. A 2007 Danish study looked at the possible correlation between multiple sclerosis and infectious mononucleosis and found that the risk of multiple sclerosis was persistently increased for more than 30 years after contracting infectious mononucleosis.
Mono may also be responsible for chronic fatigue syndrome. EBV persistence in the muscles biopsy samples, when looked at in patients with post-viral muscle fatigability, is seen far less commonly (9%) then in patients recovering from enterovirus infections (24%) according to a study done by the Department of Biochemistry at Charing Cross and Westminster Medical School, London, UK.

http://www.livescience.com/34784-mono-symptoms-treatment-diagnosis.html

 

 

Or it (EBV reactivation) is caused by Lyme or LYMErix vaccination, since Lyme and LYMErix are fungal-ish immune suppressors, and deliberately target the lymph nodes, and damage the B cell maturations or germination centers there, rendering the victims unable to fight off non-fungal infections, says Ucal, Davis:

PLoS Pathog. 2015 Jul 2;11(7):e1004976. doi: 10.1371/journal.ppat.1004976. eCollection 2015.

Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection.

Elsner RA1, Hastey CJ1, Olsen KJ2, Baumgarth N3.

Author information

Abstract

Lyme Disease caused by infection with Borrelia burgdorferi is an emerging infectious disease and already by far the most common vector-borne disease in the U.S. Similar to many other infections, infection with B. burgdorferi results in strong antibody response induction, which can be used clinically as a diagnostic measure of prior exposure. However, clinical studies have shown a sometimes-precipitous decline of such antibodies shortly following antibiotic treatment, revealing a potential deficit in the host’s ability to induce and/or maintain long-term protective antibodies. This is further supported by reports of frequent repeat infections with B. burgdorferi in endemic areas. The mechanisms underlying such a lack of long-term humoral immunity, however, remain unknown. We show here that B. burgdorferi infected mice show a similar rapid disappearance of Borrelia-specific antibodies after infection and subsequent antibiotic treatment. This failure was associated with development of only short-lived germinal centers, micro-anatomical locations from which long-lived immunity originates. These showed structural abnormalities and failed to induce memory B cells and long-lived plasma cells for months after the infection, rendering the mice susceptible to reinfection with the same strain of B. burgdorferi. The inability to induce long-lived immune responses was not due to the particular nature of the immunogenic antigens of B. burgdorferi, as antibodies to both T-dependent and T-independent Borrelia antigens lacked longevity and B cell memory induction. Furthermore, influenza immunization administered at the time of Borrelia infection also failed to induce robust antibody responses, dramatically reducing the protective antiviral capacity of the humoral response. Collectively, these studies show that B. burgdorferi-infection results in targeted and temporary immunosuppression of the host and bring new insight into the mechanisms underlying the failure to develop long-term immunity to this emerging disease threat.
https://www.ncbi.nlm.nih.gov/pubmed/26136236

 

 

 

 

 

Diseases caused by enterovirus infection (Cocksackie, Foot and Mouth Disease)

  • Poliomyelitisprimarily via the fecal-oral route
  • Polio-like syndromefound in children who tested positive for enterovirus 68.[23][24]
  • Nonspecificfebrile illness is the most common presentation of enterovirus infection. Other than fever, symptoms include muscle pain, sore throat, gastrointestinal distress/abdominal discomfort, and headache. In newborns the picture may be that of sepsis however, and can be severe and life-threatening.
  • Enteroviruses are by far the most common causes ofaseptic meningitis in children. In the United States, enteroviruses are responsible for 30,000 to 50,000 meningitis hospitalizations per year as a result of 30 million to 50 million infections.[2]
  • Bornholm diseaseor epidemic pleurodynia is characterized by severe paroxysmal pain in the chest and abdomen, along with fever, and sometimes nausea, headache, and emesis.
  • Pericarditisand/or myocarditis are typically caused by enteroviruses; symptoms consist of fever with dyspnea and chest painArrhythmias, heart failure, and myocardial infarction have also been reported.
  • Acute hemorrhagic conjunctivitiscan be caused by enteroviruses.
  • Herpanginais caused by Coxsackie A virus, and causes a vesicular rash in the oral cavity and on the pharynx, along with high fever, sore throatmalaise, and often dysphagia, loss of appetite, back pain, and headache. It is also self-limiting, with symptoms typically ending in 3–4 days.
  • Hand, foot and mouth diseaseis a childhood illness most commonly caused by infection by Coxsackie A virus or EV71.
  • Encephalitisis rare manifestation of enterovirus infection; when it occurs, the most frequent enterovirus found to be causing it is echovirus 9.
  • A 2007 study suggested that acute respiratory or gastrointestinal infections associated with enterovirus may be a factor inchronic fatigue syndrome.[25]
  • Diabetes mellitus type 1It has been proposed that type 1 diabetes is a virus-triggered autoimmune response in which the immune system attacks virus-infected cells along with the insulin-producing beta cells in the pancreas.[26] A team working at University of Tampere, Finland has identified a type of enterovirus that has a possible link to type 1 diabetes (which is an autoimmune disease).[27][28]

https://en.wikipedia.org/wiki/Enterovirus

 

More on enteroviruses, possibly in ticks:
https://www.ncbi.nlm.nih.gov/pubmed/?term=enterovirus+and+ticks

 

Are people getting foot and mouth disease from Plum Island-escaped ticks, too (Plum Island has always experimented with Hoof and Mouth disease)?   Imagine how sick people are with Lyme, if they have all these combined devastating illnesses? Yet, we’re all trashed aren’t we? Are we trashed because this is crime or are we trashed because we represent a bioweapons experiment (escaped ticks) gone horribly wrong? Why is the CDC lying about all this? For personal staff vaccines incomes reasons? Has this scam gone on so long the CDC and NIH finds no way of backing away from all their lies? Is the HHS.gov mortified at the prospect at having been discovered to 200% incompetent to their mission? Now they’re selling “vaccines” that actually give people the very diseases the vaccines are intended to prevent?

 

It happened with the MMRs and it happened with LYMErix (giving people an immunosuppression disease).

 

 

 

 

 

 

 

 

 

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