FMS/CFS/LYME/MPS/MOLD/TOXINS/METALS/CHEMICALS RESEARCH ARTICLES

Discussion in 'Fibromyalgia and ME & Chronic Fatigue Syndrome' started by fight4acure, Jul 26, 2006.

  1. fight4acure

    fight4acure Member

    Anyway, we need all the articles we can send to our doctors that proves CFS and FMS is real and discusses the articles of antivirals treating CFS and FMS. Also, any other articles about CFS, FMS, Lyme disease, chemical exposure, metal exposure, toxin exposure, mold exposure, and viral exposure, etc.

    If we could collect the articles here, I would so much appreciate it. Then we can all come to one post to get articles for our docs.

    Hugs! And Thanks ahead of time for your time in finding good and resent articles proving this illness is real. I'll start by posting some of my own.

    P.S. PLEASE BE SURE TO ADD THE SOURCE AND DATE OF ARTICLE AS WELL AS THE AUTHOR. THANK YOU SO MUCH!

    I pray this will not only help me but also others new to this board.


    (PLEASE KEEP THIS BUMPED FOR NEW PEOPLE)

    [This Message was Edited on 02/04/2008]
  2. fight4acure

    fight4acure Member

    THEORY EMERGES ON FATIGUE AILMENT
    Scott Hensley
    Wall Street Journal, Technology & Health, 9/19/00

    Toronto - Viruses that insidiously damage heart muscle may be the cause of chronic fatigue syndrome, a mysterious malady that many physicians have written off as a psychological condition, according to a provocative new study by an infectious disease expert.

    At a major scientific conference here, Martin Lerner, a doctor at William Beaumont hospital in Royal Oak, Mich., presented data on a series of patients, including himself, who developed the debilitating condition and were later treated, with apparent success, with potent antiviral drug regimens.

    "It is an infectious disease," that primarily attacks the heart, Dr. Lerner declared at a meeting of the American Society of Microbiology. Dr. Lerner said daylong cardiac monitoring found that 95% of chronic-fatigue patients he and his research team tested in two separate small studies had abnormal electrocardiograms indicative of heart damage.

    Dr. Lerner said he suspects the heart damage is caused by Epstein-Barr virus and cytomegalovirus, both long implication in the condition. The damage to the heart occurred, he believes, when the viruses were held in partial check by the patient's immune systems. Though the immune systems appear to have kept the viruses from reproducing, Dr. Lerner said partial bits of the viruses that were being produced appear to be causing heart damage.

    Raymond Swarts, an infectious-disease specialist unconnected to Dr. Lerner's group, called the findings "fantastic and very compelling." Dr. Swarts, who practices medicine in Reno, Nev., cautions that more studies are necessary.

    A test for the hard-to-diagnose syndrome would represent a significant clinical advance. Chronic-fatigue syndrome now is diagnosed by a rough checklist of symptoms and a process of elimination. The key clinical finding is that patients have persistent or relapsing fatigue for six months or more.

    In fact, doctors have argued whether the syndrome is a disease at all and even if it is, exactly how prevalent it might be. By some estimates, the syndrome affects about six in every 100,000 people.

    After implicating viruses as the cause of the syndrome, Dr. Lerner tested possible treatments. Many of the patients, including Dr. Lerner who were infected by Epstein-Barr virus regained cardiac function and returned to normal life after taking high doses of valacyclovir (brand name Valtrex), an antiviral drug made by Glaxo Wellcome PLC, for several months. Patients with cytomegalovirus received ganciclovir (Cytovene), another antiviral drug made by Roche Holding AG.

    Dr. Lerner became interested in chronic-fatigue syndrome when he fell ill in 1988 at age 58. He thought at first that he had heart disease, and an examination by doctors confirmed that his heart was weak. Later, he suspected there was more to the picture. In 1996, he began antiviral drug therapy and his heart function returned to normal. The smoking gun in Dr. Lerner's investigation came from patient samples of heart tissue. The viruses had weakened their hearts by scrambling the normally well-ordered muscle fibers. Glaxo Wellcome is funding a trial of antiviral treatments for chronic fatigue syndrome, that just got under way, said Robert Deeter, an antiviral clinical specialist with the drug company. Dr. Lerner holds patents to diagnose chronic-fatigue syndrome with cardiac monitors and to treat the condition with antiviral agents. He has another patent pending for the use of immunological agents to diagnose the condition.
  3. fight4acure

    fight4acure Member

    Indiana Doctor Gives Hope to Fibromyalgia Sufferers
    ImmuneSupport.com

    09-27-2004

    Local Doctor Gives Hope To Fibromyalgia Sufferers
    Reporter: Shannon Samson
    New Media Producer: Kerry Corum

    An Evansville, Indiana physician is going to the American Academy of Pain Management conference in San Antonio Wednesday, to present what could be a breakthrough finding. He suspects the chronic pain of diseases like fibromyalgia could be caused by a series of viruses.

    Anita Held, 64-years-old, needs a basket to hold all the pills she needs to get her through the day. Fibromyalgia leaves her sore all over and constantly tired. She says, "Breathing is an effort, just moving the least little bit is just an effort. So some days I actually will sleep all day long."

    Pain specialist Dr. David Johnson realized the fatigue, aches and chills many of his patients describe are the same symptoms that come with a case of the flu. So he had an idea: What if he tested them for some common viruses? "I went through and listed about three or four viruses, and didn't even know if the labs could test for them, and my gosh, they came back positive."

    He eventually came up with list of 17 viruses and found that his fibromyalgia patients were all testing positive for anywhere from three to nine viruses each. Dr. Johnson believes their immune systems aren't recognizing the viruses as pathogens and as they steal cell material to replicate, the patient is left with a host of ailments. He's prescribing anti-viral medications to try to suppress the viruses, which can take years.

    In the meantime, Johnson says, "I want to get the word out to physicians to test for the virus, use the anti-viral medication and let's all have some input and see if we can eradicate this condition."

    That would be a dream come true for Anita Held, who just found out she has three viruses. "I am glad they found something, because now we have something to work with, is the way I look at it. That's not bad news."

    She says it's good news to think maybe someday she could spend more time with her grandchildren without getting too tired.

    So far, 26 of Dr. Johnson's patients have tested positive for up to nine viruses. He says six are responding well to anti-viral medication.

    Besides fibromyalgia, the treatment is also helping sufferers of chronic fatigue and irritable bowel syndromes.

    Dr. Johnson outlined a list of the viruses he's testing for in fibromyalgia cases:

    *Epstein Barr virus EBV
    *Cytomegalovirus CMV
    *Herpes virus: 8 types
    *Parvovirus B 19
    Norwalk agent
    *Rotavirus
    *Enteric Coronavirus
    *Enterovirus
    Astrovirus
    Calcivirus
    *Varicella - Zoster virus VZV
    Torovirus
    *Adenovirus
    Picovirus
    Pogosta virus
    Sindbis virus
    *Coxsackie A and B virus

    *The most frequently involved virses. Most patients will have from three to nine of these viruses at abnormal levels.

    For more information on Dr. Johnson's research, contact his office in Indiana at 812-425-2662.

    Source: All content © Copyright 2000 - 2004 WorldNow and WFIE. All Rights Reserved. The original article is posted at: http://www.14wfie.com/Global/story.asp?S=2271049&nav=3w6rQvkD
  4. fight4acure

    fight4acure Member

    http://www.neoucom.edu/audience/research/offices_programs/comparative_med/animal_husbandry/guinea_pig
  5. fight4acure

    fight4acure Member

    http://www.bionews.in/wp2pdf/bionews_2006-06-03-346am.pdf#search='parainfluenza%20virus5'
  6. fight4acure

    fight4acure Member

    This site talks about Stat-1 being taken out of our systems due to the virus. This being gone gives us less chance to fight off illness, lowering our immune system.

    http://vir.sgmjournals.org/cgi/content/full/85/10/3007
  7. fight4acure

    fight4acure Member

    http://www.abcnews.go.com/Technology/wireStory?id=2099763

    Stem Cells Help Repair Rats' Paralysis

    By LAURAN NEERGAARD AP Medical Writer

    WASHINGTON Jun 20, 2006 (AP)— Scientists have used stem cells and a soup of nerve-friendly chemicals to not just bridge a damaged spinal cord but actually regrow the circuitry needed to move a muscle, helping partially paralyzed rats walk.

    Years of additional research is needed before such an experiment could be attempted in people.

    But the work marks a tantalizing new step in stem cell research that promises to one day help repair damage from nerve-destroying illnesses such as Lou Gehrig's disease, or from spinal cord injuries.

    "This is an important first step, but it really is a first step, a proof of principle that … you can rewire part of the nervous system," said Dr. Douglas Kerr, a neurologist at Johns Hopkins University who led the work being published Monday in the journal Annals of Neurology.

    Perhaps most importantly, the experiment illustrates that if stem cells eventually live up to their promise, treatment won't be simple they can't just be injected into a diseased body and repair it on their own.

    Instead, the new research details a complex recipe of growth factors and other chemicals that entice the delicate cells to form correctly and make the right connections. Miss a single ingredient, and the cells wander aimlessly, unable to reach the muscle and make it move.

    The study may bring "the appropriate tempering of expectations of stem cells," said Kerr, considered a leader in the field. "Some of my patients say, 'Oh, I'm going to pull into the stem-cell station and get my infusion of stem cells,' and it's never going to be that."

    Stem cells are building blocks that turn into different types of tissue. Embryonic stem cells in particular have made headlines, as scientists attempt to harness them to regenerate damaged organs or other body parts. They're essentially a blank slate, able to turn into any tissue given the right biochemical instructions. But human embryonic stem cell research is politically controversial, because culling the cells destroys embryos.

    The Hopkins experiment isn't the first to use stem cells to help paralyzed rodents move. But previous work bridged damage inside the spinal cord that blocked nerve cells from delivering their "move" messages to muscles, sort of like fixing the circuit that brings electricity to a fan.
  8. fight4acure

    fight4acure Member

    Potential Animal (Zoonotic) Virus Identified in Patients with Chronic Fatigue Syndrome, Multiple Sclerosis and Epilepsy

    5/31/2006 12:00:00 PM


    --------------------------------------------------------------------------------

    To: National Desk

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

    NEEDHAM, Mass., May 31 /U.S. Newswire/ -- 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.

