http://www.ican.com/news/fullpage.cfm/articleid/A55AECFE-2BD2-43B1-9FCCB5AD3
D4A6B8C/cx/news.news/article.cfm

More children diagnosed with MS
By Kathleen Fackelmann
USA TODAY
December 4, 2002

Kyle Wallace, age 9, loves to play football with his dad.

That's not unusual for a second-grade boy, but Wallace has multiple sclerosis, the neurological disease once thought to strike adults only. Researchers in a few medical centers in the United States and Canada say they're seeing more children like Kyle who are diagnosed with the disease.

And the last thing the young patients want to think about is a disease that can cause unpredictable bouts of paralysis, numbness, vision loss and a host of other terrifying symptoms.

MS affects about 350,000 American adults, and experts estimate that as many as 20,000 children in the United States have the disease but are undiagnosed. New medical evidence suggests that the number of pediatric patients is rising -- probably because more doctors are considering the diagnosis when they see a child with telltale symptoms such as a sudden loss of vision.

When a childhood diagnosis is made, doctors, parents and children are faced with a number of unanswered questions. Researchers don't know whether the drugs used to treat adults will work for children. They don't know how quickly the disease will progress.

MS occurs when the body's immune cells turn and mistakenly attack the thick sheath covering the nerve fibers of the brain and spinal cord. This protective coating, myelin, is like the rubber insulation on an electrical wire. When it's stripped, the nerve can be damaged, triggering a range of symptoms such as tremors or slurred speech. But the course of MS doesn't follow a predictable pattern.

Some people with MS have attacks that can last several days to a week and then fully recover. They may not get another attack for a year or even a decade. Others will get several attacks spaced out over a year. A small
number of people with MS get steadily worse with each attack.

Into the unknown
But that's the way the disease progresses for adults. No one knows what will happen to kids like Kyle. Lauren Krupp at the State University of New York-Stony Brook and her colleagues just completed a study of 21 kids with MS, one of the first studies to focus on the disease in children.

Traditionally, neurologists had been taught that MS strikes adults, most often women, between the age of 20 and 40. But Krupp's study, sponsored by the National Multiple Sclerosis Society, suggests MS can launch its attack very early in life: One child in the study was diagnosed at 6.

Other researchers say they've seen the disease in preschool children. Brenda Banwell, a neurologist at the Hospital for Sick Children in Toronto, says her team has treated 34 children with MS: The youngest was 4 and nearly half were under age 10 when they had their first attack.

Kyle Wallace had his first MS attack at age 4, says his mother, Tammy. She was getting him ready to go to preschool in the morning when suddenly he couldn't sit up.

Even today, many doctors don't consider MS a possibility in a child that young, Banwell says. In fact, Tammy Wallace says she has tried to get help at the local hospital when Kyle has an attack, only to be told there's no such thing as pediatric MS.

Now she doesn't even try to get help in their suburb outside Toronto. She drives the 45 minutes to get to Toronto's Hospital for Sick Kids. 

That lack of knowledge about pediatric MS means many kids may not get a diagnosis right away. Only a few doctors at urban centers in the United States and Canada specialize in pediatric MS. Krupp's group gets kids from all over the U.S. Banwell's group in Toronto also sees families from all over Canada and even some from the U.S.

Suffering in silence
Except for some mild tremors, no one would ever guess that 17-year-old Anna Peabody has MS. But Peabody, an honors student at Acton-Boxborough Regional High School in Acton, Mass., has lived through five flare-ups in the disease since her diagnosis in 2001.

"It's been awful," she says. "I missed three months of school last year." Peabody made up that time during the summer and went on with her classmates.

But researchers can't tell Peabody what the future might hold. "I worry," she says simply. "Will I be able to walk when I am 20?"

Although most children with MS have very mild cases, both Krupp and Banwell have seen a small group of kids with very aggressive symptoms. Instead of one or two attacks a year, these children must deal with five or more.

Krupp's study identified five out of 21 cases in which the disease took on this more severe course. No one really knows whether those kids will go on to experience progressively worsening disease, but Krupp hopes the arsenal of new drugs that can push back the malady in adults will work the same way for children.

But the drugs that have fueled a revolution among adults with MS have not been tested in children. There's no proof that these drugs will work the same way for kids as young as Kyle Wallace. But doctors like Krupp have no choice but to use the drugs, especially when faced with a young patient who has had multiple attacks in a short period.

