so are some vaccines cultured on any kind of mouse ingredient? Wouldn't surprise me...

From "across the pond":-

So, if "a virus" can cause autism then what's to prevent one or more of the Measles, Mumps and Rubella viruses causing autism? Is this a back door into an eventual admission that the MMR vaccine can cause autism in, say, a susceptible sub-set?

Such wonderful information here and certainly it is good to understand the infections that autistic individuals are prone to.
Gatogorra, thankyou for your logical , incisive comments.
One has to wonder if this virus , while perhaps real , is also a fake rabbit for the autism greyhounds to chase- one more piece of the divert and delay tactics which are very important for those who have their backs to the wall for their criminal negligence in allowing toxic materials into vaccines in quantities far above EPA "safe levels"
Now that the "Autism is genetic" card is wearing out, "Autism is caused by a virus" is quite a terrific idea. No wonder Dr. Snyderman states that viruses can cause OCD . Autism is just one small step further. AOA friends- We should have predicted this one.
Hmm... I wonder if autistic kids in other countries such as India, China, Korea have this same virus ? My guess is that they do not

If there is a virus, that wouldn't surprise me.. I've wondered if my son has a chronic blood infection due to a virus or mycoplasma that causes flare ups of inflammation and swelling in the brain. It would help if they would simply do a viral or mycoplasma screening as part of the of the diagnosing. This could change the whole treatment course.

From NY TImes .... 10/12 ...

Could a virus be the cause of chronic fatigue syndrome?

A study published last week in the journal Science suggested that might be the case, reporting that many patients who had the syndrome were infected with a recently discovered virus.

Chronic fatigue syndrome has long been a medical mystery and the subject of debate, sometimes bitter, among doctors, researchers and patients. It affects at least one million Americans, causing extreme fatigue, muscle and joint pain, sleep problems, difficulty concentrating and other symptoms. Its cause is unknown, symptoms can last for years and there is no effective treatment. Researchers disagree about whether it is one disease or a collection of symptoms that may have different causes in different patients. It has sometimes been stigmatized as more mental than physical, with patients labeled neurotic, depressed or hypochondriacal. Many patients find even the name of the disorder offensive, a not-so-subtle hint that it is not a real disease.

The new report has intrigued scientists, been seen as vindication by some patients and inspired hope for a treatment.

“I just feel like the whole future has changed for us,” said Anne Ursu, 36, a writer living in Cleveland who has had the syndrome in the past.

But the new study is not conclusive, and a great deal of work remains to be done to find out whether the new virus really does play a role. Just detecting it in patients does not prove it is what made them sick; people with the syndrome may have some other underlying problem that makes them susceptible to the virus, which could be just a passenger in their cells.

Even so, thousands of patients have already contacted scientists, asking to be tested, said Dr. Judy Mikovits, the first author of the study and the research director at the Whittemore Peterson Institute in Reno, a research center created by the parents of a woman who has the syndrome. Dr. Mikovits said she expected a test to become available “within weeks.”

The new suspect is a xenotropic murine leukemia virus-related virus, or XMRV, which probably descended from a group of viruses that cause cancer in mice. How or when XMRV found its way into humans is unknown. But it has also been linked to cancer in people: it was first identified three years ago, in prostate cancer, and later detected in about one-quarter of biopsies from men with that disease (and in only 6 percent of benign biopsies). It is a retrovirus, from the same notorious family that causes AIDS and leukemia in people. .......

@mother, that is interesting re DPVIV enzyme. Clostridia does the same, at least in culture.

Now have a look at these (sorry links not working, try googling them for full versions or abstracts)

Early impairment of gut mucosal immunity in HIV-1-infected children. Quesnel A et al Clin Exp Immunol. 1994 Sep;97(3):380-5.

Poliovirus vaccine strains detected in stool specimens of immunodeficient children in South Africa. Pavlov DN Diagn Microbiol Infect Dis. 2006 Jan;54(1):23-30. Epub 2005 Nov 14.

Enteric pathogens associated with gastrointestinal dysfunction in children with HIV infection. Ramos-Soriano AG et al Mol Cell Probes. 1996 Apr;10(2):67-73.

Gastrointestinal dysfunction and disaccharide intolerance in children infected with human immunodeficiency virus. Yolken RH et al J Pediatr. 1991 Mar;118(3):359-63.

Intestinal malabsorption of HIV-infected children: relationship to diarrhoea, failure to thrive, enteric micro-organisms and immune impairment. The Italian Paediatric Intestinal/HIV Study Group. AIDS. 1993 Nov;7(11):1435-40.

