aocalypse

Monday, November 03, 2014

Reduction of Intraepidermal Nerve Fiber Density (IENFD) in the skin biopsies of patients with fibromyalgia: A controlled study

Conclusion

This is one of the largest series of FM patients demonstrating a significant reduction of IENFD in their skin biopsies. The findings indicate that in a subset of FM patients, the pain syndrome is, at least partially, of neuropathic origin. Skin biopsy may prove a useful tool and a potential biomarker in future studies of FM patients.

 http://www.jns-journal.com/article/S0022-510X%2814%2900633-9/abstract

Election Day 2014

cartoon, fauci, cdc, nih, cover-up, hhv-6

Hemispherx’s Alferon And Ampligen Effective Against Ebola Virus

http://www.bidnessetc.com/28451-hemispherxs-alferon-and-ampligen-effective-against-ebola-virus/

Ampligen inhibits human herpesvirus-6 in vitro.

http://www.ncbi.nlm.nih.gov/pubmed/7893986

 

 

New HHV-6 Research Suggests Additional Ampligen(R) Role in Treating CFS 

 http://www.prnewswire.com/news-releases/new-hhv-6-research-suggests-additional-ampligenr-role-in-treating-cfs-77022237.html

  NEW YORK, Oct. 16 /PRNewswire/ -- Hemispherx Biopharma, Inc. (Amex:   HEB)
 said today that recently reported research that indicates Human Herpes Virus 6
 (HHV-6) has a role in pathogenesis of Chronic Fatigue Syndrome (CFS) symptoms
 may further explain Ampligen's(R) potential role in treatment of the disorder.
     Earlier peer-reviewed studies from independent researchers associated with
 the National Institutes of Health (NIH), have shown that Ampligen can
 eradicate HHV-6 infection in vitro; Ampligen demonstrated the maximum
 antiviral activity from a large panel of approximately three dozen prospective
 antiviral/immunological drugs.
     The new HHV-6 research was presented in a paper this past week by
 Dr. D.V. Ablashi of Advanced Biotechnologies Inc. and Georgetown University
 School of Medicine, et. al., at the American Association for Chronic Fatigue
 Conference held in Cambridge, Massachusetts.  Dr. Ablashi, who is a Board
 member of the national association, utilized specialized techniques to
 actually harvest live, replicating virus from a group of CFS patients.
     Dr. Ablashi's scientific abstract, entitled, "Increased Activation of
 Human Herpes Virus-6 (HHV-6) but not Human Herpes Virus-7 (HHV-7) or Human
 Herpes Virus-8 (HHV-8) in Chronic Fatigue Syndrome Patients" detected the
 active replicating HHV-6 in 57% of CFS patients versus only 8% of a normal
 healthy population.
     Hemispherx said that this new finding represents the second disease marker
 to be recently announced, and provides additional evidence for a possible
 Ampligen mechanism in treatment of CFS.  As recently announced, the pioneering
 efforts of Dr. Robert Suhadolnik (U.S.), and subsequent researchers at
 Montpelier University (France) and the Free University of Brussels (Belgium)
 confirmed the identification of a specifically abnormal immune/antiviral
 factor, a natural disease barrier against many viruses, in the blood's immune
 cells from approximately 90% of CFS patients (now termed the "REDD"
 abnormality).
     Hemispherx said that while the proximate cause of CFS remains unknown,
 measuring of both HHV-6 replication and REDD may serve as powerful markers to
 evaluate the disease process itself.  In this case, the active drug would
 function as a type of bifurcated warhead -- attacking both the replicating
 virus (HHV-6) as well as the REDD abnormality which led to the breakdown in
 host defense barriers.
     According to the National Institutes of Health, during the early years of
 life, HHV-6 infection is observed in 90% of the U.S. population, but
 antibodies and the intact immune system thereafter keep the virus in check and
 present only in dormant form.  However, the dysfunctional immune system of
 many CFS sufferers thereafter allows the virus to awake from dormancy and
 renew its replication and growth.
     Currently, Ampligen is the only drug being developed worldwide for
 treatment of CFS at the Phase III clinical trial level.
 