    ------

    Founded in 1997, the National CFIDS Foundation has grown to become the largest, all-volunteer patient organization of its type in the United States. The Foundation has no paid employees and is funded solely by individual donations for the primary purpose to fund medical research into the cause and treatment and/or cure of Chronic Fatigue Immune Dysfunction Syndrome (CFIDS/CFS).

    http://www.usnewswire.com/
  9. fight4acure

    fight4acure Member

    I received this article in the email, from Sherrie from AFFTER (Advocates for Fibromyalgia Funding, Treatment, Education, & Research).

    June 12,2006



    There are two related studies that involve functional MRI of the brain. The first one involves fibromyalgia patients, and the second study is on people with chronic low back pain. The findings were similar. These studies are very important because they validate with an MRI picture of the brain, that people with fibromyalgia are indeed feeling more pain than normal controls. This technology offers hope for the future of fibromyalgia research.




    “The results, which will be presented Oct. 27 at the annual meeting of the American College of Rheumatology in New Orleans, may help lead researchers to important findings on lower back pain, and on enhanced pain perception in general.

    Senior authors Richard Gracely, Ph.D., and Daniel Clauw, M.D., did the study at Georgetown University Medical Center and the National Institutes of Health, but are now continuing the work at the University of Michigan Health System. In May, they and their colleagues published a paper in the journal Arthritis and Rheumatism on pain perception in fibromyalgia patients.”



    See the two articles in their entirety below.


    Fibromyalgia Pain Isn't All In Patients' Heads, New Brain Study Finds

    ANN ARBOR, MI -- A new brain-scan study confirms scientifically what fibromyalgia patients have been telling a skeptical medical community for years: They're really in pain.

    October 28, 2002

    article source:

    http://www.sciencedaily.com/releases/2002/06/020607073056.htm

    Source: University Of Michigan Health System
    Posted: June 7, 2002

    In fact, the study finds, people with fibromyalgia say they feel severe pain, and have measurable pain signals in their brains, from a gentle finger squeeze that barely feels unpleasant to people without the disease. The squeeze's force must be doubled to cause healthy people to feel the same level of pain -- and their pain signals show up in different brain areas.

    The results, published in the current issue of Arthritis & Rheumatism, the journal of the American College of Rheumatology, may offer the proof of fibromyalgia's physical roots that many doubtful physicians have sought. It may also open doors for further research on the still-unknown causes of the disease, which affects more than 2 percent of Americans, mainly women.

    Lead authors Richard Gracely, Ph.D., and Daniel Clauw, M.D., did the study at Georgetown University Medical Center and the National Institutes of Health, but are now continuing the work at the University of Michigan Health System. In an editorial in the same issue, Clauw and U-M rheumatologist Leslie Crofford, M.D., stress the importance of fibromyalgia research and care.

    To correlate subjective pain sensation with objective views of brain signals, the researchers used a super-fast form of MRI brain imaging, called functional MRI or fMRI, on 16 fibromyalgia patients and 16 people without the disease. As a result, they say, the study offers the first objective method for corroborating what fibromyalgia patients report they feel, and what's going on in their brains at the precise moment they feel it. And, it gives researchers a road map of the areas of the brain that are most -- and least -- active when patients feel pain.

    "The fMRI technology gave us a unique opportunity to look at the neurobiology underlying tenderness, which is a hallmark of fibromyalgia," says Clauw. "These results, combined with other work done by our group and others, have convinced us that some pathologic process is making these patients more sensitive. For some reason, still unknown, there's a neurobiological amplification of their pain signals."

    Further results from the study were presented last year at the ACR annual meeting. The project will continue later this year at UMHS, joining other fMRI fibromyalgia research now under way.

    For decades, patients and physicians have built a case that fibromyalgia is a specific, diagnosable chronic disease, characterized by tenderness and stiffness all over the body as well as fatigue, headaches, gastrointestinal problems and depression. Many patients with the disease find it interferes with their work, family and personal life. Statistics show that far more women than men are affected, and that it occurs mostly during the childbearing years.

    The ACR released classification criteria for fibromyalgia in 1990, to help doctors diagnose it and rule out other chronic pain conditions. Clauw and Crofford's editorial looks at the current state of research, and calls for rheumatologists to take the lead in fibromyalgia care and science.

    But many skeptics have debated the very existence of fibromyalgia as a clearly distinct disorder, saying it seemed to be rooted more in psychological and social factors than in physical, biological causes. Their argument has been bolstered by the failure of research to find a clear cause, an effective treatment, or a non-subjective way of assessing patients.

    While the debate has raged, neuroscientists have begun to use brain scan technology to identify the areas of the normal human brain that become most active during pain. A few studies have even assessed the blood flow in those areas in fibromyalgia patients during baseline brain scans. The new study is the first to use both high-speed scanning and a painful stimulus.

    In the study, fibromyalgia patients and healthy control subjects had their brains scanned for more than 10 minutes while a small, piston-controlled device applied precisely calibrated, rapidly pulsing pressure to the base of their left thumbnail. The pressures were varied over time, using painful and non-painful levels that had been set for each patient prior to the scan.

    The study's design gave two opportunities to compare patients and controls: the pressure levels at which the pain rating given by patients and control subjects was the same, and the rating that the two different types of participants gave when the same level of pressure was applied.

    The researchers found that it only took a mild pressure to produce self-reported feelings of pain in the fibromyalgia patients, while the control subjects tolerated the same pressure with little pain.

    "In the patients, that same mild pressure also produced measurable brain responses in areas that process the sensation of pain," says Clauw. "But the same kind of brain responses weren't seen in control subjects until the pressure on their thumb was more than doubled."

    Though brain activity increased in many of the same areas in both patients and control subjects, there were striking differences too. Patients feeling pain from mild pressure had increased activity in 12 areas of their brains, while the control subjects feeling the same pressure had activation in only two areas. When the pressure on the control subjects' thumbs was increased, so did their pain rating and the number of brain areas activated. But only eight of the areas were the same as those in patients' brains.

    In all, the fibromyalgia patients' brains had both some areas that were activated in them but not in controls, and some areas that stayed "quiet" in them but became active in the brains of controls feeling the same level of pain. This response suggests that patients have enhanced response to pain in some brain regions, and a diminished response in others, Clauw says.

    The study was supported in part by the National Fibromyalgia Research Association, the U.S. Army and the NIH. In addition to Clauw and Gracely, the research team included Frank Petzke, M.D.; and Julie M. Wolf, BA. For more information on fibromyalgia research and treatment at UMHS, visit http://www.med.umich.edu/intmed/rheumatology/fmweb

    ----------------------------------------------------

    Brain study of back pain sufferers yields intriguing results

    Article source: http://www.med.umich.edu/opm/newspage/2002/backpain.htm

    Scans show amplified pain signals in patients with back pain of unknown origin

    ANN ARBOR, MI - Patients with lower back pain that can't be traced to a specific physical cause may have abnormal pain-processing pathways in their brains, according to a new study led by University of Michigan researchers.

    The effect, which as yet has no explanation, is similar to an altered pain perception effect in fibromyalgia patients recently reported by the same research team.

    In fact, the study finds, people with lower back pain say they feel severe pain, and have measurable pain signals in their brains, from a gentle finger squeeze that barely feels unpleasant to people without lower back pain. People with fibromyalgia felt about the same pain from a squeeze of the same intensity.

    But the squeeze's force must be increased sharply to cause healthy people to feel the same level of pain - and their pain signals register p in different brain areas.

    The results, which will be presented Oct. 27 at the annual meeting of the American College of Rheumatology in New Orleans, may help lead researchers to important findings on lower back pain, and on enhanced pain perception in general.

    Senior authors Richard Gracely, Ph.D., and Daniel Clauw, M.D., did the study at Georgetown University Medical Center and the National Institutes of Health, but are now continuing the work at the University of Michigan Health System. In May, they and their colleagues published a paper in the journal Arthritis and Rheumatism on pain perception in fibromyalgia patients.

    To correlate subjective pain sensation with objective views of brain signals, the researchers used a super-fast form of MRI brain imaging, called functional MRI or fMRI. They looked at the brains of 15 people with lower back pain whose body scans showed no mechanical cause, such as a ruptured disk, for their pain. They also looked at 15 fibromyalgia patients and 15 normal control subjects.

    As a result, they say, the study offers the first objective method for corroborating what lower back pain patients report they feel, and what's going on in their brains at the precise moment they feel it. And, it continues to give researchers a road map of the areas of the brain that are most - and least - active when patients feel pain. The researchers hope that further study on larger groups of patients will yield more information on altered pain processing.

    "The fMRI technology gave us a unique opportunity to look at the neurobiology underlying tenderness, which is a hallmark of both lower back pain and fibromyalgia," says Clauw. "These results, combined with other work done by our group and others, have convinced us that some pathologic process is making these patients more sensitive. For some reason, still unknown, there's a neurobiological amplification of their pain signals."

    Lower back pain affects nearly all Americans from time to time, especially those who are overweight, sedentary or work in physically demanding jobs. The pain can interfere with life and work; problems stemming from lower back pain are the second most frequent cause of lost work days in adults under the age of 45, ranking below only the common cold.

    Much of the pain may be due to pulled muscles, strained ligaments, damaged joints or small tears in the disks that act as cushions between the bones of the spine - all causes that don't show up well on X-rays but often can be seen on CT or conventional MRI scans. These physical causes often disappear after a few weeks, but many patients have chronic or recurring lower-back pain.

    In the study, the lower-back pain patients were examined by CT scan to rule out mechanical causes of their pain. Then they, the fibromyalgia patients and the healthy control subjects had their brains scanned by fMRI for more than 10 minutes while a small, piston-controlled device applied precisely calibrated, rapidly pulsing pressure to the base of their left thumbnail. The pressures were varied over time, using painful and non-painful levels that had been set for each patient prior to the scan.

    The study's design gave two opportunities to compare patients and controls. The subjective comparison measured the pressure levels at which the pain rating given by back pain patients, fibromyalgia patients and control subjects was the same. The objective comparison looked at the rating that the three types of participants gave when the same level of pressure was applied.

    The researchers found that it only took a mild pressure to produce self-reported feelings of pain in the lower-back pain and fibromyalgia patients, while the control subjects tolerated the same pressure with little pain.

    "In both the back pain patients and the fibromyalgia patients, that same mild pressure also produced measurable brain responses in areas that process the sensation of pain," says Clauw. "But the same kind of brain responses weren't seen in control subjects until the pressure on their thumb increased substantially."