Intestinal permeability in patients infected with the human immunodeficiency virus. Tepper RE Am J Gastroenterol. 1994 Jun;89(6):878-82.Efficacy of oral pancreatic enzyme therapy for the treatment of fat malabsorption in HIV-infected patients. Carroccio A et al Aliment Pharmacol Ther. 2001 Oct;15(10):1619-25.

The effect of antenatal vitamin A and beta-carotene supplementation on gut integrity of infants of HIV-infected South African women. Filteau S et al J Pediatr Gastroenterol Nutr. 2001 Apr;32(4):464-70.

uncanny or what?

HIV inhibit the enzyme CD26/DPPIV, and if XMRV do the same, that might explain why autists react to gluten and casein whithout allergy. The CD26/DPPIV is essential to digest prolin-rich proteins, and with DPPIV inhibited, the proteins will end up as casomorphins and glutenmorphins (opioids).

It´s said that that this viral infection do not explain all the symptomes in CFS, but add the burden of opioids from food, and the picture is clearer.

Why more boys? A virus maybe the set up but something is happening to mostly boys. Mercury seems to fit that bill as the final push.

I think we should look at the cell cultures. How else would a mouse virus jump to humans.

Another VERY interesting thing about RnaseL: CFS people with high low molecular weight (fragmented) RnaseL have been found to have a hightened sensitivity to MERCURY

Donna Alvado - there is some information on this CFS forum on how to get tested for XMRV. http://forums.aboutmecfs.org/forumdisplay.php?f=54 You might have to wait 6 months. I would also check the Whittemore Peterson Institute website, they will have the best information. http://www.wpinstitute.org/xmrv/index.html

There may also be information on prohealth, but I'm not registered there, so I can't read it.

julie - you asked "How prevalent is this virus in the general population?"

4% of controls.

Biomed Pharmacother. 1998;52(9):386-90. Links
The 2-5A system in viral infection and apoptosis.Castelli J, Wood KA, Youle RJ.
Biochemistry Section, NINDS, NIH, Bethesda, MD 20892, USA.

The 2-5A system is an established endogenous antiviral pathway. Interferon treatment of cells leads to an increase in basal, but latent, levels of 2-5A-dependent RNase (RNase L) and the family of 2'-5' oligoadenylate synthetases (OAS). Double-stranded RNA, thought to be derived from viral replication intermediates, activates OAS. Activated OAS converts ATP into unusual short 2'-5' linked oligoadenylates called 2-5A [ppp5'(A2'p5')2A]. The 2-5A binds to and activates RNase L which cleaves single stranded RNA with moderate specificity for sites 3' of UpUp and UpAp sequences, and thus leads to degradation of cellular rRNA. During apoptosis, generalized cellular RNA degradation, distinct from the differential expression of mRNA species that may regulate specific gene expression during apoptosis, has been observed. The mechanism of RNA breakdown during apoptosis has been commonly considered a non-specific event that reflects the generalized shut down of translation and homeostatic regulation during cell death. Due to the similar RNA degradation that occurs during both apoptosis and viral infection we investigated the potential role of RNase L in apoptosis. To investigate whether RNase L activity could lead to apoptosis, NIH3T3 cells were transfected with a lac-inducible vector containing the human RNase L gene. Treatment of these cells with isopropylthiogalactoside (IPTG) caused loss of cell viability that was confirmed as an apoptotic cell death by morphological and biochemical criteria. Similarly, specific allosteric activation of endogenous RNase L by introduction of 2-5A directly into L929 cells also induced apoptosis. In L929 cells poly(I).poly(C) treatment in combination with interferon caused an increase in apoptosis whereas neither interferon or double stranded RNA alone altered cell viability. Therefore, increased expression or activation of RNase L causes apoptosis. Inhibition of RNase L, specifically with a dominant negative mutant, suppressed poly(I)Ypoly(C)-induced apoptosis in interferon-primed fibroblasts. Poliovirus, a picornovirus with a single-stranded RNA genome, causes apoptosis of HeLa cells. Expression of the dominant negative inhibitor of RNase L in HeLa prevented virus-induced apoptosis and maintained cell viability. Thus, reduction or inhibition of RNase L activity prevents apoptosis. Both apoptosis and the 2-5A system can provide defense against viral infection in multicellular organisms by preventing production and therefore spread of progeny virus. RNase L appears to function in both mechanisms, therefore, initiation of apoptosis may be one mechanism for the antiviral activity of the 2-5A system.
RNA. 2008 Jun;14(6):1026-36. Epub 2008 Apr 21. Links
A viral RNA competitively inhibits the antiviral endoribonuclease domain of RNase L.Townsend HL, Jha BK, Han JQ, Maluf NK, Silverman RH, Barton DJ.
Department of Microbiology, University of Colorado Denver, School of Medicine, Aurora, Colorado 80045, USA.