     Information contained in this news release other than historical
 information, should be considered forward-looking and is subject to various
 risk factors and uncertainties.  For instance, the strategies and operations
 of Hemispherx involve risks of competition, changing market conditions,
 changes in laws and regulations affecting these industries and numerous other
 factors discussed in this release and in the Company's filings with the
 Securities and Exchange Commission.  Accordingly, actual results may differ
 materially from those in any forward-looking statements.
 
 

SOURCE  Hemispherx Biopharma, Inc.
 
 cartoon, ampligen, ebola, treatment, cdc,nih, fauci

The Price of CDC/NIH/Fauci's HHV-6 Indifference

Congenital herpes tied to lower developmental test scores in infants

Infants with congenital human herpesvirus-6 (HHV-6) infections are more likely to score lower on a 12-month mental development test, according to a new URMC study published in the journal Pediatrics.

http://medicalxpress.com/news/2014-11-congenital-herpes-tied-developmental-scores.html

Early Developmental Outcomes of Children With Congenital HHV-6 Infection

CONCLUSIONS: Congenital HHV-6 infection may have a detrimental effect on neurodevelopment at 12 months of age and requires further study given that congenital infection with HHV-6 is present in ∼1 in every 101 births.

 http://pediatrics.aappublications.org/content/early/2014/10/29/peds.2014-0886.abstract


HHV-6 and Autism
In most cases, “autism” like behaviors are caused by the break down of the child’s immune system; allowing viruses, candida, fungi and parasites to set up shop in our beautiful children’s body and brain. A better name for this condition is Neuro-Immune Dysfunction Syndrome (NIDS).  

Serological Association of Measles Virus and Human Herpesvirus-6 with Brain Autoantibodies in Autism
Vijendra K. Singh, Sheren X. Lin, Victor C. Yang
Clinical Immunology and Immunopathology Volume 89, Issue 1, October 1998, Pages 105-108
Abstract
Considering an autoimmunity and autism connection, brain autoantibodies to myelin basic protein (anti-MBP) and neuron–axon filament protein (anti-NAFP) have been found in autistic children. In this current study, we examined associations between virus serology and autoantibody by simultaneous analysis of measles virus antibody (measles-IgG), human herpesvirus-6 antibody (HHV-6-IgG), anti-MBP, and anti-NAFP. We found that measles-IgG and HHV-6-IgG titers were moderately higher in autistic children but they did not significantly differ from normal controls. Moreover, we found that a vast majority of virus serology-positive autistic sera was also positive for brain autoantibody: (i) 90% of measles-IgG-positive autistic sera was also positive for anti-MBP; (ii) 73% of measles-IgG-positive autistic sera was also positive for anti-NAFP; (iii) 84% of HHV-6-IgG-positive autistic sera was also positive for anti-MBP; and (iv) 72% of HHV-6-IgG-positive autistic sera was also positive for anti-NAFP. This study is the first to report an association between virus serology and brain autoantibody in autism; it supports the hypothesis that a virus-induced autoimmune response may play a causal role in autism.

