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    You are here : Home » MS Research News » New Discoveries » Potential Viral Causes of MS

    Potential Viral Causes of MS

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    New research to look for viral cause of Primary Progressive MS

    MS MRIA team of investigators from the University of Utah has received a two-year, $275,000 grant from the National Institutes of Health (NIH) to fund novel research that may help to uncover a viral cause for the most acute and severe form of multiple sclerosis.

    These studies will use an advanced technology called deep sequencing to analyze brain tissue from patients who died of primary progressive multiple sclerosis.

    Multiple sclerosis (MS), which affects an estimated 2.5Million people world-wide and 400,000 people in the United States, is an autoimmune disease that leads to nerve damage in the brain and spinal cord. This damage is caused by inflammation that occurs when the body's own immune system attacks the myelin sheath, a fatty protective covering that surrounds nerve cells. Loss of myelin affects the ability of nerve cells in the brain and spinal cord to conduct the electrical signals needed for them to communicate with each other. To date, it is not known what prompts the damaging inflammation, but many investigators believe there is an environmental trigger, possibly a viral or other infection.

    "Our preliminary data has already led to identification of a virus in the brain of one patient who died of primary progressive MS," says John D. Kriesel, M.D., research associate professor in the Division of Infectious Diseases at the University of Utah School of Medicine. "Using a technology called deep sequencing, we will now be studying brain tissue from a group of primary progressive MS patients, with the hope of isolating one or more viruses that might prove to be the cause of this severe type of MS."

    Deep sequencing, otherwise known as high-throughput sequencing, is a technology that allows scientists to sequence very large amounts of DNA more quickly and at a lower cost than traditional sequencing methods. Kriesel and his colleagues will utilize deep sequencing to study the brain tissue of 15 patients who died of primary progressive MS and compare it to brain tissue from a population of controls, including normal patients and people with other neurologic diseases.

    The sequencing data generated will then be analyzed for viral genetic material in order to identify viruses that are unique to the brain tissue of people with primary progressive MS.

    MS is classified into four types, which differ in symptom intensity and rate of disease progression. While treatment has been effective for some forms of MS, the standard medications for MS have not been shown to slow the progression of neurologic decline in people with primary progressive multiple sclerosis (PPMS). Identifying viruses that might play a role in the development of PPMS could eventually lead to the development of screening tests, prevention, or anti-viral treatments for the disease.

    "Currently, there is no approved or highly effective treatment for PPMS," says Kriesel. "The goal of our research is to define a cause for PPMS, so that future investigation can be directed at developing medicines that can slow or stop the progression of this devastating neurologic disease."

    Kriesel's collaborators include Brad Cairns, Ph.D., Jon & Karen Huntsman Presidential Professor in Cancer Research and professor in the University of Utah Department of Oncological Sciences, and Kael Fischer, Ph.D., research associate professor in the University of Utah Department of Pathology and scientific director of the Pathogen Microarray laboratory at ARUP Laboratories.

    Source: Eureka Alert! (13/10/11)

    Nose is gateway for virus tied to brain disorders

    HHV-6The nose apparently can be a portal for a cousin of the herpes virus that is linked to brain disorders, scientists have discovered.

    These findings reveal a new way the brain can get infected.

    Scientists investigated human herpes virus-6 (HHV-6), a member of the family of viruses that includes genital herpes as well as oral herpes, which causes cold sores. HHV-6 is linked with brain disorders such as multiple sclerosis, encephalitis and a form of epilepsy, and causes roseola, a disease common among infants that leads to a high fever and skin rash.

    "This is a virus that we've all been exposed to, that we all pretty much acquired in childhood," said researcher Steven Jacobson, a neurovirologist at the National Institute of Neurological Disorders and Stroke in Bethesda, Md. "Most of the time it's utterly benign."

    The way this virus entered the brain had remained a mystery, as the seat of our intelligence is largely protected by the so-called blood-brain barrier, which filters out many germs and drugs.

    However, researchers had known that other viruses, such as influenza and rabies, apparently could use the sensory network hooked up to the nose as a kind of highway into the central nervous system.

    To see how HHV-6 enters the brain, scientists analyzed tissue samples from autopsies, including a patient who had multiple sclerosis. Although viral DNA was seen throughout the brain, it was found largely in the olfactory bulb, the brain region involved in detecting odors.

    In addition, the researchers found DNA from HHV-6 in nasal mucus samples from healthy people, those suffering a loss of smell, and people with multiple sclerosis. This suggests the nasal cavity might harbor the virus in both healthy and diseased individuals.