    Though brain activity increased in many of the same areas in both patients and control subjects, there were striking differences, too. All the subjects had increased activity in eight areas of their brains, but lower-back pain patients showed no increased activity in two areas that were active in both fibromyalgia patients and normal control subjects. Meanwhile, fibromyalgia patients showed increased activation in two other areas not active in back pain patients and healthy subjects.

    This response suggests that lower-back pain patients have enhanced response to pain in some brain regions, and a diminished response in others, Clauw says.

    The study was supported in part by the National Fibromyalgia Research Association, the U.S. Army and the NIH. In addition to Clauw and Gracely, the research team included Thorsten Giesecke and Masilo Grant of UMHS, Karen Munoz of NIH, Reshma Kumar of Georgetown, and Alf Nachemson of the University of Gotenberg, Sweden.

    For more information on fibromyalgia research at UMHS, visit www.med.umich.edu/intmed/rheumatology/fmweb.
  10. fight4acure

    fight4acure Member

    1. It is also known as Simian Virus-5 or SV5.

    2. SV5 was first isolated in 1956 from uninoculated rhesus and cynomolgus monkey kidney
    cell cultures.

    3. In 1959, the SA strain was obtained from the nasal washings of a human volunteer with a
    common cold showing acute upper respiratory infection.

    4. In 1959, the DA strain was isolated
    from a specimen obtained from a fatal case of infectious hepatitis.

    5. In 1963, a second DA strain
    isolate was made from monkey kidney cell cultures inoculated with the throat swab of a child
    suffering from respiratory illness.

    6. In 1970, an SV5 related virus was isolated from the brain cell
    cultures which were derived from biopsy specimens of a patient suffering from Creutzfeldt-
    Jacob disease.

    7. It is important to note that rubulaviruses have also been associated with Chiari malformation,
    hydrocephalus, viral myocarditis, and nephritis.

    8. As we mentioned earlier in this article, after conversing with Oxford University scientists, epidemiologic considerations moved to the forefront. The NCF found an excellent and intriguing medical journal article titled "Risk Factors Associated with Chronic Fatigue
    Syndrome in a Cluster of Pediatric Cases." This was written by Dr. David Bell and colleagues who represented the Monroe County Health Department in upstate New York, the University
    of Rochester School of Medicine, as well as Roswell Park Memorial Institute. Here, the authors discussed pediatric CFS cases associated with the Lyndonville outbreak. In this paper the authors stated, "Highly significant positive associations were observed for the presence of other
    family members with symptoms of CFS, ingestion of raw milk either recently or in the past, ingestion of raw eggs, and history of allergies or asthma. Exposure to hot air heating, the presence of cats on the property, and appendicitis also had significant positive associations
    with CFS. The presence of dogs in the house was inversely associated with CFS." As a result of their study, these authors concluded that, "These data suggest that a combination of host and environmental factors, including an infectious agent or agents, are involved in the etiology of
    CFS."

    9. Paramyxoviruses are known to be contagious diseases.

    10. having other family members with CFS symptoms
    is consistent with a paramyxovirus.

    11. Secondly, ingestion of raw milk either recently or in the past as well as ingestion of raw eggs suggests an infectious agent that is passed from a farm animal,
    such as a cow or a chicken, to humans. As we have pointed out and as the medical literature suggests, a zoonotic virus that passes from animals to humans would fit that for a paramyxovirus. Third, the history of allergies or asthma would be consistent with a paramyxovirus (parainfluenza virus) due to the respiratory nature of the infection. In fact, a recent medical article has provided new insight into this very process. In a medical model associated with asthma, chronic bronchitis, and chronic obstructive pulmonary disease, it was found that respiratory paramyxoviruses can cause a "hit and run" phenomenon that is manifested by the development of a permanent airway disease phenotype long after the infection has cleared. Can you imagine what happens when a paramyxovirus infection becomes persistent?

    Fourth, exposure to hot air heating would be consistent with an airborne pathogen. One definition we found for paramyxoviruses was the following. Paramyxoviruses are a group of RNA viruses that are responsible predominantly for acute respiratory diseases and are usually transmitted in an airborne manner.

    Fifth, the presence of various associations with cats and dogs should not come as a surprise. Paramyxoviruses are known to infect numerous animal species so any association with common animals would not be surprising. Given the possible association with cows and chickens makes us wonder if any of these other animals in the Lyndonville study included feral cats, known to live in barns in rural communities.

    Lastly, what about appendicitis? Well, believe it or not, paramyxoviruses have been found to be associated with appendicitis. In the medical literature, there were several articles associating measles with appendicitis. In summary, the NCF is confident that paramyxoviruses provide an attractive epidemiologic fit for CFIDS, especially after examining the data from the cluster of pediatric cases associated with the Lyndonville outbreak.

    (Information gathered from article on website: http://www.ncf-net.org/library/PIV5HostChallenge-0606.htm)
  11. fight4acure

    fight4acure Member

    http://www.arches.uga.edu/~tye/bcmb8010/boynton.pdf#search='history%20of%20Simian%20Virus5'
  12. fight4acure

    fight4acure Member

    Posted by WakeMeUp...

    ImmuneSupport.com Treatment & Research Information

    “Previously Undetected” Virus Implicated In Developmentof Chronic Fatigue Syndrome and other Conditions
    by Editor
    ImmuneSupport.com

    06-27-2006
    Note: This article includes our follow-up suggestions regarding its implications for Chronic Fatigue Syndrome patients.

    Medical science may be just a few research steps away from cracking the secret of Chronic Fatigue Syndrome (CFS), according to news from the National CFIDS Foundation (NCF). Bottom line, states NCF’s Medical Committee: “Parainfluenza Virus-5 plays what the Foundation sees as a predominant and primary role in the development of CFS.”


    This is news that the NCF believes can “change the very nature of this disease.” CFS has been an unexplained ailment, characterized by chronic debilitating fatigue and a combination of flulike symptoms.

    Virus in the Cross-Hairs

    Independent research and detective work funded by the nonprofit NCF has confirmed evidence of a “previously undetected” viral infection in patients with CFS. The research “dovetails” with work by virologists at the private biotechnology research firm Cryptic Afflictions, LLC. It also builds on years of NCF sleuthing for clues in the work of dozens of scientists around the globe, both published and held proprietary.


    The NCF defines the CFS culprit as a strain of the recently named Parainfluenza Virus-5 (PIV-5); formerly called Simian Virus-5, or SV5, owing to its initial isolation in monkey tissue. It is an RNA virus, or “rubulavirus” in the category of viruses known to be associated with diseases such as mumps, encephalitis, and meningitis. And, as an RNA virus, it might be a mutating “chameleon.” At least a dozen strains of mumps virus have been identified, for example.

    It is further defined as a "zoonotic" virus - one that in mutating can be transmitted between animals and people. And, at least as found in an initial CFS patient test performed by NCF-funded researchers, it exactly matches the “SER” strain of PIV-5 virus isolated in diseased swine by German researchers in 1994.

    The Research-Detective Story So Far

    NCF-funded scientists identified a new viral “footprint” in the blood of Chronic Fatigue Syndrome patients, in the form of a deficiency of the Stat-1 protein, which “plays a vital role in immunity.” The researchers then created a “short list” of viruses known to “directly attack and degrade the Stat-1 protein” as part of a viral strategy for evading the host’s immune response. PIV-5 was on that list.

    Meanwhile, they learned that Steven Robbins, MD, a virologist and CEO of Cryptic Afflictions, LLC, had tested blood samples from 56 CFS patients, and cerebrospinal fluid samples from 11 CFS patients, for antibodies specific to an RNA virus he calls “Cryptovirus.” Dr. Robbins found that the vast majority (96 percent) of his CFS blood samples and 91 percent of the CFS spinal fluid samples tested positively for “Cryptovirus-specific” antibodies.

    The NCF also learned that a recent medical journal article suggests Cryptovirus “is most similar to PIV-5” – and that Cryptic Afflictions has “extensive U.S. and international patents pending and owns the intellectual property rights” for Cryptovirus, according to a report from its parent company, Century Pacific Financial Corp.

    Dr. Robbins also found that the Cryptovirus could “cause virtually identical disease in experimentally-infected animals,” according to Century Pacific. Further, he found that “nucleotide sequence data indicate that the virus is pandemic and represents a single virus ‘species’ more akin to measles virus than hypervariable viruses like HIV.”

    In addition to the Cryptovirus’s association with Chronic Fatigue Syndrome, Cryptic Afflictions reports it is also believed implicated in other neurological disorders, including multiple sclerosis and idiopathic (unexplained) epilepsy. For example, the company reports it found Cryptovirus antibodies “in the cerebrospinal fluid and blood of over 90 percent of patients tested with multiple sclerosis.”

    Next Steps for CFS Research?

    At a minimum, Century Pacific says Cryptic Afflictions is now pursuing tests of brain lesions in multiple sclerosis patients, and next plans to ask the FDA for approval of the diagnostic tests. Their testing plans for CFS seem to be unstated.

    The National CFIDS Foundation, meanwhile, reports it is working to get this information out to “medical and health groups that may be interested in further research,” and says it is “interested in funding those researchers who have expertise in the area.”

    The NCF is an all-volunteer patient organization with no paid employees, and is funded solely by individual donations for the primary purpose of funding CFS research.

    To review the NCF press release on this discovery, as well as a highly detailed, sourced report on the National CFIDS Foundation Medical Committee’s detective work, titled “Parainfluenza Virus-5: A new paradigm and a serious host challenge,” visit the Foundation’s site at http://www.ncf-net.org/Discoveries.htm

    What does this mean for you?

    1. Clearly, this and further research that may establish Chronic Fatigue Syndrome as a pathogen-triggered disease would lend medical validity to the condition.


    2. Further, increasing knowledge regarding this virus or viruses may lead to preventive measures such as vaccines and epidemic surveillance, and/or effective treatments.


    3. This news of the dedicated efforts by NCF-funded researchers and others underscores the importance of contributions to CFS research. We at Pro Health are proud to report that as a patient-owned company we have raised and donated more than $2.5 million to CFS and Fibromyalgia research to date, and contribute a portion of all our product sales to this cause.