The hope is that such drugs, especially if started early, will stave off the worst consequences of the disease. For kids with the worst attacks, Krupp has even used more than one drug in combination to push the disease back. That's worked, at least so far.

But even for Krupp, the battle with pediatric MS is a day-by-day struggle that takes on an air of urgency: Each attack can cause a little more damage to the brain. Researchers worry that repeated attacks can leave a child with memory and learning problems. Krupp says about 30 percent of the children in the study had trouble with cognitive skills, such as remembering information for a test.

Some adults with MS also have such deficits but often can get around their problems by relying on their past experience. Unlike adults with MS who have already completed their academic careers, kids are still trying to lay down a foundation of knowledge.

And even for children without cognitive damage, the effects of MS can be devastating. Anna Peabody says that her vision often fades, a problem that makes reading more than two pages of text almost impossible. But Peabody refuses to let go of her dream: attending college.

To get there, Peabody says she's had to change her attitude toward the disease. She says she spent two years denying the existence of her MS, an effort that exhausted her. Now she accepts the tremor that makes it hard for her to write a paper.

Watching that struggle can be pure anguish for a parent. "Your job as a parent is to fix it," her father, George Peabody, says. "And here comes this disease and we can't make it go away."

But researchers say they're struck by the resiliency that both children and parents show in the face of the disease. Tammy Wallace says her son's first attack left the preschooler unable to walk. She taught him to walk again and told him, "We're going to beat this."
 

Link Between Epstein-Barr and Multiple Sclerosis

[This goes to one of the immune disorder theories of autism that suspects this type of virus as a trigger.]
http://www.ivanhoe.com/channels/p_channelstory.cfm?storyid=5741

Ivanhoe Newswire - New research shows there may be an association between the Epstein-Barr virus and the development of multiple sclerosis. Epstein-Barr virus is a herpes-like virus that causes infectious mononucleosis, a type of viral illness typically called "mono." The virus is also associated with Burkitt's lymphoma and nasopharyngeal cancer. Researchers conducted a study using blood samples collected several years before the onset of multiple sclerosis. They wanted to determine whether antibodies to Epstein-Barr virus are elevated before multiple sclerosis develops. Participants included more than 3 million U.S. military personnel. Among them, 83 cases were identified as individuals granted temporary or permanent disability due to multiple sclerosis. Each of these cases were matched with two cases of healthy participants. Results of the study show antibodies to Epstein-Barr virus were consistently higher among participants who later developed multiple sclerosis. The authors write, "Similarly strong positive associations between EBV antibodies and risk of MS were already present in samples collected five or more years before MS onset." These findings suggest a long lag time between EBV infection and occurrence of multiple sclerosis. Researchers have examined the relationship between Epstein-Barr virus and multiple sclerosis for 20 years but results have not been consistent. About 350,000 Americans have multiple sclerosis. It is an autoimmune disease, meaning the body's immune system, which normally targets and destroys foreign substances, mistakenly attacks normal tissues. The cause of MS is unknown.

 

http://www.docguide.com/news/content.nsf/news/8525697700573E1885256D020062D3F4?

OpenDocument&id=03E05ADF052F2F3E852568C000807CA5&c=Paediatrics&count=10

AAN: Child-Onset Multiple Sclerosis More Likely to Have epstein-barr virus Antibodies than Controls

By Paula Moyer

HONOLULU, HI -- April 8, 2003 -- Children who have multiple sclerosis (MS) are more likely than healthy children to be seropositive for Epstein-Barr virus (EBV), according to researchers.

"EBV seropositive status is significantly associated with paediatric MS," said Brenda L. Banwell, MD, the director of the paediatric MS unit at the Hospital for Sick Children in Toronto, Ontario, Canada. Because of EBV's lifelong effects on B cell proliferation and T cell surveillance, it "may play a pivotal role in the autoimmune milieu that fosters MS." She presented findings of her team's study here at the 55th Annual Meeting of the American Academy of Neurology.

Dr. Banwell and her colleagues wanted to compare the seropositive status for common viruses in patients with paediatric multiple sclerosis and in controls. Their rationale was that several investigators have postulated that infection by a common virus such as EBV in a genetically pre-disposed host may be a pathobiological mechanism for MS.

