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AUTO-IMMUNE DISCOVERIES
*****


Information on this page pertains to Multiple Sclerosis, Lou Gehrigs, A.L.S., cystitis, R. Arthritis, Lupus, Fibromyalgia, Graves disease, Crohns disease, and other autoimmune disorders.

The Mission of This Page is to demonstrate that the majority of Autoimmune Diseases may be caused by viruses.


DISCLAIMER

If someone reading this publication has a shred of concrete or even corroborated, anecdotal evidence that a virus cannot be linked to almost all common autoimmune disorders
please send me the scientific
papers or files!!!!!
**
In a Superior Court of law, testimony does not need to be backed up by an expert if the facts being presented are facts that,
“are widely accepted in the field and commonly
 relied upon by experts.”
***
In law, a person cannot be restricted, fined, or imprisoned
 for relating personal experiences or expressing
personal opinions!
***

Bret Peirce is a licensed nuse and descendant of Benjamin Osgood Peirce and
 Charles Saunders Peirce.  Information on this page is derived from the research paper
Unified Theory Of Disease.

 

 

 

Introduction

Even lay-people who take high school biology know that B-cells and T-cells are anti viral and are almost always associated with onset
 of any viral illnesses.

Why can’t it be that these anti-viral cells happen to just be
doing exactly what they are suppose
 to be doing?

Why can’t the obvious even be considered as an answer?

Why does it have to go anywhere beyond this?

Lymphocytes are merely attacking a virus that has attacked a stressed tissue in a compromised host?

Why can’t we start with the obvious?
Right here!

Or would you rather believe, against the all laws of nature and biology, our immune body decides to attack us for a
 time period and then stop for no
apparent reason?

Are you willing to bet a lot of money on this
autoimmune theory any more,
since Tulane?

 How many lives will you bet  that autoimmune
 is a condition where our bodies commit
suicide and then suddenly 
stop?

When bacterial cells attack our own tissue it’s always
because of one thing,…there is a
bacterium in that
very tissue!

But when a lymph cell attacks tissue, why does it have to become so
 much more confusing and expensive?

That very white cell that’s attacking the collagen can have a
virus that infects it, for goodness sake!

To have thought a virus couldn’t infect collagen
was completely illogical!

Why did anybody ever think that collagen
couldn’t have a virus that infects it?

 



CONCLUSION

We should all see that it is very unintelligent to think that where there is one
virus there can’t be two!

It would be equally unintelligent to think that we are finished discovering microorganisms at the heart of some of 
our most terrible diseases.

**** 


**HUGE DISCOVERY**

Every year or so someone who is very brilliant discovers that there is a new virus at the heart of a serious
chronic disease.

Most recent virus associated with terrible illnesses are seen below. Before we can understand autoimmune we have to
understand viruses.

Please review this latest discovery by Tulane Medical School.
This is an actual excerpt from Tulane's Article....

 

THE AUTOIMMUNE DISEASE VIRUS ASSAY (ADVA)

This material is not intended to take the place of a physician's advice.

Researchers at Tulane Medical School have discovered a human retrovirus called the Human Intracisternal A-type Particle, or HIAP. It is the first A-type retrovirus to have been found in humans.

Research data strongly suggests that this virus is the cause of four well-known autoimmune disorders.
These disorders are lupus (systemic lupus erythematosus), Sjögren's syndrome, Graves' disease, and juvenile rheumatoid arthritis.

The Autoimmune Disease Virus Assay (ADVA) detects
antibodies against HIAP. These antibodies appear in approximately 95% of patients with one or more of those four disorders but in fewer than 2% of healthy individuals. The Company believes that infection by this virus may produce the differing symptoms of the disorders in different patients because of genetic variations in the immune systems of the patients.

The published results of a study of an AIDS drug in Sjögren's patients suggest that anti-retroviral drugs may act against this virus.


The ADVA is covered by patents in the U.S. and other countries.   