Ribonuclease L (RNase L) is a latent endoribonuclease in an evolutionarily ancient interferon-regulated dsRNA-activated antiviral pathway. 2'-5' oligoadenylate (2-5A), the product of dsRNA-activated oligoadenylate synthetases (OASes), binds to ankyrin repeats near the amino terminus of RNase L, initiating a series of conformational changes that result in the activation of the endoribonuclease. A phylogenetically conserved RNA structure within group C enteroviruses inhibits the endoribonuclease activity of RNase L. In this study we report the mechanism by which group C enterovirus RNA inhibits RNase L. Viral RNA did not affect 2-5A binding to RNase L. Rather, the viral RNA inhibited the endoribonuclease domain. We used purified RNase L, purified 2-5A, and an RNA substrate with a 5' fluorophore and 3' quencher in FRET assays to measure inhibition of RNase L activity by the viral RNA. The group C enterovirus RNA was a competitive inhibitor of the endoribonuclease with a K(i) of 34 nM. Consistent with the kinetic profile of a competitive inhibitor, the viral RNA inhibited the constitutively active endoribonuclease domain of RNase L. We call this viral RNA the RNase L competitive inhibitor RNA (RNase L ciRNA).
A scientific journey through the 2-5A/RNase L system.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17681844

Proc Natl Acad Sci U S A. 2007 Jan 30;104(5):1655-60.
An infectious retrovirus susceptible to an IFN antiviral pathway from human prostate tumors.Dong B, Kim S, Hong S, Das Gupta J, Malathi K, Klein EA, Ganem D, Derisi JL, Chow SA, Silverman RH.
Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA.

We recently reported identification of a previously undescribed gammaretrovirus genome, xenotropic murine leukemia virus-related virus (XMRV), in prostate cancer tissue from patients homozygous for a reduced activity variant of the antiviral enzyme RNase L. Here we constructed a full-length XMRV genome from prostate tissue RNA and showed that the molecular viral clone is replication-competent. XMRV replication in the prostate cancer cell line DU145 was sensitive to inhibition by IFN-beta. However, LNCaP prostate cancer cells, which are deficient in JAK1 and RNase L, were resistant to the effects of IFN-beta against XMRV. Furthermore, DU145 cells rendered deficient in RNase L with siRNA were partially resistant to IFN inhibition of XMRV. Expression in hamster cells of the xenotropic and polytropic retrovirus receptor 1 allowed these cells to be infected by XMRV. XMRV provirus integration sites were mapped in DNA isolated from human prostate tumor tissue to genes for two transcription factors (NFATc3 and CREB5) and to a gene encoding a suppressor of androgen receptor transactivation (APPBP2/PAT1/ARA67).

Our studies demonstrate that XMRV is a virus that has infected humans and is susceptible to inhibition by IFN and its downstream effector, RNase L.

What is the role of RNase L??

Biochimie. 2007 Jun-Jul;89(6-7):789-98. Epub 2007 Feb 20. Diverse functions of RNase L and implications in pathology.Bisbal C, Silverman RH.
IGH UPR CNRS 1142, 141 rue de la Cardonille, 34396 Montpellier, France.

The endoribonuclease L (RNase L) is the effector of the 2-5A system, a major enzymatic pathway involved in the molecular mechanism of interferons (IFNs). RNase L is a very unusual nuclease with a complex mechanism of regulation. It is a latent enzyme, expressed in nearly every mammalian cell type. Its activation requires its binding to a small oligonucleotide, 2-5A. 2-5A is a series of unique 5'-triphosphorylated oligoadenylates with 2'-5' phosphodiester bonds. By regulating viral and cellular RNA expression, RNase L plays an important role in the antiviral and antiproliferative activities of IFN and contributes to innate immunity and cell metabolism. The 2-5A/RNase L pathway is implicated in mediating apoptosis in response to viral infections and to several types of external stimuli. Several recent studies have suggested that RNase L could have a role in cancer biology and evidence of a tumor suppressor function of RNase L has emerged from studies on the genetics of hereditary prostate cancer.

