Eerdere topics over dit onderwerp:
- MS-Like Disease Discovered in Monkeys / [URL="http://www.msweb.nl/forum/showthread.ph ... stein+barr"][U]Herpes-virus[/U][/URL]
- [URL="http://www.msweb.nl/forum/showthread.ph ... stein+barr"][U]Epstein Barr virus[/U][/URL]
Virussen
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Marsei
Retrovirussen: Hoe oude virussen ons kunnen blijven achtervolgen (2001)
Retrovirussen: Hoe oude virussen ons kunnen blijven achtervolgen (2001)
Hoe [URL="http://www.mecvs.net/module-ME_CVS_docs ... d-751.html"][U]oude virussen[/U][/URL] ons kunnen blijven achtervolgen
[QUOTE]Het menselijk genoom is bezaaid met de genetische overblijfselen van oude virussen die ooit mensen geïnfecteerd hebben maar nu in het lichaam slapen of sluimeren. Tot voor kort geloofden wetenschappers niet dat ze een rol speelden in moderne ziektes.
Nieuw onderzoek zorgt ervoor dat veel wetenschappers hierover opnieuw gaan nadenken. Recente studies suggereren dat deze oude virus partikels mogelijk een rol spleen in Hodgkin lymfoom, multiple sclerosis, reumatoïde artritis en andere ziekten.
De wetenschappers die oude virussen bestuderen zijn het meest geïnteresseerd in gegevens van golven van infecties die plaatsvonden zoals 100.000 en 200.000 jaar geleden. Bij de moderne mensen waren de meeste genen geërfd van een gemeenschappelijke voorouder geïnfecteerd met retrovirussen, waarschijnlijk van knaagdieren. In tegenstelling tot andere soorten virussen, kopiëren retrovirussen hun eigen genen in het DNA van de gastheer. Er wordt verondersteld dat sommige van de retrovirussen spermacellen en eitjes geïnfecteerd hebben, zodat het virus zou worden doorgegeven van generatie op generatie in het genoom.[/QUOTE]
[QUOTE]Onderzoekers schatten dat 8% van het menselijk genoom uit virusgenen en de resten ervan bestaan, wat betekent ongeveer 80.000 genen verspreid in het DNA van een individu.[/QUOTE]
[QUOTE]Het probleem lijkt te beginnen wanneer oude retrovirus genen – afgebroken en beschadigd door de tijd, en slapend in gezonde mensen – worden gekaapt, opnieuw geactiveerd worden of voor ander gebruik gaan dienen. “Retrovirussen nestelen zichzelf in ons genoom – of kapen kopieën weg van andere genen om binnen te dringen in ons genoom – ravages aan te richten,” zegt Stephen Tapscott van het Fred Hutchinson Cancer Research Center, die deel uitmaakt van een team die vorig jaar een paper gepubliceerd heeft over het verband tussen het oude proces en waarom sommige mensen een veelvoorkomende vorm van spierdystrofie krijgen.[/QUOTE]
[QUOTE]Brigitte Huber, een professor pathologie aan de Tufts University School of Medicine, en een team van onderzoekers toonde aan dat het Epstein-Barr virus en twee herpesvirussen een oud retrovirus gen kunnen activeren. De onderzoekers zijn van plan om een theorie te testen in muizen met de vraag of chronische low-level reactivatie van het retrovirus een rol speelt in de ontwikkeling van multiple sclerose.[/QUOTE]
Hoe [URL="http://www.mecvs.net/module-ME_CVS_docs ... d-751.html"][U]oude virussen[/U][/URL] ons kunnen blijven achtervolgen
[QUOTE]Het menselijk genoom is bezaaid met de genetische overblijfselen van oude virussen die ooit mensen geïnfecteerd hebben maar nu in het lichaam slapen of sluimeren. Tot voor kort geloofden wetenschappers niet dat ze een rol speelden in moderne ziektes.
Nieuw onderzoek zorgt ervoor dat veel wetenschappers hierover opnieuw gaan nadenken. Recente studies suggereren dat deze oude virus partikels mogelijk een rol spleen in Hodgkin lymfoom, multiple sclerosis, reumatoïde artritis en andere ziekten.