    ©2006 ProHealth, Inc. Copyright Policy
    By: http://www.ImmuneSupport.com
  13. fight4acure

    fight4acure Member

    Posted by 1sweetie:

    An article from NewScientist.com news service dated June 16, 2006 states that: Chronic Fatigue Syndrome has been given as an official cause of death - apparently for the first time in the world.

    Parts of the article include:

    On Tuesday, coroner Veronica Hamilton-Deeley of Brighton & Hove Coroners Ct, UK, recorded the cause of death of a 32 year old woman as acute aneuric renal failure (failure to produce urine) due to dehydration as a result of CFS. The deceased women, Sophia Mirza, has suffered from CFS for six years.

    The coroner's verdict is a breakthrough for those who argue that CFS is a physical condition, possibly with its roots in the immune system. Dominic O'Donovan, N neuropathologist at Oldchurch Hospital in Romford, UK, who gave evidence at the inquest, said that Sophia's spinal cord showed inflammation caused by dorsal root ganglionitis - a clear physical manifestation of the disease.

    CFS specialist Jonathan Kerr of St. George's, University of London, says he is not surprised that inflammation in the spinal cord has been found in someone with the disease, as it is known to be associated with it. He says that the immune system tends to be over-activated in people with CFS and this may underlie the inflammation of the neurological tissue.

    The article has more information and you may can find it at www. newscientist.com/article/dn9342-first-official-death-from-chronic-fatigue-syndrome-.html. The article was titled First official death from chronic fatigue syndrome and was written by Rowan Hooper.

    (I received this article because I am subscribed to alerts on Google search for articles on Chronic Fatigue Syndrome & Fibromyalgia.)
  14. fight4acure

    fight4acure Member

    Posted by Ulala:

    May 31, 2006

    Parainfluenza Virus-5: A new paradigm and a serious host challenge


    National CFIDS Foundation, Inc.
    Medical Committee

    © 2006
    Written Permission Required for Reprinting or Distributing

    As reported in the latest National CFIDS Foundation's press release, we have learned
    that Parainfluenza Virus-5 plays what the Foundation sees as a predominant and primary role in
    the development of CFS/CFIDS/ME. This is highlighted by both our own preliminary research,
    medical articles and dissertations, and most importantly by the highly advanced research
    completed by Dr. Steven Robbins.

    In this article, we will try to convey several critical factors to our readers. Some data
    will refer to what is known about Parainfluenza Virus-5 (PIV-5). Other data will marry research
    completed in the field of CFIDS with that for PIV-5. Additional notes will be provided to fill
    in the blanks as necessary. In addition, we have chosen to not include supportive evidence for
    either Multiple Sclerosis or Epilepsy in this report.

    Parainfluenza Virus-5 is the new name adopted by virologists for a virus that was
    previously known as Simian Virus-5 or SV5. The parainfluenza virus PIV-5 is a member of
    the paramyxovirus family of negative-strand RNA viruses that has an RNA genome of
    approximately 15,000 nucleotides.

    SV5 was first isolated in 1956 from uninoculated rhesus and cynomolgus monkey kidney
    cell cultures. Very little attention was paid to this virus until the discovery of the hemadsorption
    method in 1957 which greatly facilitated the recognition of myxovirus infection in cell cultures.
    In 1959, the SA strain was obtained from the nasal washings of a human volunteer with a
    common cold showing acute upper respiratory infection. In 1959, the DA strain was isolated
    from a specimen obtained from a fatal case of infectious hepatitis. In 1963, a second DA strain
    isolate was made from monkey kidney cell cultures inoculated with the throat swab of a child
    suffering from respiratory illness. In 1970, an SV5 related virus was isolated from the brain cell
    cultures which were derived from biopsy specimens of a patient suffering from Creutzfeldt-
    Jacob disease.

    Let us digress somewhat. As our conversations with Dr. Robert Possee at Oxford
    University matured in Spring 2003, one important factor came to the surface above everything
    else. Of course by that time Dr.Yoshitsugi Hokama's work was underway. We knew from his
    preliminary results that the ciguatera epitope played an important role in the disease process but
    the exact nature of this needed to be elucidated. Our funding for Dr. Hokama came on the heels
    from our discoveries made through careful examination of Dr. W. John Martin's world patent
    which divulged his use of the ciguatera monoclonal antibody to detect his "stealth virus" in
    CFIDS patient blood. By bringing this work to scientists at Oxford, we found our conversations
    centered around epidemiology more and more! As of late April 2003, we chose to examine two
    paths for obtaining further information that we felt would be most helpful and would add
    clarification to this problem; CFIDS epidemiology and the current research of Dr. DeMeirleir's.
    The first was to examine the work of Dr. DeMeirleir who previously had confirmed the
    aberrations in RNaseL, a key component in the antiviral pathway, which had been based on
    prior work completed by Dr. Robert Suhadolnik at Temple University. The NCF also carefully
    examined Dr. DeMeirleir's book and learned of the Stat-1 protein defect. Most importantly
    however, we found the patent associated with his finding which provided additional explanations
    and information that had been left out of the book!

    Within days of reading the patent, the NCF contacted three major scientists who had
    completed extensive research work in the Stat-1 field. The first two had been mentioned in
    a previous column written for Forum readers. They were Dr. Joan Durbin from Columbus
    Children's Research Institute and Dr. David Levy from New York University School of
    Medicine. Both scientists had been responsible for the development of one of the first animal
    models for Stat-1 deficiencies and both were well published in the field. The other scientist we
    discussed this with was Dr. Curt Horvath, from Northwestern University, who also had
    published extensively in the Stat-1 field. The NCF shared Dr. DeMeirleir's data with each of
    these scientists. Each had commented on how unfortunate it really was that Dr. DeMeirleir
    hadn't published his findings in a peer-review journal. What the NCF had learned some time ago
    applied once more. Peer-review was a touchy subject for those who desired to protect their
    intellectual property rights. Given that Dr. DeMeirleir first found the lack of Stat-1 protein
    in CFIDS patient blood, that it appeared to correlate with RNaseL, and that it underwent
    proteasomal degradation, we asked each of the three researchers if they thought that a virus
    could be directly involved in this activity. Fortunately, we received some excellent feedback.

    During this time, the NCF created a "short list" that included viruses that were known
    to directly attack and degrade the Stat-1 protein as part of their viral evasion strategy. Stat-1
    degradation has been seen as a means for providing interferon antagonism by certain viruses as
    a method to escape the host's immune response. As a direct consequence of this process, one
    specific virus rapidly rose to the top of our list and that was Parainfluenza Virus-5 (PIV-5),
    also previously referred to as Simian Virus-5 (SV5) in the published medical literature.

    By this time the NCF had provided Stat-1 evidence, from various medical journal
    articles, to both Dr. Konnie Knox and to Dr. Donald Carrigan to see if they had an interest in
    pursuing this type of research. They subsequently filed a research application with us that
    received formal approval and research funding via our Research Grant Program. Both scientists
    were off and running as they would soon be exploring the possible role of Stat-1 in CFIDS.

    During this same time period, the NCF had also contacted Dr. Robert Suhadolnik
    directly regarding Dr. DeMeirleir's Stat-1 finding. In fact, Dr. Suhadolnik informed the NCF
    that he was in communication with Dr. DeMeirleir regarding Stat-1 and he inquired as to
    whether the Stat-1 findings were to be published in peer-review. Dr. Suhadolnik would later
    inform the NCF that his group subsequently tested for the Stat-1 protein in CFIDS patient
    samples that had been provided to them by NIH physicians and researchers. These samples were
    found to be deficient in Stat-1 echoing the importance of Stat-1 in CFIDS. Dr. Suhadolnik had
    also commented that Stat-1 acted as a "front-end component" to RNaseL and the antiviral
    pathway. Though Dr. DeMeirleir's finding for Stat-1 was published in his book, a book in which
    Dr. Suhadolnik contributed a written chapter, Dr. Suhadolnik had commented to the NCF that
    he himself had been unaware of the Stat-1 information provided in the book!

    Fortunately, with feedback from Drs. Durbin, Levy, and Horvath, the NCF went on to
    examine everything that was written in the PIV-5 field. Our primary informational sources
    included the National Library of Medicine, both the U.S. and World Patent databases, the CRISP
    database, the U.S. and World Dissertation databases, as well as biological tools such as Genbank
    and BLAST. Of course important books, such as Field's Virology, also made their way onto our
    bookshelf. The NCF had read every possible piece of information that they could get their hands
    on. We felt that ultimately the knowledge gained from this information along with the scientific
    verification or proof that would accompany it would become the driving force for changing the
    very nature of this disease. In other words, the NCF felt that the combination of information and
    scientific proof would become the primary means to an end for providing legitimate answers to
    a disease that had boggled researchers for decades and had destroyed the lives of patients
    worldwide.

    Late in the summer of 2003, we first learned of Dr. Steven Robbins' research in Australia.
    Dr. Robbins was a virologist with the Neurovirology Research Unit of the Sir Albert Sakzewski
    Virus Research Centre associated with the Royal Children's Hospital in Herston, Queensland in
    Australia. The NCF had learned that Dr. Robbins had obtained his Ph.D. from the University
    of Kansas in 1978. His dissertation was titled "Proteins Associated with Measles Virus
    Nucleocapsids in Acute and Chronic Infections." We found this interesting because measles
    and PIV-5 are both viruses from the paramyxovirus family.

    In Australia, Dr. Robbins had used viral isolation techniques to assist in the identification
    of this new virus. The entire virus was then sequenced using PCR techniques and was
    subsequently identified using Genbank. His research highlighted Multiple Sclerosis, Epilepsy,
    and CFIDS. This knowledge came directly from his world patent and from Security and
    Exchange Commission documents filed by the companies involved in this research as well as
    from press release documents that were available from corporate websites. Of significance
    to the NCF was the fact that Dr. Robbins, backed by legal U.S. corporations, had approached
    the FDA for approval for a test that had been developed to identify this pathogen in humans.
    This test would have wide ranging consequences for patients because of its direct association
    with these diseases. Attempts by the NCF to learn of the current status of this test at the FDA
    have failed.