Therea Binstock on HHV-6 and Autism:
"In recent years a number of parents have sent me immune-panels, medical charts, and medical histories of their autism-spectrum child. Remarkably, most of these immune panels report various immune atypicalities, such as (i) atypical elevations of IgG antibodies against common pathogens (eg, CMV, EBV, and/or HHV6), (ii) missing antibodies against a vaccinal antigen, and (iii) other signs of immune dysfunctin (eg, reduced NK cell count, impaired NK function, etc).
In retrospect, what I've observed in the immune panels of these children (n<15 thus far) ought not be surprising, because if a child has a general immune impairment (eg, a null allele of the C4b gene), then he or she would seem likely to have atypical responses to pathogens. "
Med Hypotheses. 2001 Apr;56(4):523-31.
Intra-monocyte pathogens delineate autism subgroups.
http://www.ncbi.nlm.nih.gov/pubmed/11339860
Abstract
Immune panels of many autism-spectrum children reveal signs of atypical infections and shifted cell counts. In conjunction with trait-related cerebral hypometabolism and hypoperfusion, these findings suggest a hypothesis: Several autism-spectrum subgroups derive from intra-monocyte pathogens such as measles virus, cytomegalovirus, human herpesvirus 6, and Yersinia enterocolitica. Furthermore, with much inter-child variation, their effects manifest as diminished hematopoiesis, impaired peripheral immunity, and altered blood-brain barrier function often accompanied by demyelination. In some such children, one or more of these pathogens persists as a chronic-active, seemingly subclinical infection etiologically significant to the child's autistic traits. Within these subgroups, immune impairments and atypical infections may be treatable.
Copyright 2001 Harcourt Publishers Ltd.
NY Times' Sins Of Omission In Autism Article: Commentary by Binstock
Thursday, December 30, 1999

     [This open letter is addressed to Sandra Blakeslee writer for Science
Times of the The New York Times.  It is in response to "New Theories Help
Explain Mysteries of Autism", published in that paper and this newsletter
last Thursday, December 28.  It is an authored opinion of autism researcher
Teresa Binstock.]

      Science Times articles often achieve a level of excellence beyond that
of articles in scientific journals. Your recent article about autism was an
exception. Instead of presenting diverse sides of an important issue, you
focused upon a single model summarized as "it must be genetic and must occur
in utero". Increasing data indicate that this model of causation and timing
is relevant only to a subgroup of children within the autism-spectrum.
      In support of the genetic-autism theory, you presented opinions of
Marie Bristol-Power and Bennett Leventhall; regarding in-utero timing, you
presented speculations from Patricia Rodier and Margaret Bauman.
      The flaw in your article arises from its omissions. You did not
mention the immune-atypicality findings of Reed Warren, VK Singh, HH
Fudenberg, S Gupta, AV Plioplys, and others (e.g., 3-24). Nor did you
present the autoimmune and infection-related ramifications of these
researchers' findings.
      You did not present ideas from the Autism Research Institute's Bernie
Rimland (2), long credited as the person who removed autism from the tainted
"science" of Bruno Bettelheim; nor did you mention or interview any of the
physicians who are treating etiologically significant immune and/or
infection-related processes in specific autism-spectrum children, some of
whom improve sufficiently so as to lose their diagnosis, some of whom
advance to inclusion within mainstream classes.
      At least you offered Eric Courchesne's statements indicating he no
longer accepts Bauman's "autism must occur in-utero" model. I myself came to
a similar position several years ago as I perused Dr. Bauman's articles and
primary citations along with newer articles unavailable as she was forming
her theory of in-utero timing (1).
      Many parents and professionals within the autism community believe
that Dr. Bristol-Powers and her "it must be genetic and must occur in-utero"
cohorts constitute a primary stumbling block to advances in diagnostics,
research, and treatment regarding children of the autism-spectrum.
      In contrast to the one-sided, paradigm-enforcing nature of your
article, Science Times recently presented a summary of human migrations into
North, Central, and South America (11.9.1999). The article presented
traditional theories alongside newer data showing that the older theories
are in need of revision.
      A similarly structured autism article would have been consistent with
Science Times' usual level of excellence and would have done justice to the
research and clinic-based findings offering new models of causation,
diagnostics, and treatment of autism-spectrum children.
      In my opinion, now that the "autism must be genetic and in-utero"
clique has had its say, Science Times ought prepare and publish another
autism article, wherein the "necessarily in-utero" model is more thoroughly
challenged and wherein the immune-atypicality and infection-related data and
researchers are fairly presented.
       Sincerely,
       Teresa Binstock
       Researcher in Developmental & Behavioral Neuroanatomy
    