De wetenschappers die oude virussen bestuderen zijn het meest geïnteresseerd in gegevens van golven van infecties die plaatsvonden zoals 100.000 en 200.000 jaar geleden. Bij de moderne mensen waren de meeste genen geërfd van een gemeenschappelijke voorouder geïnfecteerd met retrovirussen, waarschijnlijk van knaagdieren. In tegenstelling tot andere soorten virussen, kopiëren retrovirussen hun eigen genen in het DNA van de gastheer. Er wordt verondersteld dat sommige van de retrovirussen spermacellen en eitjes geïnfecteerd hebben, zodat het virus zou worden doorgegeven van generatie op generatie in het genoom.[/QUOTE]
[QUOTE]Onderzoekers schatten dat 8% van het menselijk genoom uit virusgenen en de resten ervan bestaan, wat betekent ongeveer 80.000 genen verspreid in het DNA van een individu.[/QUOTE]
[QUOTE]Het probleem lijkt te beginnen wanneer oude retrovirus genen – afgebroken en beschadigd door de tijd, en slapend in gezonde mensen – worden gekaapt, opnieuw geactiveerd worden of voor ander gebruik gaan dienen. “Retrovirussen nestelen zichzelf in ons genoom – of kapen kopieën weg van andere genen om binnen te dringen in ons genoom – ravages aan te richten,” zegt Stephen Tapscott van het Fred Hutchinson Cancer Research Center, die deel uitmaakt van een team die vorig jaar een paper gepubliceerd heeft over het verband tussen het oude proces en waarom sommige mensen een veelvoorkomende vorm van spierdystrofie krijgen.[/QUOTE]
[QUOTE]Brigitte Huber, een professor pathologie aan de Tufts University School of Medicine, en een team van onderzoekers toonde aan dat het Epstein-Barr virus en twee herpesvirussen een oud retrovirus gen kunnen activeren. De onderzoekers zijn van plan om een theorie te testen in muizen met de vraag of chronische low-level reactivatie van het retrovirus een rol speelt in de ontwikkeling van multiple sclerose.[/QUOTE]
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Marsei
HHV6-en-ME/CVS-konferentie van 2008
HHV6-en-ME/CVS-konferentie van 2008
Meer over [B]Brigitte Huber[/B] (zie vorig bericht) tijdens de [URL="http://www.hetalternatief.org/HHV6-konf ... %20442.htm"][U]HHV6-en-ME/CVS-konferentie[/U][/URL] van 2008:
[QUOTE]Brigitte Huber heeft aangetoond dat een oud, in het genoom geïntegreerd virus (HERV-K18) aktief lijkt te zijn bij veel CVS- en MS-patiënten. Dit "lichaamseigen" virus is een superantigeen: een eiwit dat tot een heftige reaktie van het afweersysteem leidt, die mogelijk (op langere termijn) gepaard met ontregeling van de T-cellen (de regisseurs).
Bekend was al dat interferon-alfa en reaktivering van het EBV-virus leidt tot aktiviteit van het "lichaamseigen" HERV-K18. De "aanstekerwerking" blijkt ook voor HHV6 te gelden.[/QUOTE]
[QUOTE]Uit het verhaal van Huber: >75% van de MS-patiënten voldoet aan de CVS-kriteria.
Dat geeft opnieuw maar weer eens aan wat die CVS-diagnosekriteria waard zijn....[/QUOTE]
[B]Caruso en Di Luca[/B]
[QUOTE]Caruso en Di Luca hebben ontdekt dat een slapende HHV6-infektie van de endotheliaalcellen, cellen die de binnenkant van de aders bekleden, er toe bij dragen dat die cellen minder goed kunnen groeien, waardoor bloedvaten veel minder makkelijk vernieuwd en gerepareerd worden.
Het eiwit U94, dat door een slapende HHV6-infektie geproduceerd wordt, is direkt verantwoordelijk voor dit schadelijke effekt van die "onschuldige" infektie.[/QUOTE]
Meer over [B]Brigitte Huber[/B] (zie vorig bericht) tijdens de [URL="http://www.hetalternatief.org/HHV6-konf ... %20442.htm"][U]HHV6-en-ME/CVS-konferentie[/U][/URL] van 2008:
[QUOTE]Brigitte Huber heeft aangetoond dat een oud, in het genoom geïntegreerd virus (HERV-K18) aktief lijkt te zijn bij veel CVS- en MS-patiënten. Dit "lichaamseigen" virus is een superantigeen: een eiwit dat tot een heftige reaktie van het afweersysteem leidt, die mogelijk (op langere termijn) gepaard met ontregeling van de T-cellen (de regisseurs).
Bekend was al dat interferon-alfa en reaktivering van het EBV-virus leidt tot aktiviteit van het "lichaamseigen" HERV-K18. De "aanstekerwerking" blijkt ook voor HHV6 te gelden.[/QUOTE]
[QUOTE]Uit het verhaal van Huber: >75% van de MS-patiënten voldoet aan de CVS-kriteria.