The literature has also shown that adults with MS have higher seropositivity for EBV than controls do and that EBV infection has been associated with other demyelinating disorders, including optic neuritis and central nervous system demyelination. Further, research has shown that infection with acute mononucleosis in adulthood increases the risk of MS several times over.

One complication to testing the theory in adults is that EBV seropositivity is nearly universal by adulthood, with 90% of adults having EBV antibodies. Therefore, comparative analysis is limited between adult MS patients and controls. It was necessary to study paediatric patients, instead, she said, since fewer children are EBV-positive than are adults. Dr. Banwell and her colleagues theorised that MS patients might be EBV-positive before their healthy peers have had exposure to the virus.

The investigative team obtained serum samples from 25 children with clinically diagnosed MS and 75 age-matched controls, who were matched at a 3:1 ratio for birth year for each MS patient. Control samples were obtained from previously healthy children for whom serology had been drawn previously due to acute symptoms of abdominal pain, pharyngitis, or rash.

All 100 samples were analysed for EBV capsid antigen (EBV-VCA), EBV nuclear antigen (EBV-EBNA), and EBV early antigen (EBV-EA). The researchers also analysed all 25 MS samples and a random sampling of 15 of the age-matched control samples for parvovirus B19 (parvo B19), cytomegalovirus (CMV), and varicella zoster (VZV). The investigators coded and analysed all samples in a uniform manner by the ELISA technique (as per manufacturer s instructions). The study virologist then interpreted results in a blinded manner.

Dr. Bandwell and her co-investigators found that EBV seropositivity differed markedly between paediatric MS patients and age-matched controls. Although 89% of paediatric MS patients were positive for EBV-VCA and EBV-EBNA, which indicated a temporally remote infection, 31% of controls had such infections (p 0.0004). Among the MS patients, 3 (12%) were negative for all three EBV antigens.

The investigators found no statistical significance regarding seropositivity for the other viruses between MS patients and controls. For parvovirus B19 the infection rates were 49% and 64%, respectively (p=NS). For CMV the rates were 42% and 64%, respectively (p=NS). For VZV those rates were 88% and 92%, respectively (p=NS).

This discrepancy in EBV seropositivity between paediatric MS patients and controls is "considerably more robust" than similar studies of EBV in adult MS patients, Dr. Banwell said. The finding demonstrates the advantage of comparative studies in which healthy subjects are relatively naïve to common infections.

Because exposure to other common viruses does not differ between paediatric MS patients and controls, the findings suggest that the association between MS and EBV may be specific, Dr. Banwell said. The study was supported by a grant from The Hospital for Sick Children Foundation.


[Study title: Viral Studies in Pediatric Multiple Sclerosis. Abstract:
S41.002]

 

From: Robert Bransfield, MD

Subject: High Frequency of Human Herpesvirus 6 DNA in Multiple Sclerosis Plaques Isolated by Laser Microdissection

The Journal of Infectious Diseases 2003;187:1377-1387
2003 by the Infectious Diseases Society of America.  All rights reserved.

0022-1899/2003/18709-0004$15.00

High Frequency of Human Herpesvirus 6 DNA in Multiple Sclerosis Plaques Isolated by Laser Microdissection

Claudio Cermelli,Rossana Berti, Samantha S.  Soldan,Michael Mayne,James M.  D'ambrosia, Samuel K. Ludwin,and Steven Jacobson Neuroimmunology Branch and Biostatistics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, and Department of Neuropharmacology and Molecular Biology, Walter Reed Army Institute of Research, Silver Spring, Maryland; Institute for Biomedical Sciences, Department of Genetics, George Washington University, Washington, DC; Department of Hygiene, Microbiology, and Biostatistics, University of Modena and Reggio Emilia, Modena, Italy; Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, and Department of Pathology, Queen's University, Kingston, Ontario, Canada

published 9 April 2003.