    With the Stat-1 work underway by Drs. Knox and Carrigan, the NCF began to share
    information on PIV-5 with them. As it would turn out, Dr. Carrigan had received his Ph.D.
    from the University of California at San Francisco in 1979. His dissertation was titled
    "Experimental Chronic Myelitis in Hamsters Associated with a Variant of Measles." The NCF
    felt that this was a real plus because Dr. Carrigan also had experience with paramyxoviruses.
    As a consequence, both Dr. Carrigan and Dr. Knox were interested in pursuing this additional
    research. Ultimately, they provided the NCF with a research proposal titled "Potential Role of
    Persistent Paramyxovirus Infection in CFS." The NCF had also provided them with additional
    funding as the result of an addendum that was added on to their original proposal. Their
    scientific research would therefore come to encompass both Stat-1 and PIV-5. Furthermore,
    the NCF would also gain valuable insight into possible interactions between HHV-6 and
    Stat-1. Interestingly, double infections have been demonstrated with PIV-5 and herpes viruses.

    As time progressed, the NCF began to closely examine the nucleotide sequence data
    from Dr. Robbins' research. From what we have been told, an independent company had
    sequenced the entire virus that Dr. Robbins had isolated. One key protein, known as the fusion
    protein, was associated with viral infection of host cells. Though Dr. Robbins had identified
    this viral component of Cryptovirus as a porcine rubulavirus, the NCF wanted to know the
    originating source. In other words, what was the source of the infection? Where did it come
    from? By running this sequence thru BLAST, a tool used to identify nucleotide sequence
    matches in Genbank, an NIH database, the NCF had learned that the fusion protein from the viral
    isolate that Dr. Robbins had identified (Genbank Assession number AX586949) had in-fact
    matched 100% with that for the fusion protein for the SER strain of PIV-5 (Genbank Assession
    number AJ278916). The SER strain had first been discovered in 1994 by three scientists at
    Bayer AG in Germany who had isolated it from swine with PRRS or Porcine Reproductive and
    Respiratory Syndrome. Additional nucleotide sequencing for the SER strain of PIV-5 had been
    completed by Dr. Hans-Dieter Klenk at the Institute for Virology at Phillipps University in
    Marburg, Germany and Dr. Christoph Klenk at the Institute of Pharmacology at the University of
    Wurzburg in Wurzburg, Germany. It is important to note that the SER strain had initially been
    characterized as PIV-2 but was subsequently classified as PIV-5.

    Simply stated, it now appeared that Dr. Robbins' virus that he had isolated from very
    ill patients potentially came from swine! This discovery would make this virus an animal or
    zoonotic virus, a virus that had crossed over from one species (animal) to infect another
    (people)! Interestingly, this would be no different than the current focus on the bird flu in the
    media and the concerns about it infecting people! Likewise, current media attention given to the
    mumps virus, a rubulavirus similar to PIV-5, and its rapid spread in the Midwest was also found
    to be equally worthy of growing public awareness. The NCF pondered, "Should Cryptovirus/
    PIV-5 receive any less airplay?"

    The NCF wondered if this was a plausible explanation? After careful consideration
    our conclusion was "Absolutely!" It made sense to us here at the NCF, along with the many
    scientists who we shared this information with, largely because of the following logic: If you
    can have the swine flu (swine influenza) then you certainly can have swine parainfluenza! These
    types of infections have been involved in epidemics and pandemics throughout history. Hmmm,
    CFS was also previously called the "Yuppie Flu!" Pretty close if you ask us!

    After running these sequences through BLAST, the NCF began to ask additional
    questions. Why would running Dr. Robbins' viral fusion sequence through BLAST generate a
    100% match with that for the fusion sequence for the SER strain BUT when you ran the fusion
    sequence for the SER strain through BLAST, Dr. Robbins' fusion sequence is NOT returned and
    listed as a possible match even though it actually is a 100% match? The NCF has shown this to
    several research people who use this tool daily and they have run these BLAST sequences on
    their own and have questioned this much like us! After all, BLAST acts as a sophisticated
    pattern recognition program that shouldn't depend on the source of the data. So, we naturally
    began to wonder if this could actually somehow represent scientific misconduct or a coverup of
    some type at the national/federal level or is it just some type of error in the BLAST program or
    perhaps an unfriendly user error? At this point we just don't know. Certainly it doesn't make
    any sense because any scientist who would run this sequence through BLAST looking for
    sequence matches would never learn of Dr. Robbins' own sequence discovery. Therefore, should
    our interpretation of this situation be correct, scientists may perhaps never associate this swine
    virus with human disease. We also wondered if this was an isolated sequence that this happened
    to. As it would turn out, it wasn't. The fusion protein filed in Genbank from the original
    scientists at Bayer, as part of their patent, also didn't return a sequence match for that from
    Dr. Robbins' research. This is something that the NCF continues to ponder over.

    Next, the NCF's funded research progressed to where Dr. Konnie Knox made a formal
    presentation at the Seventh International AACFS Conference on Chronic Fatigue Syndrome,
    Fibromyalgia, and other Related Illnesses in October 2004. There, Dr. Knox presented data
    on the "Deficiency in the Expression of Stat-1 Protein in a Subpopulation of Patients with
    CFS."

    With the new year, 2005 would ultimately bring exciting information to the NCF.
    Dr. Knox and Dr. Carrigan had performed numerous tests for the Foundation which included
    antibody as well as PCR specific probes. As stated in our press release, antibody testing
    provided some initial hints however a PCR specific probe picked up the infection in a former
    patient of Dr. David Bell's and Dr. Paul Cheney's. The NCF realized that this longtime CFIDS
    patient had their spleen removed years ago due to hemolytic anemia. This perhaps aided in PCR
    detection due to the fact that cells that circulated in the marrow could reach the periphery due to
    the lack of a spleen. Amazingly, many years prior this very same patient had been labeled by
    Dr. Thomas Evans, then Head of Infectious Diseases at the University of Rochester's School of
    Medicine, as an HIV-negative AIDS patient. This patient had profound immunosuppression
    and it was Dr. Cheney who had identified this patient as one with ICL or idiopathic CD4
    lymphocytopenia. Recent bone marrow biopsies from this patient have served to confirm several
    problems in the bone marrow compartment. PIV-5 has been known to infect bone marrow cells
    according to the medical literature.

    Though Drs. Knox and Carrigan had used PCR for identification of the fusion protein
    for PIV-5 in this patient, the NCF climbed the virology ladder to share this data with Dr. Robert
    Lamb. Dr. Lamb is a Professor of Molecular and Cellular Biology at Northwestern University.
    He is also Professor of Microbiology-Immunology at Northwestern University's Feinberg School
    of Medicine as well as an Investigator at the Howard Hughes Medical Institute. Dr. Lamb is a
    past president of the American Society for Virology and is co-editor of Field's Virology. In
    our communications with Dr. Lamb, he informed us that there were only three scientists who
    had isolated PIV-5 in human blood. These included Dr. Edith Hsiung at Yale University,
    Dr. Richard Randall at the University of St. Andrews in Scotland, and Dr. Steven Robbins. The
    NCF learned from Dr. Lamb that we had unequivocally found the virus in this patient. We were
    very grateful for this feedback. The NCF was then able to track down one of Dr. Hsiung's
    colleagues at Yale University. Dr. Marie Landry, who is Professor of Laboratory Medicine and
    Director of the Virology Laboratory at Yale, encouraged the NCF to stay focused and to remain
    on the trail of PIV-5. Dr. Landry told us that Dr. Hsiung felt very strongly that PIV-5 played an
    important role in human disease. As the NCF's confidence began to grow though, we realized
    certainly that we had much more research to do. We concluded however that Dr. Knox and
    Dr. Carrigan had helped us to reach a new intermediate point in our research by providing what
    the NCF felt was some preliminary evidence that supported Dr. Robbins' discoveries. The NCF
    had also concluded that spinal fluid and bone marrow biopsy samples would greatly assist in the
    detection of this virus.

    Along this part of the journey, the NCF had learned several things. One is that very few
    reagents were available to researchers for PIV-5. This was a field where special monoclonals
    and other reagents had evolved over time and therefore had been developed by those scientists
    who had worked in this field for many years. Typically, these reagents weren't shared with
    researchers outside the field. Next, we learned that fewer than 300 journal articles existed for
    PIV-5 in the National Library of Medicine. That represented "slim pickings" at best. Lastly, the
    NCF was appreciative of what Drs. Knox and Carrigan were trying to do and that was to develop
    their own specific technologies to directly support our research grant. RNA viruses such as this
    one mutate and trying to hit a moving target by developing a research test isn't exactly an easy
    task. It's a high-wire balancing act between specificity and sensitivity, just two hurdles from the
    many technical considerations that had to be made.

    From our information sources, the NCF had also learned that some strains of PIV-5
    appeared to cause an acute but limited illness while other strains caused viral encephalitis and
    neurological disease. The NCF had discovered that some of the encephalitic strains of PIV-5
    could directly infect ependymal cells. Ependymal cells are the cells that line the ventricles of the
    brain as well as the central canal of the spinal cord. Dr. Robbins had determined that the virus
    directly infected B-cells and that these cells acted as a reservoir for the virus. The scientists at
    Bayer concluded that this virus was involved in respiratory and reproductive diseases. This was
    due to the fact that this virus was classified as a parainfluenza virus. Parainfluenza viruses are
    known to adversely affect the respiratory system. Furthermore however, this virus was in the
    genus rubulavirus. Rubulaviruses, such as mumps, are known to adversely affect the
    reproductive system. Several years ago, the NCF had the good fortune of having numerous
    conversations with Dr. John McClaskey, an endocrinologist and pathologist with Rochester
    General Hospital, who had completed his residency at the NIH. Dr. McClaskey told the NCF
    that virtually every male, with longstanding CFS that he had examined at the NIH, suffered from
    hypogonadism and that these men were unable to generate testosterone. This is consistent with
    orchitis and hypogonadism associated with another rubulavirus, mumps. This is proof perhaps
    that the research world does meet up eventually with clinical practice! Of additional interest,
    it is important to note that rubulaviruses have also been associated with Chiari malformation,
    hydrocephalus, viral myocarditis, and nephritis.

    How then could a single virus be involved in diseases such as CFIDS, MS, and epilepsy?
    First of all, these viruses differ by strain variations. For example, HHV-6 has both an A-variant
    as well as a B-variant. Each has their own unique characteristics even though they are part
    of the same virus family. With mumps, a dozen strains have been identified. This is really no
    different than PIV-5 where some strains have been associated with encephalitis while others
    have caused limited illness. Secondly, we suspect that even variations within a disease could
    also occur simply because RNA viruses mutate. With each replication cycle, this virus is
    capable of mutating to subtly change some of its characteristics. These changes will likely
    translate into changes that can then occur in the host. In other words, this virus acts just like a
    "cunning chameleon." Lastly, it may turn out that animal strains of the virus, that are capable of
    infecting people, may have a greater propensity to mutate since they probably did so to jump
    species initially. As you can now appreciate, virology involves very tedious work!