                



BASIC VIROLOGY

 

  • MOST LAY-PEOPLE DO NOT KNOW THAT EVERY LIVING TISSUE, ORGANISM, BACTERIA, FUNGUS, ALGAE, PARASITE, INSECT, PLANT, TREE, ANIMAL, MOLUSC, FISH, AND SINGLE BLOOD CELL CAN HOST A VIRUS.

 

  • THEY DO NOT KNOW THAT JUST ABOUT EVERY KIND OF TISSUE IN YOUR BODY HAS A VIRUS THAT CAN ATTACK IT! EVEN YOUR RETINA OR A SINGLE WHITE BLOOD CELL,(REMEMBER H.I.V. and LEUKEMIA)

 

  • THEY DO NOT KNOW THAT THERE IS A VIRAL GENE EXPRESSED IN MANY, AUTOIMMUNE, LEUKEMIAS, LYMPHOMAS, SARCOMAS, AND SEVERAL CANCERS.

 



Multiple Sclerosis

I have compiled a very short collection a research conclusions that indicate M.S. is in fact a virus! Epstein Barr, retrovirus, and cytomegalo viruses are implicated. (But not herpes)

Abstract I

A strain of cytomegalovirus (CMV) was isolated during the third subcultivation of explants from the left frontal lobe of a chimpanzee that developed paralysis more than 3 years after intracerebral inoculation at birth with brain cell cultures derived from a patient with multiple sclerosis. Another strain of CMV was also isolated from a lymph node culture taken from the same chimp. The isolates, designated MZM-13 and MZM-14, produced a cytopathic effect characteristic for CMV when inoculated into brain, ganglion, or fibroblast cultures of human or simian origin. Infected cells contained characteristic Cowdry A intranuclear as well as intracytoplasmic inclusion bodies, and 100-nm spherical herpes-like virus particles were detected by electron microscopy in the nucleus and cytoplasm of infected cells. Virus was further identified as CMV with convalescent human anti-CMV serum. Complement-fixing antibody to CMV was present at a titer of 1:32 when the acutely ill chimpanzee was sacrificed. No antibody was detected at birth or at 1 or 2 years of age. A newborn chimpanzee inoculated intracerebrally with MZM-13 developed clinically asymptomatic lesions in the central nervous system characterized by acute and chronic inflammation and degeneration of myelin in cranial and spinal nerve roots. Restriction endonuclease analysis of viral deoxyribonucleic acid isolated from these two viruses indicated that MZM-13 and MZM-14 are identical and are closely related to chimpanzee CMV. No similarity in restriction endonuclease fragment patterns was found between MZM virus and the Towne and Clegg strains of human CMV. 



Abstract II....   linked PDF

 

 

             

           [PDF]

R Alvarez-Lafuente, M Garcia-Montojo, V De Las Heras, M. Dominguez-Mozo, M Bartolome, M. Benito-Martin, and R Arroyo
Herpesviruses and human endogenous retroviral sequences in the cerebrospinal fluid of multiple sclerosis patients
Multiple Sclerosis, June 1, 2008; 14(5): 595 - 601.

            
           

 Abstract III 

                             Multiple Sclerosis and Epstein-Barr Virus

Objective 
To determine whether antibodies to EBV are elevated before the onset of MS.

Design, Setting, and Population  Nested case-control study conducted among more than 3 million US military personnel with blood samples collected between 1988 and 2000 and stored in the Department of Defense Serum Repository. Cases were identified as individuals granted temporary or permanent disability because of MS. For each case (n = 83), 2 controls matched by age, sex, race/ethnicity, and dates of blood sample collection were selected.

Main Outcome Measures  Antibodies including IgA against EBV viral capsid antigen (VCA) and IgG against VCA, nuclear antigens (EBNA complex, EBNA-1, and EBNA-2), diffuse and restricted early antigens, and cytomegalovirus.