The frequency of human herpesvirus 6 (HHV-6) DNA was assessed in autopsy material from multiple sclerosis (MS) plaques and normal-appearing white matter (NAWM) from brains of persons with MS, healthy brains, and brains of persons with other neurologic diseases.  Specific areas from formalin-fixed, paraffin-embedded brain tissue samples were isolated by laser microscope.  DNA was extracted from laser microdissected brain material, and HHV-6 genomic sequences were amplified by nested polymerase chain reaction.  We analyzed 44 NAWM samples and 64 MS plaques from 13 patients with MS, 46 samples from 13 patients with non-MS neurologic disorders, and 41 samples from 12 healthy control brains.  Of the 44 NAWM samples, 7 (15.9%) were positive for HHV-6 DNA sequences, versus 37 (57.8%) of 64 MS plaques (P < .0005).  HHV-6 DNA was detected in 10 (21.7%) of 46 samples from patients with non-MS neurologic disorders and in 11 (26.8%) of 41 samples from patients without known neurologic disease.  Although the frequency of HHV-6 DNA did not differ significantly by sample type, HHV-6 DNA was significantly more common in MS plaques, suggesting that HHV-6 may play a role in MS pathogenesis-

-------
Presented in part: 4th International Conference on Herpesviruses Paris, 1012 May 2001 (abstract O22).

Informed consent was obtained from patients or their parents/guardians, and human experimentation guidelines of the US Department of Health and Human Services were followed.

Financial support: Fondazione Cassa di Risparmio di Carpi (to C.C.).

Present affiliation: Department of Neurology, University of Pennsylvania, Philadelphia.

Once again the findings do not go along with the subject title. When will it ever?
Cindy

http://www4.nationalacademies.org/news.nsf/isbn/0309090865?OpenDocument

Read Full Report

Date: Oct. 6, 2003
Contacts: Christine Stencel, Media Relations Officer
Andrea Durham, Media Relations Assistant
Office of News and Public Information 202-334-2138; e-mail <news@nas.edu>

FOR IMMEDIATE RELEASE

Flu Vaccines Do Not Trigger Relapses in Multiple Sclerosis Patients; Guillain-Barré Syndrome Linked Only to 1976 Swine Flu Vaccine

WASHINGTON -- Scientific evidence shows that influenza vaccines do not trigger relapses of multiple sclerosis (MS) in adults with the disease, says the latest report on vaccine safety from the Institute of Medicine of the National Academies.  In addition, the report confirmed the well-studied link between the specific influenza vaccine used to ward off an anticipated epidemic of the "swine flu" in 1976 and several hundred cases of the rare paralytic disorder  Guillain-Barré syndrome (GBS) that occurred in vaccinated adults. The majority of studies suggest that flu vaccine formulations used after 1976 have no link to GBS, but inconsistencies in data and the designs of studies that investigated this question preclude a more definitive assessment. Although flu vaccinations soon might be recommended for young children, too, no studies have directly addressed whether these vaccines may cause or exacerbate GBS, MS, and other demyelinating conditions in this population, said the committee that wrote the report.

"Because flu vaccines are so widely used in adults, the possibility that neurological disorders might be related to the vaccines must be given serious consideration," said committee chair Marie McCormick, professor and chair, department of maternal and child health, Harvard School of Public Health, Boston. "At the same time, it is just as important that the possible risks are weighed appropriately against the burdens of illness and death associated with flu, which ranked among the leading killers in the United States during the 1990s." Flu viruses caused an average of 36,000 deaths among Americans every year throughout the last decade.

The committee determined that there is only weak evidence for biological mechanisms by which flu vaccines might work through the immune system to trigger neurological disorders. Also, without experimental data or evidence from studies in humans, the biological means by which the vaccine could influence a person's risk of developing GBS or MS through a direct toxic effect on the nervous system are only theoretical.

The Centers for Disease Control and Prevention advises that all people over age 50 be vaccinated, as these individuals are at greatest risk of suffering serious illness or death brought on by a flu virus infection. CDC also recommends immunization for younger individuals who have an underlying health condition, such as diabetes, asthma, or HIV infection. The agency's Advisory Committee on Immunization Practices is considering whether to recommend annual vaccinations in young children as well. Before it does so, CDC should increase its surveillance of vaccine-related adverse events, and particularly its ability to detect and assess potential neurological complications, the committee said.

GBS affects roughly one to two of every 100,000 Americans. About two-thirds of cases occur within several days or weeks of a bacterial or viral infection, particularly by the Campylobacter jejuni bacterium. Eighty-five percent of GBS patients will return to normal functioning within six to nine months, althoug h some patients experience relapses or prolonged illness.