    Let us turn our attention to PIV-5 and discuss some of its unique characteristics. The
    SER strain of PIV-5 is unusual because it exhibits no observable cell fusion activity in several
    cell types. Simply stated, this SER strain fails to induce syncytium formation. Syncytium
    formation means that the uninfected cell and the infected cell fuse together to form a
    multinucleated giant cell. The SER strain lacks this characteristic! Scientists have determined
    that this apparent lack of fusion activity is the result of an alteration to the SER fusion protein.
    Next, PIV-5 directly targets two important components associated with the innate
    immune response. The first target has already been discussed and that is the Stat-1 protein.
    Since Stat-1 is responsible for type I and type II interferon responses (alpha, beta, and gamma)
    within the cell, its role in cellular immunity cannot be understated. Medical science has revealed
    that Stat-1 deficient cells are unresponsive to interferons thus leaving the host defenseless
    against viral and bacterial infections. PIV-5 directly targets and degrades Stat-1 via one of its
    viral proteins known as the V protein. This V protein of PIV-5 acts to block interferon signaling.
    This is an important part of its viral evasion strategy against the host. Because of this strategy,
    the Stat-1 deficiency seen in patients with CFIDS represents an acquired host condition due to
    viral infection by PIV-5. Dr. DeMeirleir had previously identified a correlation between Stat-1
    and RNaseL ratios. RNaseL is an important component of the antiviral pathway. It is worth
    noting that Ampligen is a mismatched double-stranded RNA (dsRNA) based interferon inducer.
    The V protein of PIV-5 has been shown to block intracellular dsRNA signaling thus limiting the
    yield of beta-interferon during infection.

    The second target associated with PIV-5 is IRF-3. IRF-3 is notation for interferon
    regulatory factor-3. The mechanism associated with IRF-3 can best be described as follows.
    When a virus infects a cell, double-stranded RNA (dsRNA) activates the transcription factor
    IRF-3 which then stimulates type I interferon (alpha/beta) gene expression. The V protein
    of PIV-5 acts to block interferon production by blocking IRF-3. The blocking of IRF-3 is
    a strategy employed by another virus, hepatitis C (HCV).

    To summarize, PIV-5 blocks two distinct pathways of the innate immune response
    due to the fact that its V protein blocks both interferon signaling, by causing the degradation
    of Stat-1, and interferon production, by blocking IRF-3 nuclear import. Therefore, PIV-5
    infection acts as an interferon antagonist in the host. It is important to remember that for
    persistent infections to become possible, viral inhibition of host defenses must play a significant
    role in the viral evasion process. We believe that these are the characteristics that potentially
    make PIV-5 a very formidable virus.

    As we mentioned earlier in this article, after conversing with Oxford University
    scientists, epidemiologic considerations moved to the forefront. The NCF found an excellent
    and intriguing medical journal article titled "Risk Factors Associated with Chronic Fatigue
    Syndrome in a Cluster of Pediatric Cases." This was written by Dr. David Bell and colleagues
    who represented the Monroe County Health Department in upstate New York, the University
    of Rochester School of Medicine, as well as Roswell Park Memorial Institute. Here, the authors
    discussed pediatric CFS cases associated with the Lyndonville outbreak. In this paper the
    authors stated, "Highly significant positive associations were observed for the presence of other
    family members with symptoms of CFS, ingestion of raw milk either recently or in the past,
    ingestion of raw eggs, and history of allergies or asthma. Exposure to hot air heating, the
    presence of cats on the property, and appendicitis also had significant positive associations
    with CFS. The presence of dogs in the house was inversely associated with CFS." As a result
    of their study, these authors concluded that, "These data suggest that a combination of host and
    environmental factors, including an infectious agent or agents, are involved in the etiology of
    CFS."

    Let's take a look at each one of these associations that were found to be highly significant
    and provide our interpretation based on what we have learned about paramyxoviruses. First, the
    presence of other family members with symptoms of CFS certainly suggests an infectious agent.
    Paramyxoviruses are known to be contagious diseases. Anyone who has witnessed the spread
    of measles or mumps in children in families can attest to this. These are perhaps the most
    commonly recognized paramyxoviruses. So having other family members with CFS symptoms
    is consistent with a paramyxovirus. Secondly, ingestion of raw milk either recently or in the past
    as well as ingestion of raw eggs suggests an infectious agent that is passed from a farm animal,
    such as a cow or a chicken, to humans. As we have pointed out and as the medical literature
    suggests, a zoonotic virus that passes from animals to humans would fit that for a
    paramyxovirus. Third, the history of allergies or asthma would be consistent with a
    paramyxovirus (parainfluenza virus) due to the respiratory nature of the infection. In fact, a
    recent medical article has provided new insight into this very process. In a medical model
    associated with asthma, chronic bronchitis, and chronic obstructive pulmonary disease, it was
    found that respiratory paramyxoviruses can cause a "hit and run" phenomenon that is manifested
    by the development of a permanent airway disease phenotype long after the infection has
    cleared. Can you imagine what happens when a paramyxovirus infection becomes persistent?
    Fourth, exposure to hot air heating would be consistent with an airborne pathogen. One
    definition we found for paramyxoviruses was the following. Paramyxoviruses are a group of
    RNA viruses that are responsible predominantly for acute respiratory diseases and are usually
    transmitted in an airborne manner. Fifth, the presence of various associations with cats and dogs
    should not come as a surprise. Paramyxoviruses are known to infect numerous animal species so
    any association with common animals would not be surprising. Given the possible association
    with cows and chickens makes us wonder if any of these other animals in the Lyndonville study
    included feral cats, known to live in barns in rural communities. Lastly, what about
    appendicitis? Well, believe it or not, paramyxoviruses have been found to be associated with
    appendicitis. In the medical literature, there were several articles associating measles with
    appendicitis. In summary, the NCF is confident that paramyxoviruses provide an attractive
    epidemiologic fit for CFIDS, especially after examining the data from the cluster of pediatric
    cases associated with the Lyndonville outbreak.

    A prominent feature of CFIDS is a dysregulated immune system. As such, one
    research article that the NCF took particular interest in involved that from Dr. Charles Lapp
    and colleagues. In this study, the researchers chose to examine apoptosis, also known as
    programmed cell death, in the lymphocytes of patients. Also measured was alpha-interferon as
    well as the interferon-induced protein kinase RNA (PKR). The authors concluded that increased
    apoptotic cell population was observed in patients compared to healthy controls. In fact, this
    increased apoptotic subpopulation in patients was accompanied by an abnormal cell arrest in the
    S phase and the G2/M boundary of the cell cycle as compared to the control group and these
    effects were mediated by PKR. The cell cycle or cell division cycle is the cycle of events in a
    eukaryotic cell from one cell division to the next. It consists of interphase, mitosis, and usually
    cell division. As cells proceed through this process, a surveillance system of checkpoints
    monitors the cell for damage and failure to perform critical processes. Checkpoints can block
    progression through the phases of the cell cycle if certain conditions are not met. What the NCF
    found most interesting is that this finding for cell cycle and apoptosis in-vivo in patient blood is
    in agreement with in-vitro research published by Dr. Robert Lamb. The infection of cells by
    viruses can affect the cell division cycle of the host cell to favor viral replication. In Dr. Lamb's
    article, PIV-5 was found to affect cell cycle progression in a manner identical to that described in
    CFIDS patients by Dr. Lapp.

    Thus, Parainfluenza Virus-5 infection produces deleterious effects on the host due to
    the following characteristics. First, PIV-5 compromises immunity due to the virus's ability to
    directly infect B-cells which serve to act as a reservoir for the virus. Secondly, PIV-5 further
    compromises immunity due to interferon antagonism. Third, PIV-5 can induce serious immune
    suppression. Since the virus is capable of infecting bone marrow cells, the bone marrow
    compartment and its corresponding microenvironment is therefore compromised. The ability to
    subsequently generate appropriate cell lineages is adversely affected. Fourth, PIV-5 alters the
    cell cycle to affect apoptosis in infected cells. These various characteristics make for a powerful
    and distinctive combination of viral evasion strategies aimed at avoidance of and alteration to the
    host's immune system.

    At the NCF, we had decided to take things a step further in our understanding of this
    virus so we turned to the medical literature for information about porcine rubulavirus. There
    we learned that swine suffered from interstitial pneumonia and encephalitis; that T-cells late in
    infection do not acquire CD8 phenotype (which probably accounts for the CD8 depletion); that
    in immunosuppressed convalescent swine, viral RNA was found in the brain and lung after
    recovery from acute infection and that the viral genome is active in these pigs; that there are
    alterations in the numbers of T-cells and B-cells in this infection; that boars experimentally
    infected with porcine rubulavirus formed lesions in their reproductive tract with testicular
    atrophy, degeneration of the seminiferous tubules, reduced sperm motility and quality, with
    overall results indicating that porcine rubulavirus caused severe epididymo-orchitis; that
    porcine rubulavirus can establish persistent infections in porcine kidney cells; that porcine
    rubulavirus is an emerging virus responsible for meningoencephalitis, respiratory distress,
    and reproductive alterations in pigs; that porcine rubulavirus causes the induction of apoptosis
    as an important mechanism in the pathogenesis of this infection and that this virus induces
    changes in lymphocyte subpopulations in peripheral blood. To us, this certainly was in
    agreement with our observations for our disease as CFIDS patients.