Results  The average time between blood collection and MS onset was 4 years. The strongest predictors of MS were serum levels of IgG antibodies to VCA or EBNA complex. The risk of MS increased monotonically with these antibody titers; relative risk (RR) in persons in the highest category of VCA ( 2560) compared with those in the lowest ( 160) was 19.7 (95% confidence interval [CI], 2.2-174; P for trend = .004). For EBNA complex titers, the RR for those in the highest category ( 1280) was 33.9 (95% CI, 4.1-283; P for trend <.001) vs those in the lowest category ( 40). Similarly strong positive associations between EBV antibodies and risk of MS were already present in samples collected 5 or more years before MS onset. No association was found between cytomegalovirus antibodies and MS.

Conclusion  These results suggest a relationship between EBV infection and development of MS.
Epstein-Barr Virus in Pediatric Multiple Sclerosis
Suad Alotaibi, MD; Julia Kennedy, MSc; Raymond Tellier, MD; Derek Stephens, MSc; Brenda Banwell, MD
JAMA. 2004;291:1875-1879.

Context  Infection with common viruses, particularly Epstein-Barr virus (EBV), has been postulated to contribute to the pathobiology of multiple sclerosis (MS). Detailed virological studies in pediatric MS have not been previously reported.

Objective  To evaluate whether children with MS are more likely to be seropositive for EBV or other common viruses than their healthy age-matched peers.

Design, Setting, and Patients  Case-control study of viral samples collected from March 1994 to February 2003 from 30 pediatric MS patients, 90 emergency department controls matched 3:1 with the MS patients by year of birth, and 53 healthy control children.

Main Outcome Measures  Archived serum samples were analyzed for the presence of IgG antibodies directed against EBV viral capsid antigens, nuclear antigens, and early antigens, cytomegalovirus, parvovirus B19, herpes simplex virus, and varicella zoster.

Results  Serological evidence for remote EBV infection was present in 83% of pediatric MS patients compared with 42% of emergency department and healthy controls (P<.001). Five pediatric MS patients were negative for all 3 EBV antigens. Pediatric MS patients were less likely than controls to have been exposed to herpes simplex virus (P = .003), while seropositivity for cytomegalovirus, parvovirus B19, and varicella zoster did not differ between MS patients and controls.
Conclusion  These results suggest an association between EBV infection and pediatric MS.


                                                                          

Abstract IV

Selective association of multiple sclerosis with infectious mononucleosis 

The average age of onset of IM in the population of MS cases (16.5 years) did not differ from controls (16.8 years). Our data confirm previous much smaller studies to show that the risk for MS is significantly enhanced by prior IM, and extend those previous data by showing that this association is far stronger than with other common childhood infections or afflictions. Multiple scelerosis 2008; 14: 307—313. http://msj.sagepub.com

 Conclusion  These results suggest an age-dependent relationship between EBV infection and development of MS.


 Commentary On Viral Relationships To Autoimmune
(Excerpts From Unified Theory Of Disease)






   WHY DO WE NEED ANY MORE EVIDENCE? 



So, Anyone Who Thinks Viruses Cannot Cause
 Autoimmune Diseases Please
Solve These Riddles.

How many different hepatitis viruses are there now?

What causes cervical cancer?

Remember the days when there was no HantaVirus,
no West Nile, no HIV?

Remember when Leukemia and Lymphoma
was a cancer?

Look up myocarditis! We can see the names of viruses
 that can cause this  illness.

Also see that Lupus, Rheumatoid Arthritis, Scleroderma
 ALSO causes the exact
 same disease!

Ask yourself this question,...

"Why does a virus cause the exact same conditions
as an autoimmune?"

 Can anyone look in the mirror and say with certainty that
 all these conditions are
not related?
 

Well, according to Tulane it never has been a coincident that the retroviruses implicated in myocarditis was
also seen lurking in Lupus and other related
 disorders that also happen
 to cause,....what?

 Myocarditis!

