All I know about the HHV-6 Foundation’s interest in autism is what I read on April 5th in Kent Heckenlively’s post on Age of Autism:

“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.”

Mr. Heckenlively’s autistic daughter apparently was started on ganciclovir, the experimental treatment, even before they got the test results for HHV-6.

On April 14th, Mr Heckenlivey wrote:

“After one blood draw went awry and we finally got a sample to Viracor [a company that performs HHV-6 tests], three weeks after starting on ganciclovir. On Friday I got the result back. It was 100 copies, a weak positive reading.

Curiously, though, she showed no antibodies to HHV-6, suggesting an immune system issue. This puzzled our virologist until I mentioned again to him our belief that autistic children are immune-compromised. He acknowledged my point, but I don’t think he believes me yet.

So, what are the possibilities? After three weeks on the medication maybe it’s done a pretty good job at knocking the virus down? That is a reasonable assumption and to me the most likely one. I’m seeing some clinical improvements, but she often seems to have an up and down cycle over a month, so I’m not breaking out the champagne just yet.”

Unless I’ve missed it, Mr. Heckenlively hasn’t written anything else about HHV-6 since then.

His blog:
http://www.ageofautism.com/legal/index.html

The HHV-6 Foundation’s site says this about treatment for HHV-6:

“The Foundation is actively working with drug companies to spur an interest in the development of new treatments for HHV-6. The Foundation has also funded extensive in-vitro testing on natural compounds or compounds that are already approved for other conditions.

Although they are not FDA-approved for treatment of HHV-6 infection, many doctors treat HHV-6 encephalitis with intravenous ganciclovir (Cytovene) or foscarnet (Foscavir). Ganciclovir is also available in an oral form (Valcyte ). In vitro studies have shown that cidofovir (Vistide) which is also approved for CMV retinitis, is more effective than either ganciclovir or foscarnet (DeClercq 2003, Long 2003). However it is not known how well cidofovir crosses the blood brain barrier.

Both foscarnet and cidofovir must be administered with a great deal of hydration to avoid kidney toxicity. Typically a full liter of water is given by IV before each dose. Probenecid is given with cidofovir to protect the kidney.

Valcyte (valganciclovir) is an antiviral pill that is turned into ganciclovir in the body. Because it is better absorbed than ganciclovir pills, it causes much higher levels of ganciclovir in the blood. It is manufactured by Roche pharmaceuticals. The drug is primarily used to treat cytomegalovirus infections, which is most common in transplant patients, however it has been shown in uncontrolled studies to effectively treat co-infection of HHV-6 and Chronic Epstein Barr virus. Stanford University researchers are undergoing a trial of Valcyte in a subset of CFS patients with elevated antibodies to HHV-6 and EBV. They call this condition Virus Induced CNS Dysfunction. (See info on Stanford Trial of Valcyte in VICD.)

In an in vitro study at The Rega Institute funded by the Foundation, the influenza antiviral and Parkinson’s drug, amantadine, generated a reproducible inhibition of HHV-6 replication, albeit at relatively high (subtoxic) concentrations. Researchers at the Rega institute also found lamotrigine, an anti-epileptic drug, was effective against HHV-6B but not HHV-6A (Naesens et al, 2006).”
http://www.hhv-6foundation.org/treatment.html

And Carantech, Inc., the company I mentioned in my first post, lists a number of “antibody therapeutics” that they are exploring. (See the link above.)

It’s all up in the air. The sooner we know one way or another if HHV-6 in involved in autism, the better.

The mitochondrial mutations observed in this study were mainly hetereoplastic, that is cells contained both mitochondria with the mutation and mitochondria without the mutation. These mitochondria were in blood cells, which derive from blood stem cells which over a lifetime multiply many times more than do somatic cells.

Interesting stuff, but I’m feeling confused again. The study seems to indicate they were looking for ten ‘common’ mutations that could lead to defective mitochonrdrial function. If the loss of such mutations isn’t rare, I’m struggling to figure out how these particular mutations could be identified as common causes; i.e., how are they identifiable if they are lost to regeneration?

This is reminiscent (sp?) of a discussion I had on this board previously regarding CNVs versus environmentally acquired mutations, I can see pretty easily how acquired mutations could be lost to new cell generation, but not how a more global mutation could fall to the wayside. Likewise, I’m having trouble with acquired mutations accumulating to such a point that they are identifiable as problematic mutations, and not everyday mutations that we all tend to have.

Can you give us some more insight?

Thanks

-pD

The mitochondrial mutations observed in this study were mainly hetereoplastic, that is cells contained both mitochondria with the mutation and mitochondria without the mutation. These mitochondria were in blood cells, which derive from blood stem cells which over a lifetime multiply many times more than do somatic cells. It is not rare for people to lose a genetic defect from their blood stem cells as they age. What that means is that the stem cells with the genetic defect didn’t continue to replicate and were replaced by blood stem cells without the defect. They allude to this in the article, suggesting that some mothers may have been heteroplastic for the mitochondrial defect and lost that heteroplasty over time. The reason this happens is because stem cells with the defect don’t replicate as well and so over time good stem cells out replicate them and eventually replace them.

If you did happen to have a mitochondrial defect that was heteroplastic, putting your cells under sufficient metabolic stress to challenge those defective mitochondria to the point of failure might be an excellent therapy strategy. If all the defective mitochondria in a cell are destroyed, the only ones left are the non-defective ones. Periodic infections and fevers might be a natural mechanism to do that.

One indirect way of answering that would be to figure out how common HHV-6 infections are in autistic individuals because mitochondrial dysfunction seems to be associated with HHV-6.
(HHV-6 has been suggested as a potential trigger for autism by the director of the HHV-6 Foundation.)

This abstract discusses HHV-6B and mitochondria:
http://tiny.cc/55Ius

Also, the few safety tests I’ve seen have not had any long term safety studies done that I can tell, so the only way they are considering a reaction is if it is immediately obvious and allergic in nature. Also, the Hep B doesn’t seem to have any newborn safety studies that I can tell. My child’s doctors refused to believe it was the vaccines (particularly Hep B) that caused my daughter’s fevers that lasted several weeks, rash from head to toe, vomiting, diarrhea and dehdyration. She was hospitalized for care after each of her vaccines and yet the doctors would not acknowledge any reaction. Would scientists have a greater sense of integrity or insight? I hope so, but it worries me when a medical community does not (in our experience with our doctors and children’s hospital).