    Is there any dedicated current research being done on the SER strain of Parainfluenza
    Virus-5? Yes, but it comes with many questions. According to the CRISP database, an NIH
    grant was given to Dr. Richard Compans. Dr. Compans is a Professor and Chair of
    Microbiology and Immunology at Emory University's School of Medicine. Dr. Compans' grant,
    funded by NIAID, began on July 1, 1997. His grant titled "Regulation of Viral Membrane
    Fusion" is funded through January 31, 2009. The NCF found this to be very interesting for
    several reasons. First, Dr. Compans received his grant in 1997. The scientists at Bayer AG in
    Germany hadn't had their research accepted for publication to the Archives of Virology until July
    of 1998. This was one year after Dr. Compans had received funding from NIAID. Therefore,
    the NCF asked, "Where did Dr. Compans get his informational heads-up from because this strain
    had never appeared before in any of the medical literature?" We speculate that perhaps this
    came from either the World or the U.S. patent applications that had been filed during 1994 and
    1995 respectively. Perhaps information came from colleagues at either the NIH or the CDC?
    We just don't know. Secondly, the way the NCF looked at this, a twelve-year grant represented a
    pretty big chunk of change for a virus that hadn't been noticed by the scientific community yet!
    In other words, why would NIAID spend big money to research this virus? What did they
    know? Third, publications by Dr. Compans on this SER strain included colleagues at the CDC.
    So, the NCF came to realize that the NIH knew about this strain via the grant from NIAID. The
    CDC knew about this strain because of the publications from people who assisted Dr. Compans
    in his work. Granted, the NCF hasn't been able to find out the grant amount for this twelve-year
    project, but we're working on it! As a side-note, we also found it interesting that Dr. Compans
    was a co-editor along with Dr. Brian W.J. Mahy for a book titled "Immunobiology and
    Pathogenesis of Persistent Virus Infections" that was published in 1996. Dr. Mahy, as you may
    recall, was the former Director of the Division of Viral and Rickettsial Diseases at the CDC who
    was reassigned due to deceptive accounting practices. Implicated were the misappropriation of
    funds for CFS. Last of all, the NCF wondered about the potential impact regarding the findings
    for the SER strain of Parainfluenza Virus-5 in Porcine Reproductive and Respiratory Syndrome
    (PRRS). PRRS outbreaks have occurred on several continents. According to an article
    published in 2005, "PRRS affected breeding herds and growing-pig populations as measured by
    a decrease in reproductive health, an increase in deaths, and reductions in the rate and efficiency
    of growth....PRRS imposes a substantial financial burden on U.S. swine producers and causes
    approximately $ 560.32 million in losses each year." The NCF now realized that since this SER
    strain had first been identified in swine and apparently now in humans, this puzzle piece would
    carry with it serious ramifications, especially if we were dealing with a pandemic. For all those
    dealing with this disease, this would alter their lives forever often making it a true living hell.


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    16. Hydrocephalus: a fatal late consequence of mumps encephalitis; Gonzalez-Gil J,
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    17. Early ependymal changes in experimental hydrocephalus after mumps virus
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    18. Fatal mumps nephritis and myocarditis; Kabakus N, Aydinoglu H, Yekeler H,
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    19. Viral infection of the myocardium in endocardial fibroelastosis. Molecular
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    20. Abortive versus productive viral infection of dendritic cells with a paramyxovirus
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    21. Potential role of persistent paramyxovirus infection in Chronic Fatigue Syndrome:
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    22. The V proteins of simian virus 5 and other paramyxoviruses inhibit induction of
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    23. Recovery of paramyxovirus simian virus 5 with a V protein lacking the conserved
    cysteine-rich domain: the multifunctional V protein blocks both interferon-beta
    induction and interferon signaling; He B, Paterson RG, Stock N, Durbin JE,
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    303(1):15-32

    24. Conserved cysteine-rich domain of paramyxovirus simian virus 5 V protein plays
    an important role in blocking apoptosis; Sun M, Rothermel TA, Shuman L, Aligo JA,
    Xu S, Lin Y, Lamb RA, He B; J Virol 2004 May;78(10):5068-78

    25. Cell mediated and humoral immune responses to mumps virus: Recent developments;
    Flynn M, Mahon BP; Chapter 6: Immune response to mumps viruses; Recent research
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    26. Induction of interferon synthesis by the PKR-inhibitory VA RNAs of adenoviruses;
    Weber F, Wagner V, Kessler N, Haller O; J Interferon Cytokine Res. 2006 Jan;
    26(1):1-7

    27. Regulation of interferon regulatory factor-3 by the hepatitis C virus serine protease;
    Foy E, Li K, Wang C, Sumpter R Jr, Ikeda M, Lemon SM, Gale M Jr; Science 2003
    May 16;300(5622):1145-8

    28. Acute and chronic airway responses to viral infection: implications for asthma and
    chronic obstructive pulmonary disease; Holtzman MJ, Tyner JW, Kim EY, Lo MS,
    Patel AC, Shornick LP, Agapov E, Zhang Y; Proc Am Thorac Soc. 2005; 2(2):132-40
    29. Measles-related appendicitis; Paik SY, Oh JT, Choi YJ, Kwon KW, Yang WI; Arch
    Pathol Lab Med. 2002 Jan; 126(1):82-4

    30. Measles-associated appendicitis: two case reports and literature review; Pancharoen C,
    Ruttanamongkol P, Suwangool P, Likitnukul S, Thisyakorn U; Scand J Infect Dis. 2001;
    33(8):632-3

    31. Latent in vitro infection of hamster cells by SV5 and herpes virus. Electron microscope
    demonstration of a double viral production; Delain E, Le Francois D, Youn JK, Barski G;
    C R Acad Sci Hebd Seances Acad Sci D. 1969 Aug 18;269(7):805-8

    32. Relationships and host range of human, canine, simian and porcine isolates of simian
    virus 5 (parainfluenza virus 5); Chatziandreou N, Stock N, Young D, Andrejeva J,
    Hagmaier K, McGeoch DJ, Randall RE; J Gen Virol. 2004 Oct;85(Pt 10):3007-16

    33. Elevated apoptotic cell population in patients with chronic fatigue syndrome: the pivotal
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    J Intern Med. 1997 Dec;242(6):465-78

    34. Detection of chronic fatigue syndrome by increased apoptosis and cell cycle arrest of
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    Vojdani A ; Issued: 12/29/98; Filed: 4/17/97

    35. The paramyxovirus simian virus 5 V protein slows progression of the cell cycle; Lin GY,
    Lamb RA; J Virol. 2000 Oct;74(19):9152-66

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    37. Comparative evaluation of the CD4+CD8+ and CD4+CD8- lymphocytes in the immune
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    Montano LF, Zenteno E; Vet Immunol Immunopathol. 2001 May 30;79(3-4):249-59

    38. Porcine rubulavirus LPMV RNA persists in the central nervous system of pigs after
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    McNeilly F, Adair B, Moreno-Lopez J, Berg M; J Neurovirol. 1998 Oct;4(5):545-52

    39. Immunity to porcine rubulavirus infection in adult swine; Hernandez J, Reyes-Leyva J,
    Zenteno R, Ramirez H, Hernandez-Jauregui P, Zenteno E; Vet Immunol Immunopathol.
    1998 Aug 31;64(4):367-81

    40. Lesions in the reproductive tract of boars experimentally infected with porcine
    rubulavirus; Ramirez-Mendoza H, Hernandez-Jauregui P, Reyes-Leyva J, Zenteno E,
    Moreno-Lopez J, Kennedy S; J Comp Pathol. 1997 Oct;117(3):237-52

    41. Establishment and characterisation of a porcine rubulavirus (LPMV) persistent
    infection in porcine kidney cells; Hjertner B, Linne T, Moreno-Lopez J; Acta Vet Scand.
    1997;38(3):213-24

    42. Purification of the Porcine rubulavirus attachment protein by liquid isoelectric focusing;
    Santos-Lopez G, Flores E, Banos R, Herrera-Camacho I, Reyes-Leyva J; Protein Expr
    Purif. 2004 May;35(1):120-5

    43. Apoptosis in lymph nodes and changes in lymphocyte subpopulations in peripheral
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    Jauregui P, Sanchez-Torres L, Favila-Castillo L, Estrada-Parra S, Moreno-Lopez J,
    Kennedy S; J Comp Pathol. 2003 Jan;128(1):1-8

    44. Regulation of Viral Membrane Fusion; Compans RW; Emory University, Department
    of Microbiology and Immunology; Grant # 5R01AI054337-28 funded by the National
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    Project End: 31-Jan-2009

    45. Mutations in the cytoplasmic domain of a paramyxovirus fusion glycoprotein rescue
    syncytium formation and eliminate the hemagglutinin-neuraminidase protein requirement
    for membrane fusion; Seth S, Vincent A, Compans RW; J Virol. 2003 Jan;77(1):167-78

    46. Activation of fusion by the SER virus F protein: a low-pH-dependent paramyxovirus
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    47. Assessment of the economic impact of porcine reproductive and respiratory syndrome
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    2005 Aug 1;227(3):385-92

  15. fight4acure

    fight4acure Member

    http://en.wikipedia.org/wiki/Simian_immunodeficiency_virus
  16. fight4acure

    fight4acure Member

    Posted by Ulala:

    Molecular Structure Of Viral Protein, Parainfluenza Virus 5 Fusion (F) Protein, Identified By Scientists At Northwestern University


    Main Category: Biology / Biochemistry News
    Article Date: 06 Jan 2006 - 0:00am (PDT)This Article
    Also Appears In
    Flu / SARS




    Scientists at Northwestern University have determined the molecular structure of a viral protein, the parainfluenza virus 5 fusion (F) protein.

    The parainfluenza virus 5 is part of a family of viruses (paramyxoviruses) that causes everything from pneumonia, croup and bronchiolitis to cold-like illness and is responsible for many hospitalizations and deaths each year. The results will be published Jan. 5 by the journal Nature.

    Details of the protein's structure in its metastable state -- the state of the protein on the virus surface responsible for infecting cells -- has significant implications for developing improved protein-based vaccines, designing novel anti-viral agents and understanding the entry mechanisms of other viruses.

    Knowing the structure of the F protein will aid understanding of all members of the paramyxovirus family, which are among the most significant human and animal pathogens, causing both respiratory and systemic disease.

    "The development of antiviral drugs is helped by knowledge of the structure, shape and mechanism of the target molecules, which is what we can now provide for the F protein," said Theodore S. Jardetzky, professor of biochemistry, molecular biology and cell biology, who co-led the study. "Knowing how the virus gets into the cell will allow us to better inhibit this key part of the viral life cycle."

    Tens of thousands of different proteins are at work in the human body, each folded into a very specific shape to do its job properly.

    Most proteins have just one shape for their lifetimes, but a handful -- in particular, proteins associated with enveloped viruses such as HIV, influenza virus and the paramyxoviruses -- have two dramatically different shapes, one before the virus attacks and enters a cell and one after.