 

I’ve been screaming this viral connection for twenty plus years. Even biochemically when analyzed immune markers, (antibodies and cytokines,)  are the same for both
autoimmune and viral
 infections. 


 On the "Proof," page is a description of these actual biochemical and antibody studies which have discovered identical
 characteristics between supposedly,
"unrelated," disorders.

Heck! What better link did we need!

If one examines just the basic patterns associate with the autoimmune disorders they all have the same
variations or presentations as severe
viral infections,  just in their
 epidemiology and
characteristics
alone.

*** 

 

  


WORLD'S MOST POWERFUL
ARGUMENT TO DATE


  The A.M.A. Cannot Answer Any of These Questions



  --} Why does the tissue destruction start first in original tissues, but then spread to adjacent Tissues like an infection would do?     

--} Why does the body attack tissues in pockets and not the entire system of tissues.

--}Why does the body stop attacking itself once it has started? (auto immune remission,) which normally never happens in transplant rejection?

--} Once rejected A tissue is always rejected but who not in Auto immune?

--}Why hasn’t modern medicine produced any kind of evidence that indicates there can’t be a virus linked to A.I. disorders?

--} Why does the Guilliam Barre’, "virus" behave identically as A.L.S. and M.S causing de-myelination by way of lymphocytes? Why can’t A.L.S. and M.S. be treated ? Why can’t G.B. be treated?

--} Why do almost all alternative therapies touted for treating viruses and also get touted by different scientist for treating auto immune diseases as well?

--}If autoimmune is not caused by a biological agent or a chemical/physical agent, then why can’t we see it passed on to children and grandchildren, a genetic disorder?

--} Why is the number of A.I. growing but not in descending relatives acting just like a comunicable disease? 

--} Why do autoimmune diseases present identical bio-chemical markers as are found in serious viral infections? (Identical!!)

--}
Why don’t antibacterial cells have any autoimmune diseases where they try to kill us?

--} Why in autoimmune always anti viral cells doing the destruction?

--}If our immune system actually rejects our own tissues, why doesn’t cortisone help stop rejection?

--} Why does almost every autoimmune disease have a licensed doctor somewhere saying he thinks it’s a viral infection?.

--}  Why did Iceland have zero incidents of multiple sclerosis throughout its entire history until English troops landed there during WWII?

--} Why did Iceland have not one but several brand new cases show up in local population following British Arrival.

--}Why do autoimmune diseases seem to target, (low oxygen) tissues

--} Why do anaerobes target low oxygen tissues?

--}Why do some autoimmune diseases have geographical factors? Does our body just decide to kill us because of where we live

--}Why do some viruses have geographical factors like some autoimmunes?
 

--} Why can polio be a virus but other disorders mimicking polio, like Distrophy, can’t be? 

--} Why are viruses so difficult to find! Why are autoimmune riddles difficult to solve?
 
--}Why do demyelinating diseases prefer women at a certain age group?

--}  Why do some blood born pathogens prefer women at a certain age groups.

--} Why are researches finding identical antibody proteins in autoimmune disorders as they find in severe viral infections ?

--} Why, in alternative medicine and traditional medicine, are treatments for HIV and hepatitis being associated with autoimmune disorders treatments as well?

--} Why does stress trigger dormant viral infections (shingles, herpes, hepatitis c, etc.)

--} Why does stress trigger autoimmune reactions too?    

--}Why does severe injury or secondary infection bring out dormant viral infections?

--} Why does severe injury or secondary infection bring out dormant autoimmune disorders too?

--} Why is Epstein Barr infection so common in Lupus and other inflammatory disorders?  

--} Why is there such strong association between autoimmune and viruses?

--} Why are M.S. patients reporting favorable course during hyperbaric oxygen treatments?

--} Why are M.S. patients now getting better using gamma globulin and interferon? These are in fact  
     anti viral treatments.

--} Why are autoimmune patients so susceptible to secondary infections if their immune systems are 
      in fact, over reactive.