MS is the most common inflammatory disease of the central nervous system, affecting between 250,000 and 350,000 Americans. Eighty percent of MS patients experience a relapsing-remitting form of the disease, in which exacerbations of symptoms are followed by complete or partial recovery. The cause of MS has yet to be determined, but susceptibility appears to involve both genetic factors and environmental triggers. While the evidence refuting a link between flu vaccines and MS relapses suggests that the vaccines also do not trigger the onset of MS, a dearth of quality studies specifically examining flu vaccination and the development of the disease means that a causal association can be neither accepted nor ruled out at this time.
 

Subject: researcher spent three decades exploring MS mystery

U. researcher spent three decades exploring MS mystery
Molecular mimicry: Robert Fujinami suspects a virus may be tricking the body into attacking the coating of the nerve fibers
By Greg Lavine
The Salt Lake Tribune

When Robert Fujinami started his research 30 years ago, multiple sclerosis was a black box - a dark void to scientists. Few had illuminated much about the debilitating disease that eats away at the lining of the brain and spinal cord. Attacking the problem from various angles, Fujinami and colleagues around the world have made progress. "Now we have flashlights we can shine into the black box to see parts of the disease," said the University of Utah School of Medicine neurologist. "Instead of flashlights, someone will develop a floodlight to show what's inside the black box."

Fujinami has turned his narrow beam of light on molecular mimicry. In multiple sclerosis, this means that a virus may fool the human body's immune system into attacking healthy parts of the body. MS involves the destruction of a substance known as myelin that covers nerve fibers. Without that coating, normal nerve transmissions are disrupted. Researchers have no cure for the disease, though drugs are now available to help treat the problem. Scientists continue to chip away at what causes the disease.

Multiple sclerosis presents a challenge to medicine. Cases appear to cluster in areas in higher latitudes, such as the northern United States, Canada and Sweden. Southern latitudes, like Italy, seem to have fewer cases of multiple sclerosis and a lower risk of the disease. If a woman born in Sweden, for example, moves to Italy after turning 15, she maintains her birth country's high risk of developing the disease. A Swedish-born woman who moves to Italy before the age of 15 takes on her new home's lower risk of the disease. This leads some researchers, including Fujinami, to suspect that a virus found at northern latitudes may lead to MS.

"Maybe something early in life would prime a genetically susceptible individual for developing MS later in life," he said. MS may begin damaging myelin only after a second virus sets the disease into action, a theory being tested in mice, Fujinami said. What the priming or triggering viruses may be remain speculation. Some suggest Epstein Barr virus, while a few suspect human herpes virus 6. Molecular mimicry may occur when an invading virus carries proteins that are similar in structure to proteins found on myelin. As the immune system mounts an attack against the invading virus, it targets the protein. The immune system's response also takes on the proteins on the healthy myelin.

J. Richard Barringer, a fellow neurologist at the U. School of Medicine, said Fujinami has garnered international recognition for his MS work on molecular mimicry. "He's been one of the real pioneers in developing that concept over the years," said Barringer, who has served on the board of directors for the National MS Society. Risk factors: If researchers can finger the culprit virus, they might be able to develop vaccines or drugs to treat the disease before it attacks the brain's covering. Genetics and gender are considered to be among the factors that put people at risk for MS. Aside from viruses, other researchers are examining environmental factors such as heavy metals or trauma as potential causes, according to the National Multiple Sclerosis Society.

Fujinami has been exploring various aspects of the disease since graduating from the U. in 1972 with a microbiology degree. He has logged time behind the lab bench at Northwestern University, in Chicago, and the Scripps Clinical and Research Foundation, in La Jolla, Calif. In 1990, he returned to Utah with his wife, Christine, whom he went to school with at Salt Lake City's East High School. Fujinami set up a laboratory at the U. to continue his work on MS. It is easy to imagine growing tired of a topic after 30 years, but Fujinami remains committed to the field. "Most researchers are pretty stubborn," he said. "I think we're getting closer and closer, which is the exciting part." The prospects of a brighter future help motivate Fujinami, but there are times when other thoughts dart through his mind. "I wish I could move to another disease," he joked.