HUMAN HERPES VIRUS 6
a Resource Page for Physicians, Researchers, and Parents
of Autism-Spectrum Children

by Teresa Binstock
Researcher in Developmental and Behavioral Neuroanatomy

http://members.jorsm.com/~binstock/hhv6.htm

" The Warren et al autism-spectrum studies about null alleles of the
complement C4b gene and about reduced levels of complement C4b in blood. These
studies were based upon a specific gene and a specific protein, and yielded an
important insight, namely, that autism-spectrum children have an above-average
frequency of immune-impairment.

2. In recent years a number of parents have sent me immune-panels, medical
charts, and medical histories of their autism-spectrum child. Remarkably, most
of these immune panels report various immune atypicalities, such as (i) atypical
elevations of IgG antibodies against common pathogens (eg, CMV, EBV, and/or
HHV6), (ii) missing antibodies against a vaccinal antigen, and (iii) other signs
of immune dysfunctin (eg, reduced NK cell count, impaired NK function, etc).

In retrospect, what I've observed in the immune panels of these children (n<15
thus far) ought not be surprising, because if a child has a general immune
impairment (eg, a null allele of the C4b gene), then he or she would seem likely
to have atypical responses to pathogens "

"HHV-6 is a commensal inhabitant of brains; various neurologic
manifestations, including convulsions and encephalitis, can occur during primary
HHV-6 infection or in immunocompromised patients." (7), and HHH6 has been
reported within "oligodendrocytes and microglia" (8), and focal HHV6-
encephalitis has been documented (10

" If the autism-spectrum child's anti-HHV6 titres are elevated, you might
consider evaluations of peripheral blood via PCR for HHV6 (9, 9b), which would
provide an indication of the extent to which various aspects of immunity were
being altered by such an infection. Interestingly, cytomegalovirus (CMV) can be
present in monocytes of individuals who have no anti-CMV antibodies (9a), thus
raising the possibility that HHV6 *might* have a similar effect in some autism-
spectrum children, ie, be etiologically significant despite a lab finding of "no
elevated anti-HHV6 antibodies".