Med Sci (Paris). 2008 Oct;24(10):859-64.
[RNase L, a crucial mediator of innate immunity and other cell functions
Bisbal C, Salehzada T.
Inserm ERI25-EA 4202, Muscle et Pathologies, Bâtiment Crastes de Paulet, CHU Arnaud de Villeneuve, 371, avenue du Doyen Gaston Giraud, 34295 Montpellier Cedex 5, France.

The 2-5A/RNase L pathway is one of the first cellular defences against viruses. RNase L is an unusual endoribonuclease which activity is strictly regulated by its binding to a small oligonucleotide, 2-5A. 2-5A itself is very unusual, consisting of a series of 5'- triphosphorylated oligoadenylates with 2'-5' bonds. But RNase L activity is not limited to viral RNA cleavage. RNase L plays a central role in innate immunity, apoptosis, cell growth and differentiation by regulating cellular RNA stability and expression. Default in its activity leads to increased susceptibility to virus infections and to tumor development. RNase L gene has been identified as HPC1 (Hereditary Prostate Cancer 1) gene. Study of RNase L variant R462Q in etiology of prostate cancer has led to the identification of the novel human retrovirus closely related to xenotropic murine leukemia viruses (MuLVs) and named XMRV.

PLoS Pathog. 2009 Oct;5(10):e1000602. Epub 2009 Oct 2.
RNase L mediated protection from virus induced demyelination.Ireland DD, Stohlman SA, Hinton DR, Kapil P, Silverman RH, Atkinson RA, Bergmann CC.
Department of Neuroscience, Lerner Research Institute, The Cleveland Clinic, Cleveland, Ohio, United States of America.

IFN-alpha/beta plays a critical role in limiting viral spread, restricting viral tropism and protecting mice from neurotropic coronavirus infection. However, the IFN-alpha/beta dependent mechanisms underlying innate anti-viral functions within the CNS are poorly understood. The role of RNase L in viral encephalomyelitis was explored based on its functions in inhibiting translation, inducing apoptosis, and propagating the IFN-alpha/beta pathway through RNA degradation intermediates. Infection of RNase L deficient (RL(-/-)) mice with a sub-lethal, demyelinating mouse hepatitis virus variant revealed that the majority of mice succumbed to infection by day 12 p.i. However, RNase L deficiency did not affect overall control of infectious virus, or diminish IFN-alpha/beta expression in the CNS. Furthermore, increased morbidity and mortality could not be attributed to altered proinflammatory signals or composition of cells infiltrating the CNS. The unique phenotype of infected RL(-/-) mice was rather manifested in earlier onset and increased severity of demyelination and axonal damage in brain stem and spinal cord without evidence for enhanced neuronal infection. Increased tissue damage coincided with sustained brain stem infection, foci of microglia infection in grey matter, and increased apoptotic cells. These data demonstrate a novel protective role for RNase L in viral induced CNS encephalomyelitis, which is not reflected in overall viral control or propagation of IFN-alpha/beta mediated signals. Protective function is rather associated with cell type specific and regional restriction of viral replication in grey matter and ameliorated neurodegeneration and demyelination.

Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20816-21. Epub 2008 Dec 15. Links
An essential role for the antiviral endoribonuclease, RNase-L, in antibacterial immunity.Li XL, Ezelle HJ, Kang TJ, Zhang L, Shirey KA, Harro J, Hasday JD, Mohapatra SK, Crasta OR, Vogel SN, Cross AS, Hassel BA.
Graduate Program in Molecular Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Type I IFNs were discovered as the primary antiviral cytokines and are now known to serve critical functions in host defense against bacterial pathogens. Accordingly, established mediators of IFN antiviral activity may mediate previously unrecognized antibacterial functions. RNase-L is the terminal component of an RNA decay pathway that is an important mediator of IFN-induced antiviral activity. Here, we identify a role for RNase-L in the host antibacterial response. RNase-L(-/-) mice exhibited a dramatic increase in mortality after challenge with Bacillus anthracis and Escherichia coli; this increased susceptibility was due to a compromised immune response resulting in increased bacterial load. Investigation of the mechanisms of RNase-L antibacterial activity indicated that RNase-L is required for the optimal induction of proinflammatory cytokines that play essential roles in host defense from bacterial pathogens. RNase-L also regulated the expression of the endolysosomal protease, cathepsin-E, and endosome-associated activities, that function to eliminate internalized bacteria and may contribute to RNase-L antimicrobial action. Our results reveal a unique role for RNase-L in the antibacterial response that is mediated through multiple mechanisms. As a regulator of fundamental components of the innate immune response, RNase-L represents a viable therapeutic target to augment host defense against diverse microbial pathogens.
In Vivo. 2008 Jan-Feb;22(1):115-21. Links
Unravelling intracellular immune dysfunctions in chronic fatigue syndrome: interactions between protein kinase R activity, RNase L cleavage and elastase activity, and their clinical relevance.Meeus M, Nijs J, McGregor N, Meeusen R, De Schutter G, Truijen S, Frémont M, Van Hoof E, De Meirleir K.
Department of Human Physiology, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel, Belgium.