    Moreover, in experiments, scientists demonstrated that HHV-6 could infect lab-grown versions of the olfactory ensheathing cells, which help olfactory neurons grow and establish connections in the brain. The researchers believe the virus might use these cells as a bridge across the blood-brain barrier, the first time scientists had evidence these cells could be a route of infection.

    "Now researchers can start looking to see if other viruses might use this route as well," Jacobson told LiveScience.

    Jacobson cautioned that while this virus might help trigger brain disorders, it was not necessarily the primary cause. "We may all have it, but some might have a special genetic susceptibility to it, or maybe there's an environmental trigger that causes neurologic disease to then occur," Jacobson said.

    Further studies could also investigate whether this virus has any effect on behavior. "It all depends on where this virus goes in the brain," Jacobson said. With the new information, researchers could then look for therapies against this virus.

    The scientists detailed their findings Monday in the Proceedings of the National Academy of Sciences.

    Source: ©2011 FOX News Network (10/08/11)

    Monkey MS suggests human disease may be caused by a virus

    Viral MS?In 1986, an unknown disease began killing monkeys at the Oregon National Primate Research Center in Hillsboro. Affected animals developed an unsteady gait and a rapidly advancing paralysis of the limbs. Caregivers could do nothing to stop the disease and euthanized most of the helpless animals within a week of symptom onset.

    The disease, researchers now report, is the monkey equivalent of multiple sclerosis. And it appears to be caused by a virus – adding support to the possibility that multiple sclerosis in humans can be triggered by a viral infection. Experts say the discovery could help expedite the search for more effective treatments.

    "That's the ultimate goal," said co-author Scott Wong, a scientist at the primate center and Oregon Health & Science University's Vaccine and Gene Therapy Institute.

    Since the first case appeared at the primate center, 56 monkeys in the Japanese macaque colony have fallen ill with the neurological disease. In most years, no more than four cases appear in the population of more than 300 monkeys. In a few cases, the monkeys recovered and lived normally for many months before relapsing -- a course often seen in people with multiple sclerosis, or MS.

    Wong and colleagues studied brain and spinal cord samples from nearly all of the monkeys after death. Microscopic examination revealed damage very similar to that in MS patients, including nerve fibers stripped of their protective sheath. Brain scans performed on eight living monkeys showed scattered patches of dead and damaged nerve cells also similar to those seen in people with MS.

    The researchers isolated a previously unknown virus from a sample of damaged spinal nerve tissue taken from one animal. DNA analysis showed that the virus belongs to the herpes family of viruses. Wong's team developed a sensitive test for the virus and used it to screen samples from healthy and diseased monkeys. So far, they have detected the virus in samples of damaged nerve tissue from six monkeys that died from the disorder. The virus has not showed up in healthy samples.

    "Whether or not a similar virus might actually cause MS, that's the big issue," said Dr. Dennis Bourdette, a co-author of the study and director of OHSU's multiple sclerosis center.

    Scientists have spent decades trying to find out whether viruses play a role in triggering multiple sclerosis. So far, the evidence for a viral cause has fallen short. Still, many researchers suspect that a viral infection could be one of the factors that drive the immune system to mount a misdirected attack on the protective sheath around nerve fibers.

    Using the sensitive tests developed by Wong, Bourdette said his team is preparing to screen samples from people with MS to look for human-adapted viruses related to the monkey virus. He said the search shouldn't take longer than 18 months. If such a virus exists -- and it proves to be a triggering factor in multiple sclerosis -- Bourdette said researchers could begin developing a preventive vaccine. The National Institutes of Health funded the research.

    Dr. Kenneth L. Tyler, a professor neurology at the University of Colorado Denver who was not involved with the research, said much work remains to establish the role of viruses in multiple sclerosis.

    "It is feasible that something similar in humans is occurring, although this study does not prove it," Tyler said. He noted that the researchers have yet to present definitive evidence that the monkey virus is the cause of the MS-like disease. For instance, he said, researchers must show that exposing healthy monkeys to the virus will reliably produce the disease.

    But even if the viral connection doesn't pan out, Tyler said the discovery of the MS-like disease in Japanese macaques is significant because it gives researchers a better animal model for testing treatments because it is a naturally occurring disease – not a condition contrived by laboratory manipulation.

    "This is a very exciting and interesting animal model," Tyler said.

    Source: © 2011 Oregon Live LLC (29/06/11)

    Ancient Retrovirus May Contribute to Multiple Sclerosis
    Smoldering Infections of Two Common Viruses EBV and HHV-6 Cause Inherited Retrovirus Genes to Activate.