Binstock's Anterior Insular Cortex Hypothesis for Linkage Between Gut and Brain.
Binstock (http://www.jorsm.com/~binstock/insular.htm) has developed a hypothesis to explain the gut-brain relationships for autistic children.
The anterior insular cortex (aIC) links visceral sensation from the gastrointestinal tract with the amygdala and the hypothalamus (1-6). The anterior insular cortex also participates in oral phenomena, object recognition, and naming (5) along with "apraxia of speech" (7,8).
Twenty-five stroke patients with articulatory deficits all had a lesion within "a discrete region of the left precentral gyrus of the insula", whereas this area was "completely spared" in 19 stroke patients without these deficits (7).
Autism-spectrum children with atypical oral habits and/or disorders of naming and of language (9-10) also tend to have a typical gastrointestinal symptoms (11-12). There is also a growing volume of anecdotal data that a small subgroup of autism-spectrum children experiences improved sound production and language use in response to treatments whose focus and effects are gastrointestinal. These treatments include gluten-free and casein-free diets, anti-Candida therapies, anti-viral therapies, and antibiotic therapies (13-19,31,32) suggesting that the underlying neuronal circuitry is intact.
Binstock suggests that the aIC and associated nuclei could become disrupted by at least two mechanisms: (I) intraneuronal migration of a neurotropic virus and/or (II) chronic hyperstimulation of the gastrointestinal tract.
Gesser and colleagues have documented (I) the translocation of HSV from the gastrointestinal tract into the mesenteric nervous system (rats and humans), and (II) the migration of mesenteric HSV as far as theamygdaloid nuclei in rats (20-23). In this theory, viruses could migrate from the gastrointestinal tract through neural pathways into the central nervous system.
Given a high rate of stimulation of neuron pathways reporting gastrointestinalconditions to limbic regions and cortex, neurotransmitter or intracellular-messenger use in excess of their production or recirculation could occur, thereby inducing a change of function of neurons within the aIC.
This hypothesis provides a basis for helping autistic children through treating their gastrointestinal disturbances.
References:
  1. Krushel LA, van der Kooy D. Visceral cortex: integration of the mucosal senses with limbic information in the rat agranular insular cortex. J Comp Neurol 270.39-54 1988.
  2. Mesulam MM, Mufson EJ. Insula of the Old World Monkey. I. Architectonics of the insulo-orbito-temporal component of the paralimbic brain. J Comp Neurol 212.1-22 1982.
  3. Mesulam MM, Mufson EJ. Insula of the Old World Monkey. II. Afferent cortical inputs and comments on the claustrum. J Comp Neurol 212.23-37 1982.
  4. Mesulam MM, Mufson EJ. Insula of the Old World Monkey. III. Efferent cortical output and comments on function.
  5. Augustine JR. Circuitry and functional aspects of the insular lobe in primates including humans. Brain Res Rev 22.229-44 1996.
  6. Morecraft RJ, Geula C, Mesulam MM. Cytoarchitecture and neural afferents of orbitofrontal cortex in the brain of the monkey. J Comp Neurol 323.341-58 1992.
  7. Dronkers NF. A new brain region for coordinating speech articulation. Nature 384.159-61 1996.
  8. Donnan GA et al. Indentification of brain region for coordinating speech articulation. Lancet 349.221-2 1997.
  9. Peeters T, Gillberg C. Autism: Medical and Educational Aspects. Whurr Pub Ltd 1999.
  10. [Additional Citation]
  11. D'Eufemia PD et al. Abnormal intestinal permeability in children with autism. Acta Paediatrica 85.1076-9 1996.
  12. Horvath K et al. Gastrointestinal abnormalities in children with autistic disorder. J Pediatr 1999 135.5.559-63 1999.
  13. Bolte ER, personal communication; see also Sandler RH, Bolte ER et al. Possible gut-brain interaction contributing to delayed onset autism symptomatology. Abstract #18, Fourth Int Symp on Brain-Gut Interactions; Neurogastroenterol Mot 10.363 1998.
  14. BR..., Ph.D., Personal communication.
  15. Jane El-Dahr, MD, Personal communication.
  16. Ray Kopp, Personal communication based upon his internet experience with hundreds of parents of autism-spectrum and/or gfcf children.
  17. WM..., MD, Personal communication.
  18. PS..., Ph.D., Personal communication.
  19. Amy Holmes, MD, Personal communication.
  20. Gesser RM et al. Oral-oesophageal inoculation of mice with herpes simplex virus type 1 causes latent infection of the vagal sensory ganglia (nodose ganglia). J Gen Virol 1994 Sep;75 ( Pt 9):2379-86.
  21. Gesser RM et al. Oral inoculation of SCID mice with an attenuated herpes simplex virus-1 strain causes persistent enteric nervous system infection and gastric ulcers without direct mucosal infection. Lab Invest1995 Dec;73(6):880-9.
  22. Gesser RM, Koo SC. Oral inoculation with herpes simplex virus type 1 infects enteric neuron and mucosal nerve fibers within the gastrointestinal tract in mice. J Virol 1996 Jun;70(6):4097-102.
  23. Gesser RM, Koo SC. Latent herpes simplex virus type 1 gene expressionin ganglia innervating the human gastrointestinal tract. J Virol 1997 May;71(5):4103-6.
  24. Bourdois PS, McCandless DL, MacIntosh FC. A prolonged after-effect of intense synaptic activity on acetylcholine in a sympathetic ganglion. CanJ Physiol Pharmacol 1975 Feb;53(1):155-65.
  25. Michael Goldberg, MD, NeuroImmune Dysfunction conference; Bethesda,Maryland, 1999.
  26. Sid Baker, MD, Defeat Autism Now! conference; Cherry Hills, New Jersey,1999.