Life in the lab: While the Fujinami lab has started some research into autism, most of his contact with other disease research fields is limited to journals and talking to other scientists. He interacts with scientists studying other diseases that are related to immune system problems, such as diabetes and arthritis. The neurologist looks at what top minds are thinking about in other fields and wonders whether that could help MS research. Much of the work in his lab revolves around a strain of mice known as SJL/J. Researchers infect the mice with a virus that is thought to be similar to the priming virus in humans. None of the mice develop an MS-like disease from the first virus. Later in a lab mouse's life, a second virus is added that fools the creature's immune system into attacking its own myelin that coats nerve fibers, he said.

During a recent lab tour, Fujinami held up a plastic tray, called a plaque assay, that contained several indigo-colored circles. Any spots that let light through indicated where the virus has taken hold in the mouse tissue samples. The work going on in his lab is a far cry from what was possible when he started looking at the shadowy disease.  Despite spending three decades on this problem, he insists he will not be discouraged if his generation fails to nail down a cure for MS. "I feel like I've set down a good foundation," he said. Fujinami takes heart in thinking that one of his students might find the switch that turns on the floodlight that will bring MS out of the darkness.
glavine@sltrib.com

Subject: Molecular mimicry/virus abstracts

J Immunol. 2005 Jan 15;174(2):907-17.   Related Articles, Links    
 
Viral delivery of an epitope from Haemophilus influenzae induces central nervous system autoimmune disease by molecular mimicry.

Croxford JL, Anger HA, Miller SD.

Department of Microbiology-Immunology, and Interdepartmental Immunobiology
Center, Northwestern University Medical School, Chicago, IL 60611, USA.

Multiple sclerosis (MS) is an autoimmune CNS demyelinating disease in which infection may be an important initiating factor. Pathogen-induced cross-activation of autoimmune T cells may occur by molecular mimicry. Infection with wild-type Theiler's murine encephalomyelitis virus induces a late-onset, progressive T cell-mediated demyelinating disease, similar to MS. To determine the potential of virus-induced autoimmunity by molecular mimicry, a nonpathogenic neurotropic Theiler's murine encephalomyelitis virus variant was engineered to encode a mimic peptide from protease IV of Haemophilus influenzae (HI), sharing 6 of 13 aa with the dominant encephalitogenic proteolipid protein (PLP) epitope PLP(139-151). Infection of SJL mice with the HI mimic-expressing virus induced a rapid-onset, nonprogressive paralytic disease characterized by potent activation of self-reactive PLP(139-151)-specific CD4(+) Th1 responses. In contrast, mice immunized with the HI mimic-peptide in CFA did not develop disease, associated with the failure to induce activation of PLP(139-151)-specific CD4(+) Th1 cells. However, preinfection with the mimic-expressing virus before mimic-peptide immunization led to severe disease. Therefore, infection with a mimic-expressing virus directly initiates organ-specific T cell-mediated autoimmunity, suggesting that pathogen-delivered innate immune signals may play a crucial role in triggering differentiation of pathogenic self-reactive responses. These results have important implications for explaining the pathogenesis of MS and other autoimmune diseases.

PMID: 15634913 [PubMed - in process]   

 Recent independent scientific research funded by the National CFIDS Foundation, Inc. (NCF) of Needham, MA provided preliminary confirmation of a new virus identified in patients with Chronic Fatigue Syndrome. The Foundation's medical research dovetails with that completed to date by Cryptic Afflictions, LLC (1), a private company.

Dr. Steven J. Robbins, virologist and Chief Executive Officer of Cryptic Afflictions, LLC has discovered a major neuropathogen identified as an RNA virus designated as Cryptovirus. Substantial clinical and molecular evidence indicates that this virus is involved in the development of neurological disorders that include Chronic Fatigue Syndrome (CFS), also known as Myalgic Encephalomyelitis (M.E.) by the World Health Organization, Multiple Sclerosis (M.S.) and Idiopathic Epilepsy of unknown cause.

According to the company, "This previously undetected virus appears to be of significant importance to researchers looking for a cure to Multiple Sclerosis and many other neurological illnesses. Antibodies to the newly discovered virus were found in the cerebrospinal fluid and blood of over 90 percent of the patients tested with Multiple Sclerosis. It is believed that this newly discovered virus may prove to be responsible for a host of neurological disorders. Tests are currently being prepared for tissue samples of lesions within the brains of patients with Multiple Sclerosis. This will be the final round of tests before approaching the FDA for approval of the diagnostic tests."