    Brigitte Huber, PhD, of the Tufts University School of Medicine, presented evidence at a medical conference that suggested that a reactivated ancient retrovirus embedded in the human genome may be active in chronic fatigue syndrome (CFS) and multiple sclerosis (MS) patients. Danish scientists at the same conference suggested that the activation of this retrovirus, dormant in healthy individuals, could be the reason why autoimmune conditions worsen with viral infections.

    Chronic Fatigue Syndrome and Multiple Sclerosis Patients at Increased Risk From the Effects of HERV-K18 Activation

    "Patients with profoundly fatiguing diseases such as MS and CFS may be particularly susceptible to HERV-K18 activation," said Dr. Huber. The announcement was made at the International Symposium on Viruses in CFS and Post-Viral Fatigue, a satellite conference of the 6th International Conference on HHV-6 & 7. Using an SNP-based genotyping method, Dr. Huber found that both MS and CFS patients (whose illness had been triggered by infectious mononucleosis) were at a higher relative risk for containing HERV-K18 variants known to induce superantigen activity. Superantigens are proteins that are able to induce a strong undifferentiated T-cell response believed to deplete the immune system over time.

    Viral activity and/or immune activation has been shown to trigger HERV-K18 activity. Both Epstein-Barr virus infection (infectious mononucleosis) and interferon-alpha administration are associated with HERV-K18 activity. "HHV-6 activates HERV-K18 as well," said Danish investigator Per Hollsberg, MD and professor from the University of Aarhus In Denmark. His PhD student Vanda Lauridsen Turcanova presented this data at the same conference. "Furthermore, this retrovirus activation may have important consequences for autoimmunity," he added.

    HERV-K18 activation may be the endpoint of an HHV6/EBV interferon pathway operating in both MS and CFS. HHV-6 is being investigated as a co-factor in both diseases. Other retroviruses, HERV-H and HERV-W, have been implicated in MS by other researchers. Over 75% of MS patients meet the criteria for CFS. Fatigue is often the most disabling symptom for MS patients. The two diseases also share characteristics such as grey matter atrophy, impaired cerebral glucose metabolism, autonomic nervous system activity and altered patterns of brain activity.

    Dr. Huber's study suggests that endogenous retroviral activation in CFS and MS could produce some of the symptoms associated with both diseases. She has received a National Institutes of Health (NIH) grant to study these issues. Per Hollsberg has done extensive research on the role of EBV and HHV-6 in multiple sclerosis.

    The HHV-6 Foundation

    The HHV-6 Foundation encourages scientific exchanges and provides grants to researchers seeking to increase our understanding of HHV-6 infection in a wide array of central nervous system disorders. Daram Ablashi, the co-discoverer of the HHV-6 virus, is the Foundation's Scientific Director.

    Source: The HHV-6 Foundation (23/06/08)

    A specific viral cause of multiple sclerosis: one virus, one disease?

    "Multiple sclerosis is an autoimmune disease," is heard so often that it is widely accepted as fact by the current generation of students and physicians.

    Yet, although it is undisputed that multiple sclerosis (MS) is immune mediated, an autoimmune mechanism remains unproven. Immune-mediated tissue damage can also result from viral infections in which the host immune response is directed to viral rather than self proteins, or as a consequence of nonspecific or bystander immune responses that change the local cytokine environment.

    Increasing evidence suggests that poorly controlled host immune responses account for much of the tissue damage in chronic infections, and it has been postulated that a similar mechanism may underlie many chronic diseases with features suggestive of an infectious causative factor, including MS. A recent study suggesting that oligodendrocyte death accompanied by microglial activation is the primary event in new MS lesion formation, rather than lymphocyte infiltration, could change the current mindset almost exclusively focused on autoimmunity.

    This review presents the rationale for considering MS a single disease caused by one virus, as well as the anticipated pattern of a persistent central nervous system infection, the application of Koch's postulates to viral discovery in MS as the causative agent, and tissue culture-independent genotypic approaches to viral discovery in MS.

    Lipton HL, Liang Z, Hertzler S, Son KN. Department of Neurology, University of Illinois at Chicago, Chicago, IL 60612-7344, USA

    Source: Pubmed PMID: 17455291 (05/09/07)

    Cincinnati team focuses on infection as MS cause
    Research under way at the University of Cincinnati could one day help short-circuit the most disabling forms of multiple sclerosis.

    Istvan Pirko, a neurologist and researcher in UC's Waddell Center for Multiple Sclerosis, is leading a team of researchers studying the role certain cells in the body's immune system play in the development of multiple sclerosis.

    In the disease, the immune system seems to attack myelin, a fatty substance that insulates the nerves. As the insulation is worn away, various symptoms begin, including loss of vision, balance and coordination and muscle weakness and  fatigue.