Intra-monocyte pathogens delineate autism subgroups.


Institute for Molecular Introspections, Estes Park, Colorado, USA.
Medical Hypotheses (Impact Factor: 1.18). 05/2001; 56(4):523-31. DOI: 10.1054/mehy.2000.1247
Source: PubMed
ABSTRACT Immune panels of many autism-spectrum children reveal signs of atypical infections and shifted cell counts. In conjunction with trait-related cerebral hypometabolism and hypoperfusion, these findings suggest a hypothesis: Several autism-spectrum subgroups derive from intra-monocyte pathogens such as measles virus, cytomegalovirus, human herpesvirus 6, and Yersinia enterocolitica. Furthermore, with much inter-child variation, their effects manifest as diminished hematopoiesis, impaired peripheral immunity, and altered blood-brain barrier function often accompanied by demyelination. In some such children, one or more of these pathogens persists as a chronic-active, seemingly subclinical infection etiologically significant to the child's autistic traits. Within these subgroups, immune impairments and atypical infections may be treatable.
A Review of Autism and the Immune Response

Paul Ashwood and Judy Van De Water


HUMAN HERPES VIRUS 6

By Teresa Binstock
"If the autism-spectrum child's anti-HHV6 titres are elevated, you might consider evaluations of peripheral blood via PCR for HHV6 (9, 9b), which would provide an indication of the extent to which various aspects of immunity were being altered by such an infection. Interestingly, cytomegalovirus (CMV) can be present in monocytes of individuals who have no anti-CMV antibodies (9a), thus raising the possibility that HHV6 might have a similar effect in some autism- spectrum children, ie, be etiologically significant despite a lab finding of "no elevated anti-HHV6 antibodies"."
http://members.jorsm.com/~binstock/hhv6.htm


FEBRILE SEIZURES & HUMAN HERPES VIRUS 6
By Teresa Binstock
". . .HHV-6 (human herpes virus #6) is realized to be a common source of febrile convulsions in young children."
http://members.jorsm.com/~binstock/fs-hhv6.htm


HIV infection in children - neurodevelopmental (autistic) outcomes and clinical pathologies - and their correlations to 'common' autism
There is a striking correlation between neurodevelopmental symptoms found in children infected with HIV virus and those children diagnosed with Autism Spectrum Disorders (of unknown aetiology). Furthermore, the underlying biomedical pathologies found in HIV-positive children are in many ways identical to biomedical pathologies found in children diagnosed with ‘common’ autism.
http://autismcalciumchannelopathy.com/HIVandAutism.html