This study examined possible interactions between immunological abnormalities and symptoms in CFS. Sixteen CFS patients filled in a battery of questionnaires, evaluating daily functioning, and underwent venous blood sampling, in order to analyse immunological abnormalities. Ribonuclease (RNase) L cleavage was associated with RNase L activity (rs=0.570; p=0.021), protein kinase R (PKR) (rs=0.716; p=0.002) and elastase activity (rs=0.500; p=0.049). RNase L activity was related to elastase (rs=0.547; p=0.028) and PKR activity (rs=0.625; p=0.010). RNase L activity (rs=0.535; p=0.033), elastase activity (rs=0.585; p=0.017) and RNase L cleavage (rs=0.521; p=0.038) correlated with daily functioning. This study suggests that in CFS patients an increase in elastase activity and subsequent RNase L cleavage is accompanied by increased activity of both the PKR and RNase L enzymes. RNase L and elastase activity are related to daily functioning, thus evidence supporting the clinical importance of these immune dysfunctions in CFS patients was provided.

Now the RNAse L (Ribonuclease L) has important roles in antimicrobian and antiviral functions and inhibites the XMRV virus
I wonder what is the status of the RNAse L in different subgroups of ASD...

I'm remembering Dr. Kent Holtorf saying recently on Fox News that he has seen people with chronic fatigue syndrome and fibromyalgia devastated by vaccines (AoA 9/26).

http://www.springerlink.com/content/364313152818131w/

Another virus PASSED down from mother to child..(think of mom with CFS and has a child with autism.)
\
This virus from polio vaccines....

oops, didn't post

http://findarticles.com/p/articles/mi_m0ISW/is_279/ai_n16865315/

Interestingly, both CFS and Autism have similar biomedical problems, aka, infections, mercury toxicity, metabolism problems, mitochondrial, glutathione block, etc....

Thank you David. My head is spinning.

Like KDM, the first thing I thought of when I read that the virus is being investigated in diseases like CFS, autism and prostate cancer was "SV40"-- the cancer causing virus that was in a polio vaccine.

The second thing I thought of when I read the virus was "blood borne" is that the press is going to howl that all autism moms are sluts or intravenous drug users-- that the virus is an an STD.

Why wouldn't close to 100% of children (save for that tiny percentage with genetically "mediated" forms) with autism have this virus? I just don't believe in the "take-your-pick-could-be-anything" cause of autism. I think the cause(s) will be limited to one or two substances or set of related events that mimic each other. If this virus isn't in all children with autism, then they'll surely find that another-- perhaps a vaccine strain (maybe two or so in combination, administered at the same time)-- entirely mimics the effects and that the other remaining percentage of children are effected by that. And it could be that none of these viruses would be able to do so much damage without simultaneous mercury/metal toxicity.

Did they make any other observations about the subjects who were positive for the virus, such as...they were especially tired? Like maybe they had chronic fatigue on top of autism?

I'm wondering along with David if-- like Karposi's sarcoma and AIDS--children with autism are just especially prone to contract this. We all know that children with autism get thrush. But thrush-- while it seems to worsen symptoms of autism-- isn't the cause of autism. AIDS patients also get thrush-- not a cause there either.

Read this:

"The finding that Hpc1 maps to the RNase L gene suggested that inherited defects in RNase L might allow for infection with an oncogenic virus, leading to PC [prostate cancer]"

http://www.pnas.org/content/104/5/1449.full

So the idea is that a genetic variation makes some people more vulnerable to a cancer causing virus.