    The exact cause of multiple sclerosis is unknown, but some experts believe exposure to environmental toxins or a viral infection might trigger the attack.

    Pirko's research focuses on the infection theory. He and his team inject mice with viruses to re-create the symptoms of multiple sclerosis, including tell-tale lesions on the brain.

    Among the team's projects:

    Creating, for the first time, bleeding brain lesions in mice that mimic the effects of human paediatric multiple sclerosis.

    With the project, researchers have identified viral proteins and genes that might be responsible for triggering the response of certain "killer" immune cells that attack the nervous system.

    The project has also helped researchers map the development of the bleeding lesions. Pirko hopes the project could result in new drugs or other therapies to stop or slow formation of the lesions.

    Tracking brain shrinkage and spinal cord atrophy caused by multiple sclerosis with a series of MRI scans.

    Pirko said the scans document for the first time that the shrinkage and atrophy, long suspected, actually happen.

    The images show what specific structures in the nervous system are targeted. Now, researchers hope to find out whether the damage is caused by the myelin loss or the death of nerve cells, and what drugs or other therapies might stop the process.

    Creating very severe brain lesions in mice that are comparable to "black hole" formations found in the brains of humans with severely disabling forms of multiple sclerosis.

    "We don't always see these in patients, but we know when we do that the patients are going to be in more trouble," Pirko said.

    Researchers believe the lesions are caused by immune cells "just eating holes" in brain tissue, he said, and hope to learn how that process occurs and how to stop it.

    Source: The Enquirer Copyright © 1995-2007 (12/03/07)

    Study tests whether virus triggers MS
    The common cold — inconvenient and annoying but generally considered benign — may cause attacks of multiple sclerosis. And it may provide a clue about what causes MS in the first place.

    That's the premise of a study being launched at the University of Utah School of Medicine, which is seeking help from local MS patients. Several thousand Utahns are estimated to have the disease.

    Researchers have previously noticed that while MS patients may be less likely than other people to get a cold in the first place, a worsening of MS symptoms is three to four times more likely when they do catch a cold. Multiple sclerosis typically waxes and wanes in patients with the "relapsing-remitting" form of the disease, which accounts for 80 percent of all MS cases.

    It's possible that a cold virus is also the "inciting agent" for the initial development of MS, says Dr. John D. Kriesel, the study's principal investigator and an assistant professor of internal medicine and infectious diseases. The cause of the debilitating disease, which damages the brain and spinal cord, has long been a mystery.

    The goal of the study, which will be conducted by the U., Salt Lake City Veterans Administration Hospital, ARUP Laboratories and the University of Arizona, is to identify which specific viruses, if any, might be triggering an MS attack. These viruses could then be targeted by vaccines or treated with anti-viral drugs. Participants, each with active colds that have lasted no more than a day or two, will provide samples of blood and nasal mucous, and undergo a neurological examination. One or more additional visits will be required over a subsequent five-week period.

    The possible link between colds and MS was first discovered in 1985 by University of Arizona neurology professor William Sibley, who will be a co-investigator in the current study. The new study will use sophisticated molecular-biology techniques to parse out which particular cold viruses might be to blame, Kriesel says.

    Previous research pointing to a virus as the trigger for the initial disease and subsequent attacks includes the fact that outbreaks are often seasonal. The studies also show that disease occurs more often in people who were born in the spring rather than the late fall.

    "I would say it has something to do with maternal antibodies and resistance to viral infection," Kriesel said. Children born in the spring eventually lose the protection of their mother's antibodies within the first nine months, he said. By then it's winter or early spring, when they may be susceptible to a cold virus. Re-exposure to that virus or a similar virus may lead to MS.

    Kriesel cited the work of John Kurtzke, which provides evidence that a "priming infection" is acquired before puberty. Migration studies have borne this out, he says. For example, a person born in Africa who moves to Sweden at age 15 has a low chance of acquiring MS, whereas a person born in Sweden, where cold viruses are more prevalent, and then moves to Africa, has a much higher chance of having MS.

    An outbreak of MS in the Faroe Islands in 1943 also points to the virus hypothesis, he says. The outbreak on the remote island occurred after the British arrived in 1940.

    It's possible, though, that it's not the cold virus itself but rather "the nastiness of having the cold" that triggers MS attacks, Kriesel says. "A lot of researchers have given up on the viruses. They've tried to grow viruses out of the brains of MS patients and haven't succeeded."

    Source: Deseret © 2006 Deseret News Publishing Company (09/06/06) 

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

    (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.

    Source: US Newswire © 2006 U.S. Newswire (31/05/06)

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