Ales

It seems that CCID uses a different definition of a “stealth virus” (Copied from <a href="http://www.ccid.org):" target="_blank">www.ccid.org):</a>

“Dr. Martin's laboratory was the first to detect weak, but significant, positive polymerase chain reaction (PCR) responses in the blood of CFS patients. The initial primer sets used were based on known sequences of human herpesviruses and human retroviruses. Since the positive PCR responses required low stringency conditions for both amplification and detection of the PCR products, it was apparent that the agent(s) being detected were not identical to the viruses used to design the PCR primers.
Low stringency PCR was similarly applied to blood and cerebrospinal fluid (CSF) from patients with more severe neurological illness. Early examples included: i) A teenager with residual neurological impairment from what was initially considered a missed diagnosis of a Herpes simplex encephalitis; ii) a premature infant, failing to thrive with seizures and neurodevelopmental delay; and iii) a school teacher with a severe expressive aphasia and marked periventricular hyperintensities on magnetic resonance imaging (MRI). It soon became apparent that many of these patients showed similar weak reactivity as did CFS patients, in low stringency PCR based assays. A stereotactic brain biopsy obtained in early 1990 from the periventricular region of the school teacher was also PCR positive. Histological examination of the brain biopsy showed no evidence of inflammation, yet on electron microscopy, occasional virus-like particles were seen within vacuolated cells. The implication of the finding was that the positive PCR assays being observed in CFS patients was also be indicative of a non-inflammatory virus encephalopathy.
Renewed efforts at culturing blood of a CFS patients led to the detection of a cytopathic virus that induced a vacuolating change in cells from multiple species. The cytopathic effect (CPE) was quite distinct from that seen in the routine clinical virology laboratory and was initially suggestive of a foamy (spuma) retrovirus. The cultures were strongly reactive with the same set of retrovirus primers that gave a positive PCR when used directly on the blood of the patient. Cloning of the PCR products showed that portions of this particular virus had been derived from a cytomegalovirus , and specifically, from African green monkey simian cytomegalovirus. Similar PCR assays on positive virus cultures from other CFS patients gave differing products, leading to the conclusion that the viruses were molecularly heterogeneous. Because of the lack of inflammation in the brain biopsy and the minimal if any cellular responses seen in virus-culture-positive CSF specimens, the term “stealth” was coined to designate the type(s) of viruses being cultured.
Stealth viruses are presently defined as a molecularly heterogeneous grouping of atypically structured viruses that induce a vacuolating CPE in tissue culture. The in vitro growth characteristics and the reactivity patterns in serological and/or molecular based assays can be used to distinguish stealth viruses from conventional human cytopathic viruses. In spite of being cytopathic, stealth viruses fail to induce an effective anti-viral inflammatory response in vivo and, thereby, have the capacity to induce a persistent, active infection.
Since the original reports, stealth viruses have been cultured from a large number of patients with both CFS and with various neurological and neuropsychiatric illnesses. The early histological findings have been confirmed in other patients with severe neurological diseases who have undergone brain biopsy. The spectrum of severe clinical illnesses seen in stealth virus positive patients has included the following: i) Newborns with hepatomegaly, thrombocytopenia and choroid plexus hemorrhage, born to virus infected mothers; ii) young children with autistic, attention deficit, anorexia nervosa, and aggressive behavioral disorders; iii) young adults with schizophrenic, manic-depressive psychosis and drug addiction; iv) patients with various neurological disorders ranging from localized impairment of sensory, motor or autonomic functions, to otherwise unexplained coma, and v) elderly individuals with dementia, including patients labeled as having Alzheimer?s disease. Many of the patients tested have had concomitant disease involving various other organ system including the gut, salivary glands, liver, pancreas, thyroid, adrenal, heart, and genital organs.”


<a href="http://www.ccid.org/index.htm" target="_blank">http://www.ccid.org/index.htm</a>

states among other things:

“ It bas now been scientifically proven that stealth viruses do, indeed, exist and can be at the root of many multi-system neuro-degenrative illnesses, such as Chronic Fatigue Syndrome, fibromyalgia, attention deficit disorder, autism and other diseases causing behavorial changes.”