In most cases, “autism” like behaviors are caused by the break down of the child’s immune system; allowing viruses, candida, fungi and parasites to set up shop in our beautiful children’s body and brain. A better name for this condition is Neuro-Immune Dysfunction Syndrome (NIDS). http://www.not-autism.org/about
"The HHV-6 and measles viruses are etiologically linked to autism because they are related to brain autoantibodies and demyelinating diseases."
http://overcomingcandida.com/candida_and_autism_2.htm
"Reports of HHV-6 and autism are abundant. Many children have high herpes titres, sometimes to that of 4-6 times of normal, often correlating with autism symptoms or seizures."
http://www.canlyme.com/autismlyme.html
"Lauren [a child with autism] also had a huge variety of blood tests, which gave some amazing results. In basic terms it showed that Lauren’s natural killer cells were very low which shows there is a problem with her immune system, she also came up as having the HHV6 Human Herpes Virus. Lauren was over 250 times the acceptable limit. Speaking to Dr Goldberg on the phone about Lauren’s results he said it was literally one of the highest results he has seen."
http://www.autismfile.com/articles/issue1_11.htm
"We learned, by having blood tests and immune panels prepared from our son John's blood tests (something no physician before had thought to do), that he had high HHV6 titers and low Natural Killer (NK) cells, a condition which is not caused genetically, but which is a disease probably brought on by genetic susceptibility. However, John is now curable! Treatment began a year ago, and despite two setbacks due to illness in the process, John is improving very steadily. The life described in the beginning of this short presentation has dramatically changed, in too short a period to be attributed to maturity. We have a relationship with him. We all laugh and play together now. He always listens and sometimes follows simple directions. He doesn't mess the floor anymore. He has been sleeping through the night since December. His HHV6 titers are down. Dr. Goldberg expects John to mainstream in the next two years. With your help, it could be sooner."
http://www.whale.to/v/smythe.html
The symptoms of the “quiet” ADD child (who is likely connected to this phenomenon) is not consistent with the past training or processes used to “explain” and address the “hyper” ADD child. It seems likely that the cognitive defects described in adults and children with CFIDS may be thought of as milder, later-onset form of ""autism", as they are similar in symptomatology and possible etiologies. The continued exploration of an immune-dysfunctional epiphenomena, and the potential etiologies linked to it, is a door we must walk through if we expect to change the future of this generation of children!
http://autisticconjectureoftheday.blogspot.com
Are Autism Spectrum Disorders part of the Multisystemic HHV-6 Spectrum of Disorders?
Is the Multisystemic HHV-6 Epidemic Causing the Dramatic Rise in Autism?
Can the complications of Autism Spectrum Disorder be reduced by controlling Multisystemic HHV-6?
Why won't the Centers for Disease Control tell the truth about the role of Multisystemic HHV-6 in Autism, Chronic Fatigue Syndrome, AIDS and many other serious neuroimmunological syndromes? What exactly is Multisystemic HHV-6? Is it really just a reactivated herpes virus or is it actually some other kind of lethal virus that can be passed from person to person and can become chromsomally integrated? Does it belong in a class by itself? Where did it come from? Is it a zoonose, a virus that is circulating in people and animals?


"About six weeks back I was given the name of a woman who had approached Generation Rescue. She has a foundation which is working on the theory that the Human Herpes Virus #6 (HHV-6) is the cause of chronic fatigue syndrome. This woman’s foundation often talked with the world’s top virologists who privately tell her their belief that HHV-6 is also implicated in multiple sclerosis, autism, and seizures. She didn’t have time to pursue HHV-6 in regards to autism, but thought we should be made aware of the theory."
Kent Heckenlively, Age of Autism


Serological Association of Measles Virus and Human Herpesvirus-6 with Brain Autoantibodies in Autism
Vijendra K. Singh, Sheren X. Lin, Victor C. Yang
Clinical Immunology and Immunopathology Volume 89, Issue 1, October 1998, Pages 105-108
Abstract
Considering an autoimmunity and autism connection, brain autoantibodies to myelin basic protein (anti-MBP) and neuron–axon filament protein (anti-NAFP) have been found in autistic children. In this current study, we examined associations between virus serology and autoantibody by simultaneous analysis of measles virus antibody (measles-IgG), human herpesvirus-6 antibody (HHV-6-IgG), anti-MBP, and anti-NAFP. We found that measles-IgG and HHV-6-IgG titers were moderately higher in autistic children but they did not significantly differ from normal controls. Moreover, we found that a vast majority of virus serology-positive autistic sera was also positive for brain autoantibody: (i) 90% of measles-IgG-positive autistic sera was also positive for anti-MBP; (ii) 73% of measles-IgG-positive autistic sera was also positive for anti-NAFP; (iii) 84% of HHV-6-IgG-positive autistic sera was also positive for anti-MBP; and (iv) 72% of HHV-6-IgG-positive autistic sera was also positive for anti-NAFP. This study is the first to report an association between virus serology and brain autoantibody in autism; it supports the hypothesis that a virus-induced autoimmune response may play a causal role in autism.
http://www.sciencedirect.com/science/article/pii/S0090122998945883