--} Why does white cell counts drop so low in very late autoimmune stages?


There is one single answer that can explain these riddles ...


     
"….because autoimmune disorders are viral    
        infections!"








                          

                          MORE OBVIOUS IS TOO OBVIOUS


All sclerotic disorders, inflammatory disorders, and collagen disorders have different degrees of severity.
 
Nobody is going to argue this point!

Here is the basic general pattern; these are not exact to every disorder but they are a rough generalization that is not going to be disputed by medical professionals:

1) 30%will have one flare-up (severe or mild) and never a second, going undiagnosed in mild.  

2) 30% of the victims will have a slow, chronic course, (progressive)    

3) 30% of the victims will have a cycle of acute illness followed by remissions.

4) A fraction of the victims will have such a severe illness that they never seem to recover, death can result or permanent injury to tissues.


Now compare these variants to viral disease patterns of cytamegalo, herpatic, retro- viruses, adeno virus, epstein bar!
 
In general:

1) 30% will have one flare-up (severe or mild) and never a second, going undiagnosed in mild.

2) 30% of the victims will have a slow, chronic course. (progressive)

3) 30% of the victims will have a cycle of acute illness followed by remissions.

4) A fraction of the victims will have such a severe illness that they never seem to recover, death can result.


Does anyone see any similarities between autoimmune and viral patterns?

                    
                     Other Diseases And Viruses

Even viral-linked cancers like leukemia and lymphoma share an active vs. dormancy cycle and behave like the virus that infected its cells. (Especially Lymphomas) But note that some Leukemias have no viral associations.

Even hemorrhagic cystitis, (an autoimmune,) is now proven to be caused by adenoviruses and still is being called autoimmune in some circles! Why?
 
But what about milder forms of cystitis still being called an autoimmune?  What evidence is there saying they are not viruses?
Well, there is none.

Well, DMSO treats interstitial cystitis! It’s FDA approved.

How does it work? Couple theories but none pertaining to viruses, yet it is FDA approved! Go to FDA website if you don't believe me.
 
It would be too easy to say that DMSO, best known for carrying oxygen, deprives anaerobes of their oxygen-free environment!

That would be awfully simple and cheap. Wouldn't it!

The most suspicious thing of all is to examine all the known human viruses. See that almost every tissue, which has an immune disorder linked to it, can also have a viral illness that exists in that very same tissue! I have enclosed a list for you! These were viruses that I didn't even know existed and I've been a nurse for over a decade. 

When reading about these rare viral infections one can see clearly that the symptoms and patterns resembles autoimmune presentations.

So, the possibility that a second virus is wreaking same havoc upon the same tissue, is very, very possible. Also, the possibility that this one rare virus can be sometimes misdiagnosed as an A.I. disease is not a far- fetched prediction! It has never been really disputed by any hard evidence.

What makes fibrous tissues and collagen immune from viruses anyway? Well, they’re not anymore! Thank you Tulane for showing us that a virus infection happens in connective tissue!

We all should have seen this coming!






     A VERY BAD CRIME STORY IS OUR A.M.A. 
       
BUT LEAVE THE DOCTORS ALONE


                            

It is true. Doctors are trained, taught, molded by the A.M.A.
They are subject to their rules
and their philosophies.


  Going against A.M.A.
is a risky proposition. So don't
blaim the actual doctors
 for this very bad
 crime story.


But Imagine a CSI drama where:
 
 * Viral fingerprint at the crime scene and a viral*
 footprint as well.

* The M.O. of the perpetrator mimics that of a virus. *

*The patterns of the perpertrator mimics that of*
of virus.

* Viruses were spotted in the next block over by a *
 couple of witnesses!

* But wait the police say, "it can't be a virus who committed the crime!" *

* No one ever looks or attempts to rule out a * 
virus as the perpetrator!

* Instead they devote millions of dollars to convicting *
the victim of the original crime!

 * Yet everytime a forensic piece is examined,*
they find more and more
 viral associations!