    The parainfluenza virus 5 fusion protein is one of these. It is the change of the fusion protein from the initial metastable state to the post-virus entry state that drives the fusion of viral and cellular membranes, permitting entry of the viral genome into the cell.

    "What we've learned about the structure of the parainfluenza virus 5 fusion protein will be directly applicable to the whole family of paramyxoviruses," said virologist Robert A. Lamb, John Evans Professor of Biochemistry, Molecular Biology and Cell Biology and co-leader of the study. "The family includes viruses that cause measles, mumps, bronchitis, pneumonia, canine distemper, croup and Newcastle disease, which kills chickens.

    Measles still causes huge numbers of deaths worldwide. And while HIV, influenza and SARS are not in the same family, the viruses do share a mechanism similar to that used by paramyxoviruses for entering the host cell."

    The parainfluenza virus 5 is also closely related to two recently discovered and deadly viruses called Hendra and Nipah viruses, which are classified as select agents of concern for biodefense.

    The pre-fusion structure of the F protein combined with the structure of the protein in its post-fusion state, which was determined and reported earlier in 2005 by this same research team, gives scientists a complete picture of how the paramyxovirus F protein works to infect the cell.

    The F protein belongs to a group of fusion proteins (class I) that exist in two states: the metastable or pre-fusion state and the post-fusion state.

    This is only the second time that both the pre- and post-fusion structures have been determined for a class I viral fusion protein. The first was for the influenza virus, completed in 1994.

    While a lot of research is currently being conducted on the HIV fusion protein, its two structures -- and an understanding of how the protein works -- remain incomplete.

    "The protein we studied," explained Lamb, an Investigator for the Howard Hughes Medical Institute, "is sequestered on the virus and is responsible for bringing about a membrane merger or fusion of the viral and cellular membranes.

    The protein opens the inside of the virus to the inside of the cell, delivering the viruses genetic information into the cytoplasm of the cell to infect it."

    In the process the protein moves from its first folded state, the metastable state (pre-fusion), to its second, final and very stable state (post-fusion), undergoing a dramatic change of shape. "The protein in its metastable state has a very specific job to do -- to enable infection of the cell -- and it does this by essentially acting as a harpoon that shoots into the cell's membrane to bring about the fusion," said Jardetzky.

    "The metastable protein is a one-time-use machine," said Lamb. "It does its work and then it's finished, spent. And you want the protein to be triggered at the right time and in the right place for fusion: when the virus binds to the cell's surface."

    The research team determined the pre-fusion structure by imaging crystals of the protein, using the extremely brilliant X-rays produced by the Advanced Photon Source (APS) synchrotron at Argonne National Laboratory in Illinois and at the Howard Hughes Medical Institute beamlines at the Advanced Light Source in Berkeley, Calif.

    First the researchers had to make the protein, which included pulling a scientific trick on the protein to get it to fold properly and keep it in its metastable state.

    Because the molecules of the protein are so small they could not be imaged directly. Instead, the researchers used many of these molecules to create a crystal that could be imaged.

    Using the method of X-ray diffraction, they bombarded the crystal with X-rays, which bounced off the atoms within the crystal.

    By collecting and analyzing this information, Jardetzky, Lamb and their colleagues determined the location of each atom within the structure.

    Jardetzky credits the very high intensity X-rays for enabling the researchers to image the structure at 2.85 angstroms. (An angstrom is one ten-billionth of a meter, or about one-hundred-millionth of an inch.)

    This resolution was critical for an accurate picture of how the 10,805 atoms in the structure are assembled. In addition to Jardetzky and Lamb, other authors on the paper are postdoctoral fellow Hsien-Sheng Yin (first author) of the Howard Hughes Medical Institute and Northwestern, and research associate Xiaolin Wen and research assistant professor Reay G. Paterson, from Northwestern.

    Megan Fellman
    fellman@northwestern.edu
    Northwestern University
    www.northwestern.edu
  17. fight4acure

    fight4acure Member

    CFS and Neurology – An overview of recent research
    by Roberto Patarca-Montero, M.D., Ph.D.
    ImmuneSupport.com

    12-12-2000

    Summary: Although the following article is quite technical, it presents an overview of the latest studies into the neurological patterns and processes of CFS patients. The research discussed here suggests that cognitive difficulties in CFS are not related to mood or psychology. Studies also reveal that cognitive impairment is worse after strenuous exercise.
    The main theory investigated is that damage to an area of the upper brain called the reticular activating system (RAS) could lead to CFS. Sleep states and lethargy were two symptoms discovered to be related to the functioning of the RAS. Other tests with MRIs have also revealed reduced blood flow to the latter regions of the brain. Scientists are targeting their research to investigate where precisely these regions are, and exactly how they relate to CFS.
    Report: There is a relation in CFS between cognitive impairment and functional disability, which cannot be explained entirely on the basis of psychiatric factors. The most consistently documented neuropsychological impairments in CFS are in the areas of complex information processing speed and efficiency.
    Although the neuropathological processes underlying cognitive dysfunction in CFS are not yet known, preliminary evidence suggests the involvement of cerebral white matter and independence from mood disturbances. An organic brain dysfunction within a defined neural substrate in CFS patients is suggested by the observation of an impaired acquisition of the eyeblink response and normal sensitivity and responsivity to acoustic stimuli.
    After physically demanding exercise, CFS subjects demonstrate impaired cognitive processing (as assessed by the Symbol Digit Modalities Test, Stroop Word Test and Stroop Color Test) compared with healthy individuals. CFS patients also show specific sensitivity to the effects of exertion at the level of effortful cognitive functioning (focused and sustained attention), which may indicate reduced working memory capacity, or greater demand to monitor cognitive processes, or both.
    Many observations suggest that CFS could derive from residual damage to the reticular activating system (RAS) of the upper brain stem and/or to its cortical projections. It should be pointed out that although the larger right greater than left asymmetry in regional cerebral blood flow is found at the parietotempotal level in CFS patients as compared to healthy controls, no significant correlations are found between frontal tracer uptake and right-left parietotemporal asymmetry, on the one hand, and clinically relevant CFS dimensions on the other. Damage to the RAS could be produced by a previous viral infection, leaving functional defects unaccompanied by any gross histological changes.
    In animal experiments, activation of the RAS can change sleep state and activate or stimulate cortical functions. RAS lesions can produce somnolence and apathy. Studies by modern imaging techniques have not been entirely consistent, but generally many magnetic resonance imaging studies suggest that small discrete patchy brain stem and subcortical lesions can often be seen in CFS.
    Regional blood flow studies by single photon-emission computerized tomography have been more consistent. They have revealed blood flow reductions in many regions, especially in the hind brain. Similar lesions have been reported after poliomyelitis and in multiple sclerosis and in both conditions chronic fatigue is characteristically present. In the well-known post-polio fatigue syndrome, lesions predominate in the RAS of the brain stem. If similar underlying lesions in the RAS can eventually be identified in CFS, the therapeutic target for CFS would be better defined than it is at present.
    In this respect, fluorine-deoxyglucose positron emission tomography showed specific metabolism abnormalities in CFS patients (hypometabolism in right mediofrontal cortex and brainstem) as compared with both healthy controls and depressed patients. The most relevant abnormality is brain stem hypometabolism, which has been also reported in single-photon emission computed tomography studies and seems to be a marker for the in vivo diagnosis of CFS.
    Editor’s Note: This article originally appeared in the journal Phytotherapy of Chronic Fatigue Syndrome and appears with the permission of the Haworth Press.
  18. fight4acure

    fight4acure Member

    Recent Fibromyalgia Findings ImmuneSupport.com

    03-10-2006

    Source: The Science & Research of CFS, The CFIDS Chronicle Special Issue, 2005-2006. Just released, this issue is generating huge buzz in the CFS community. Copies are available through the CFIDS Association’s website at www.cfids.org for $12 each. Visit http://www.cfids.org/special/default.asp to browse a complete listing of articles, including links to several online samples. Source: Special Issue: The Science & Research of CFS, The CFIDS Chronicle, 2005-2006 Issue. A publication of the CFIDS Association of America.
    Although there are some immunological aberrations in FM, including a decreased number of natural killer cells, most researchers now believe that the illness is not an immune system disorder. “Essentially, there is nothing specifically immunological in fibromyalgia – and if there is, whatever little there is, I think it is secondary to the central nervous system problem that fibromyalgia patients have,” says Dr. Muhammad Yunas. “It’s a chronic, neurologic disease.”

    Numerous research studies have found biologic abnormalities in FM patients, and it’s increasingly uncommon to hear physicians suggest the illness is all in your head. “There was a time when we thought fibromyalgia was psychosomatic. We now understand the pain in fibromyalgia is caused by an abnormality in the central nervous system in which pain sensations are amplified,” explains Dr. Robert Bennett, an FM expert at Oregon Health Sciences University.

    This “central sensitization theory” is described in detail in the August 2005 issue of the Journal of Rheumatology. Basically, the theory is that fibromyalgia results from miscommunication among nerve impulses in the central nervous system – the brain and spinal cord – causing FM patients to feel intense pain when they should only feel mild discomfort or fatigue.

    Recent investigations found multiple triggers for this amped-up response to pain. For instance, FM patients have three to four times higher levels than normal of substance P, a central nervous system neurotransmitter involved in pain processing. Researchers also found lower levels of substances that diminish pain sensation, such as serotonin, norepinephrine and dopamine.

    Dr. Daniel Clauw, the director of the Center for the Advancement of Clinical Research at the University of Michigan, says, “The pain of fibromyalgia is not occurring because of some injury or inflammation of the muscles or joints. There is something wrong with the way the central nervous system is processing pain from the peripheral tissues. It’s overamplifying the pain.”

    Pharmaceutical companies are now interested in developing drug treatments base on the new research.

    Reprinted with kind permission of the CFIDS Association of America, that nation's largest non-profit organization dedicated to Chronic Fatigue Syndrome. Online at www.cfids.org.

  19. fight4acure

    fight4acure Member

    Thanks hanginin and ouch! :)

    We all basically created this list, but I was having too much brain fog to keep track of it all, so instead I decided to make an easy list we can all add on research articles in regards to chronic pain and our illnesses.

    :) Hugs!
  20. karinaxx

    karinaxx New Member

    i think this is a great idea.
    there is so much out there, but i first have to find it again, on my laptop, on the net, it will take me some time to dig it out again.
    and i am feeling so lousy in the moment.
    keep it up
    karina