HUMAN HERPES VIRUS 6
By Teresa Binstock
"If the autism-spectrum child's anti-HHV6 titres are elevated, you might consider evaluations of peripheral blood via PCR for HHV6 (9, 9b), which would provide an indication of the extent to which various aspects of immunity were being altered by such an infection. Interestingly, cytomegalovirus (CMV) can be present in monocytes of individuals who have no anti-CMV antibodies (9a), thus raising the possibility that HHV6 might have a similar effect in some autism- spectrum children, ie, be etiologically significant despite a lab finding of "no elevated anti-HHV6 antibodies"."
http://members.jorsm.com/~binstock/hhv6.htm


FEBRILE SEIZURES & HUMAN HERPES VIRUS 6
By Teresa Binstock
". . .HHV-6 (human herpes virus #6) is realized to be a common source of febrile convulsions in young children."
http://members.jorsm.com/~binstock/fs-hhv6.htm


HIV infection in children - neurodevelopmental (autistic) outcomes and clinical pathologies - and their correlations to 'common' autism
There is a striking correlation between neurodevelopmental symptoms found in children infected with HIV virus and those children diagnosed with Autism Spectrum Disorders (of unknown aetiology). Furthermore, the underlying biomedical pathologies found in HIV-positive children are in many ways identical to biomedical pathologies found in children diagnosed with ‘common’ autism.
http://autismcalciumchannelopathy.com/HIVandAutism.html (Editor's note: HIV-positive being a euphemism for HHV-6-positive.)


In most cases, “autism” like behaviors are caused by the break down of the child’s immune system; allowing viruses, candida, fungi and parasites to set up shop in our beautiful children’s body and brain. A better name for this condition is Neuro-Immune Dysfunction Syndrome (NIDS). http://www.not-autism.org/about
"The HHV-6 and measles viruses are etiologically linked to autism because they are related to brain autoantibodies and demyelinating diseases."
http://overcomingcandida.com/candida_and_autism_2.htm
"Reports of HHV-6 and autism are abundant. Many children have high herpes titres, sometimes to that of 4-6 times of normal, often correlating with autism symptoms or seizures."
http://www.canlyme.com/autismlyme.html
"Lauren [a child with autism] also had a huge variety of blood tests, which gave some amazing results. In basic terms it showed that Lauren’s natural killer cells were very low which shows there is a problem with her immune system, she also came up as having the HHV6 Human Herpes Virus. Lauren was over 250 times the acceptable limit. Speaking to Dr Goldberg on the phone about Lauren’s results he said it was literally one of the highest results he has seen."
http://www.autismfile.com/articles/issue1_11.htm
"We learned, by having blood tests and immune panels prepared from our son John's blood tests (something no physician before had thought to do), that he had high HHV6 titers and low Natural Killer (NK) cells, a condition which is not caused genetically, but which is a disease probably brought on by genetic susceptibility. However, John is now curable! Treatment began a year ago, and despite two setbacks due to illness in the process, John is improving very steadily. The life described in the beginning of this short presentation has dramatically changed, in too short a period to be attributed to maturity. We have a relationship with him. We all laugh and play together now. He always listens and sometimes follows simple directions. He doesn't mess the floor anymore. He has been sleeping through the night since December. His HHV6 titers are down. Dr. Goldberg expects John to mainstream in the next two years. With your help, it could be sooner."
http://www.whale.to/v/smythe.html
The symptoms of the “quiet” ADD child (who is likely connected to this phenomenon) is not consistent with the past training or processes used to “explain” and address the “hyper” ADD child. It seems likely that the cognitive defects described in adults and children with CFIDS may be thought of as milder, later-onset form of ""autism", as they are similar in symptomatology and possible etiologies. The continued exploration of an immune-dysfunctional epiphenomena, and the potential etiologies linked to it, is a door we must walk through if we expect to change the future of this generation of children!
http://autisticconjectureoftheday.blogspot.com

Chorea and developmental regression associated with human herpes virus-6 encephalitis.

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