*..and incredibly still they try to blame the victim for his* own poor health, still refuse to investigate the
virus!



This could be great material for RENO 911, wouldn't you agree!
But this is exactly what the Lupus Foundation, Arthritis foundation,  and the FDA are doing.


 



 
MISLEADING INTERPRETATIONS OF 
ACTUAL RESEARCH


A reputable scientist, (remaining nameless) who is published in Bentham Science, and just about everywhere else, is a brilliant man, has isolated the very
lymphokyne and interferon that are
 "over produced" in a couple
autoimmune disorders.

 
That would seem like an achievement!
Everyone is acting like its an achievement!
Going to help us make interferon blockers one day!

At Tulane they are saying, "NO KIDDING,
 we've all found the virus,  and your
not that brilliant!"

He actually represented his remarkable research as a "Target"
 for drug therapy, hoping to one day "correct"
this over-production of
  interferon.
 
Don’t laugh!
There is a twist:

He also discovered that this very same "overproduced" factors are  "found"
in viral leukemia and severe
 viral diseases!

Imagine that! Couldn’t see that coming!
 
Immune factors are the same as viral infections?
Thing that make us say,  Hmmm?

This brilliant scientist never, ever did say,
"Hey! Maybe to understand autoimmune,
we should look at this viral link?"

This brilliant man did not say, (nor did his supervisors,) "we can try to treat the leukemia virus by blocking this 
 
over- produced
enzyme."
 
Why aren't they concerned about
this over production in
 leukemia?


Isn't that peculiar how they are worried about elevated

  immune factors in only one kind 
of disease and not the other?


Why Not? 

I’ll tell you why not!

If One Leukemia is a proven virus then everybody knows it’s normal immune reaction to have these proteins and enzymes
"overproduced!"


Could it be that they have spent millions of other peoples’ money to isolate normal immune factors that they want to block some day to treat
 a viral infection they still call an
 autoimmune disorder!

 Never mind that Multiple Scerosis patients are now receiving interferon injections for their autoimmune disease.

Interferon is what some drug companies
are trying to block in other
autoimmunes!

Is this not an inconsistency. One autoimmune they are trying to block interferon and in another autoimmune they are
injecting interferon!

More than one scientist has misrepresented these chemicals or biomarkers. 
(lymphokyne and b-interferon!) 

A completely different analysis by a different chemists also has identified specific antibodies and their  proteins  which are "overproduced" in
various autoimmune disorders, 
not just chemical enzymes!

The 2nd scientist reported that these same antibodies and proteins were also merely, "found" in other severe viral infections too.

Imagine that!

Now the antibodies and antibody proteins of acute viral infections also match those in autoimmune, (not just the the chemicals,) and still we say  they are not related!

This scientist again misrepresented the nature of these immune substances by saying they are 'overproduced'  in auto-immunes!

(Maybe they're suppose to be over produced in order
to fight off an infection.)

This second researcher, unethically so,  stopped short of making the firm connection between autoimmune and the viral mimicry taking place by,
in fact,  calling it "biochemical mimicry"?

How misleading!

Did anybody in medicine ask, " I wonder why these antibodies match
 those in viral infections?"

"Hmmm, maybe they are viral infections?"

So, instead of suspecting an obvious viral link to autoimmune we try to block the immune system, and we are spending millions of dollars doing it, using desperate  patients as guine pigs!
 
(See the study below if you don’t believe me!)

You will be shocked to hear, as we speak, Lupus Foundation, is supporting a clinical trial to test immune blocking agent consisting of a monoclonal
 antibody and a lymphokyne blocker.
 

    

BEWARE RESEARCH FOUNDATIONS


At the Lupus foundation and Arthritis Foundation I contacted
them about this viral link!

Both times the heads of research didn’t even
 return my calls!

When I threatened to expose them on a website, both called back.
Neither one wanted an email of the Tulane Study.

Has anyone raised a hair?