But what if a pharmaceutical product created an immune susceptibility which mimicked this genetic "vulnerability"? For instance, it was long believed that MELAS, or "Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke" was a genetic disease and that if pharmaceuticals had anything to do with it (people have suddenly developed the full syndrome while on neuroleptics, antidepressants or anticonvulsive drugs with hugely elevated frequency), it was because the drugs-- so industry scientists said-- brought out the latant gene expression of MELAS. But now some researchers are finding that the genetic condition itself can be entirely replicated by drugs-- meaning one does not have to have any "latant" or underlying genetic defect to develop MELAS. More and more, they're finding that pharmaceuticals can entirely mimic what were once solely genetic disorders-- with or without anything "genetic" underlying.

Crazy stuff.

No one should consider this takes vaccines off the table.

It's quite possible that the retroviruses, like XMRV, are inherent in the material used to culture the vaccines and are artifacts. Similar to the SV40 virus which came from the kidneys of infected monkeys which were used for polio vaccines.

It could also be that viruses develop from mutations or recombinations of attenuated viruses or live viruses with human cellular RNA within the toxic stew of multivaccines and adjucts.

Viruses use cellular RNA to replicate themselves - such that the vaccine RNA sequences combine with cellular sequences to create new forms in order to survive. The mutation potential of chemicals like thimerosal, aluminum and others may increase the chance of sequence disruptions and recombination.

The problem is if you don't know what it is you don't know what to look for or how to develop a reliable way to find it.

Several viruses have been implicated in CFS before so it will take time to see how this plays out.

Viruses could be yet just another way the symptoms of autism are expressed (autism expression could have more than one cause since it is based on "symptoms").

sooo much more to learn about vaccines!

J Clin Invest. 1980 Apr;65(4):798-803.

Adverse effects of cytomegalovirus vaccination in mice.

* Jordan MC.

Studies of live attenuated cytomegalovirus (CMV) vaccine have recently been initiated in man. The possibilities of latent infection and disease resulting from reactivation of vaccine virus are major concerns. Because markers for attenuation of tissue culture-passaged mouse CMV (MCMV) exist, studies of potential adverse effects of vaccination were initiated in mice. Plaque-purified MCMV was passed 12 times in cell culture ("vaccine virus") and shown to be attenuated by virtue of loss of lethality and diminished replication in reticuloendothelial organs of normal mice. Although subcutaneous inoculation of 10(5) plaque-forming units of wild virus was lethal for mice immunosuppressed with antilymphocyte serum (18/18 died), "vaccine MCMV" killed only 3/18 (P < 0.05) and was thus shown to be highly attenuated even in immunosuppressed animals. 4 mo after subcutaneous inoculation of vaccine MCMV, no infectious virus was detectable in the tissues of normal C(3)H mice. However, immunosuppression with anti-lymphocyte serum and cortisone caused MCMV reactivation, dissemination, and wide-spread cytomegalic inclusion disease in 19 of 20 animals. Characterization of the reactivating virus recovered from salivary glands indicated that reversion to virulence had occurred. Thus, vaccine MCMV, although markedly attenuated initially, established latent infection, reactivated after immunosuppression, and reverted to virulence, at least in salivary gland tissue. These data from the murine model substantiate the need for careful surveillance and virologic study of patients given experimental CMV vaccine. PMID: 6244333 [PubMed - indexed for MEDLINE

so much more to learn....

Amy Becker Clark wrote: "I highly recommend the book "Osler's Web, Inside the Labyrinth of the Chronic Fatigue Syndrome Epidemic" by Hillary Johnson. The parallels between autism and CFS/ME extend far beyond a viral etiology: both epidemics are plagued by political and intellectual bungling so outrageous you'd almost think it was by design. Almost..."

The same is true of Lyme disease. The Infectious Diseases Society of America (IDSA) has done a HUGE coverup of Lyme disease, and doesn't even acknowledge the existence of chronic Lyme. "Cure Unknown" is a good book about this.

I highly recommend the book "Osler's Web, Inside the Labyrinth of the Chronic Fatigue Syndrome Epidemic" by Hillary Johnson. The parallels between autism and CFS/ME extend far beyond a viral etiology: both epidemics are plagued by political and intellectual bungling so outrageous you'd almost think it was by design. Almost...

.
It's the old question of which came first, the chicken or the egg.

Maybe that specific virus helps to cause autism.

Or maybe the various health problems -- which come along with, say, mercury poisoning, or an excess of toxic substances in vaccinations -- maybe that sets up a condition which allows this particular virus to flourish.

They'll never know, will they? Because they'll keep working on the "virus caused it" idea.

To the man with a hammer, every problem is a nail.

.

I have always suspected this to be the case.

It could be why our son is such a tough nut to crack and only make small or moderate gains with most biomeds (methylB12 and vitamin A have really helped him).