Dr. Robbins' evidence includes the presence of virus-specific antibodies in the serum and cerebrospinal fluid of patients suffering from these disorders, the ability of the virus to cause virtually identical disease in experimentally-infected animals, and nucleotide sequence data that indicates that the virus is pandemic and represents a single virus species much like measles.

A recently published medical journal article suggests that Cryptovirus is most similiar to Parainfluenza Virus-5, a rubulavirus in the paramyxovirus family. Another rubulavirus related to Cryptovirus and Parainfluenza Virus-5, that has gained national attention for its large outbreak, is the mumps virus. Rubulavirus infections have been associated with encephalitis, meningitis, orchitis, inflammation of the
testicles or ovaries, spontaneous abortion, and deafness.

The NCF has conducted its own preliminary research into the potential role of Cryptovirus and Parainfluenza Virus-5 in Chronic Fatigue Syndrome. Professor Alan Cocchetto, Medical Director for the Foundation stated, "Our own funded research first confirmed the lack of a vital protein, known as Stat-1, in the blood of patients with Chronic Fatigue Syndrome. Stat-1 plays an indispensable role in immunity. Without this protein, patients are unable to effectively fight viral and bacterial infections. Thus, the next logical question to be answered was 'Could a virus be causing this Stat-1 depletion?' " Cocchetto continued, "Parainfluenza Virus-5 is a virus that had to be seriously considered as a possible piece of this medical puzzle because it directly targets and destroys the Stat-1 protein." Gail Kansky, President of the NCF stated, "Once we determined the status of Stat-1 in patient blood samples, we knew that we had to look for possible evidence of Parainfluenza Virus-5 infection. It was during this phase of our own research that we actually learned of Dr. Steven Robbins' discovery of Cryptovirus specific antibody reactivity in patients with CFS." Dr. Robbins had tested fifty- six serum specimens from patients who had
been diagnosed with CFS along with eleven matching cerebrospinal fluid samples obtained from physicians in Brisbane and Southeast Queensland. Dr. Robbins had determined that 96 percent of the blood samples and 91 percent of the spinal fluid samples tested positively for Cryptovirus specific antibodies in these CFS patients.

The National CFIDS Foundation's own research began to dovetail with that of Dr. Robbins. Scientists funded by the Foundation performed numerous tests for Parainfluenza Virus-5 that included antibody as well as PCR specific probes. Antibody testing provided some initial hints, however a PCR specific probe picked up the infection in a former patient of David S. Bell, M.D. and Paul R. Cheney, Ph.D., M.D., both
considered well known specialists in the field of Chronic Fatigue Syndrome. Kansky commented, "Though our funded research continues in diagnostic testing, our findings have served to highlight the important work of  Dr. Robbins and the role of Cryptovirus and Parainfluenza Virus-5 infection in CFS."

NCF scientists utilized the NIH Genbank database to find the nucleotide sequence for a specific viral protein of Cryptovirus that matched 100 percent to the porcine (swine) strain of Parainfluenza Virus-5 known as the SER strain. In 1994, scientists at Bayer AG in Germany first isolated the SER strain from swine with Porcine Reproductive and Respiratory Syndrome. "This may represent a zoonotic process since zoonotic viruses are those that can be transmitted between animals and people" stated Cocchetto. Kansky commented, "Here we have what appears to be the same viral strain of Parainfluenza Virus-5 on two continents and in two different populations, swine and humans. Given that the NCF found Parainfluenza Virus-5 in one CFS patient in the United States certainly raises the bar." The Foundation is currently funding further research.

The National Institutes of Health (NIH) has several ongoing grants in the Parainfluenza Virus-5 field. Currently, however, there is only one U.S. scientist specifically funded for research on the SER strain of
Parainfluenza Virus-5 by the NIH.

(1) "Limina Biotechnologies, Inc. is a recently formed subsidiary of Global Medical Technologies, Inc. that was established for the purpose of merging Cryptic Afflictions LLC and Global Medical Technologies, Inc. It is the intent of management to spin off this newly formed corporation once the merger is completed so Limina can raise capital through its own IPO," according to the company's website,
http://www.globalmedicaltech.com.

Contact: Gail Kansky of the National CFIDS Foundation, 781-449-3535 or
gailronda@aol.com