Again, this seems to point to something else than now fully acknowledged EBV.

In this lecture
<a href="http://www.inx.net/~carolynv/jmartin/martin.htm" target="_blank">http://www.inx.net/~carolynv/jmartin/martin.htm</a>

you can read about the relation of a stealth virus to a virus from African green monkeys, simian cytomegalovirus. Here is a quotation:

“I'll mention that we've been working on this for a long time. Back in 1991, we had such a culture from a patient who still has Chronic Fatigue Syndrome. So this was a lady that was in Los Angeles, worked as a health care worker and basically became sick with a typical chronic fatigue like illness. Her virus was fortunate in a sense that it was more intact than many of the viruses you do see and by using an electron microscope and looking at the infected cells from cultures, we could begin to see particles that were indicative of a virus. This is a larger magnification. These are pretty typical viruses that generally look like the herpes virus, that would include cytomegaloviruses, Herpes Virus 6, Herpes Simplex Virus. These other larger units are the types of viral materials that viruses use to assemble themselves. So here we had a culture from a patient and it looked as if it might be a herpes virus, yet when we did all the various tests for that, it did not show to be a normal human herpes virus. Rather we found it was something different. We proceeded to do molecular studies on that virus and essentially this (Slide 2) summarizes some of the studies on it as well as results of the molecular studies. It produced, as I said, vacuolated cytopathic effects in humans and as I indicated earlier, even in animal cell lines--cat cells, even some insect cell lines. It looked like herpesvirus-like particles. This polymerase chain reaction is a very sensitive molecular technique that was used and that gave us portions of the virus genome and when we sequenced one portion it showed some relatedness to human cytomegalovirus, partial--50%--similar but not really human cytomegalovirus. And when we extended that study and the sequence analysis and had sequence analysis available for African green monkey Simian cytomegalovirus it was apparent that we had 90 - 95% relatedness of parts of that virus to this African green monkey derived cytomegalovirus. And for those people who can appreciate the numbers, this (Slide 3) is a kind of quantitative analysis that shows a measure, either by FASTA score or BLASTN score, a measure of the relative relatedness of this virus to human cytomegalovirus. The FASTA score was 348. More closely related to the cytomegalovirus from Rhesus monkeys, a score of 1000. But the highest of all with African green monkey viruses, referring to the simian cytomegalovirus. The BLASTN score shows powers to the tenfold, and 10 to the 245 is an unbelievably high number. Without any equivocation then, we can say that this virus came from African green monkeys, simian cytomegalovirus.”

Remember, that I have no serious medical education, I came across CCID only a week ago and I am interested in it since I have been suffering from a devastating illness for a long time without any explanation of the currently acknowledged medical knowledge. It appears that peer reviewed journals are reluctant to publish the scientific findings of CCID, on the other hand the information they provide doesn’t look like a nonsense. Please refer your eventual questions about these stealth viruses to <a href="http://www.ccid.org" target="_blank">www.ccid.org</a> or use search engines.

Ales

Jackalope

I'd like to point out that the statement on the CCID website isn't even close to being commonly accepted. Fibromyalgia, in particular, seems more closely related to migraines and sleep disturbances than any viral infection. Especially since patients with various chronic painful syndromes (from injury or from autoimmune disorders) often begin to exhibit the same symptoms of fibromyalgia over time. The fact that tricyclics antidepressants and various anti-seizure drugs (the most recently tried are Neurontin and Topamax) tend to significantly improve symptoms would suggest a problem with neurotransmitter levels, not a viral infection.

For a quick comaprison, there's a particularly nutty theory that arthritis and other autoimmune diseases are caused by mycobacterium infection...even though the evidence is otherwise. While antibiotics from the tetracycline family do help some arthritis patients, it's because those drugs have antimetalloproteinase activity. It has nothing to do with their antibiotic properties. I point this out because just about every disease that doesn't have a clearcut cure eventually has someone saying, "Oh it's really an infection, just one that's really hard to find!" The truth is probably closer that infections set off autoimmune activity, which continues long after the original infection is gone.

Just because someone has an official looking website out there does not mean they're actually doing good science.