Dat geeft opnieuw maar weer eens aan wat die CVS-diagnosekriteria waard zijn....[/QUOTE]
[B]Caruso en Di Luca[/B]
[QUOTE]Caruso en Di Luca hebben ontdekt dat een slapende HHV6-infektie van de endotheliaalcellen, cellen die de binnenkant van de aders bekleden, er toe bij dragen dat die cellen minder goed kunnen groeien, waardoor bloedvaten veel minder makkelijk vernieuwd en gerepareerd worden.
Het eiwit U94, dat door een slapende HHV6-infektie geproduceerd wordt, is direkt verantwoordelijk voor dit schadelijke effekt van die "onschuldige" infektie.[/QUOTE]
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Marsei
Ancient Retrovirus May Contribute to Chronic Fatigue Syndrome, Multiple Sclerosis
Ancient Retrovirus May Contribute to Chronic Fatigue Syndrome, Multiple Sclerosis
Ancient [URL="http://www.livinguncured.info/Ancient-R ... Contribute"][U]Retrovirus[/U][/URL] May Contribute to Chronic Fatigue Syndrome, Multiple Sclerosis
[QUOTE]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.[/QUOTE]
Ancient [URL="http://www.livinguncured.info/Ancient-R ... Contribute"][U]Retrovirus[/U][/URL] May Contribute to Chronic Fatigue Syndrome, Multiple Sclerosis
[QUOTE]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.[/QUOTE]
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Marsei
HHV-6 in MS
HHV-6 in MS
[URL="http://hhv-6foundation.webs.com/hhv6inms.htm"][U]HHV-6 in MS[/U][/URL]
Er wordt aangegeven dat er een groeiend bewijs is dat HHV-6 een rol speelt bij MS.
Verder worden er redenen gegeven waarom virussen waarschijnlijk een oorzaak voor MS zijn.
[QUOTE]Today, attention focuses primarily on (HHV-6), Epstein Barr virus (EBV), Chlamydia pneumonia (Cpn) and human endogenous retroviruses (HERVs). Since these viruses and pathogens potentiate each other, it is possible that there are many infections involved in a chain reaction, with the end result being an autoimmune process that continues long after the initial infections have passed.[/QUOTE]
[URL="http://hhv-6foundation.webs.com/hhv6inms.htm"][U]HHV-6 in MS[/U][/URL]
Er wordt aangegeven dat er een groeiend bewijs is dat HHV-6 een rol speelt bij MS.
Verder worden er redenen gegeven waarom virussen waarschijnlijk een oorzaak voor MS zijn.
[QUOTE]Today, attention focuses primarily on (HHV-6), Epstein Barr virus (EBV), Chlamydia pneumonia (Cpn) and human endogenous retroviruses (HERVs). Since these viruses and pathogens potentiate each other, it is possible that there are many infections involved in a chain reaction, with the end result being an autoimmune process that continues long after the initial infections have passed.[/QUOTE]
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Marsei
Active HHV-6 Infections in Patients with Early Disease (2000)
Active HHV-6 Infections in Patients with Early Disease (2000)
Active [URL="http://www.ivpresearch.org/ms_new.htm"][U]HHV-6 Infections[/U][/URL] in Patients with Early Disease
[QUOTE]The study found the incidence of active HHV-6 infection is significantly increased in MS patients with disease durations of less than or equal to 12 years. Active HHV-6 infections were found in both relapsing remitting MS patients and progressive MS patients. [/QUOTE]
[QUOTE]In summary, most if not all patients with MS have active HHV-6 infections in their central nervous system tissues, lymphoid tissues, and peripheral blood. Such infections are not seen in normal controls. Controlling active HHV-6 infection could alter the course of the disease and give us important insights into the role of this virus in initiating and perpetuating the disease process.
[/QUOTE]
Active [URL="http://www.ivpresearch.org/ms_new.htm"][U]HHV-6 Infections[/U][/URL] in Patients with Early Disease
[QUOTE]The study found the incidence of active HHV-6 infection is significantly increased in MS patients with disease durations of less than or equal to 12 years. Active HHV-6 infections were found in both relapsing remitting MS patients and progressive MS patients. [/QUOTE]
[QUOTE]In summary, most if not all patients with MS have active HHV-6 infections in their central nervous system tissues, lymphoid tissues, and peripheral blood. Such infections are not seen in normal controls. Controlling active HHV-6 infection could alter the course of the disease and give us important insights into the role of this virus in initiating and perpetuating the disease process.
[/QUOTE]
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Marsei
Retrovirus: cell stress
Retrovirus: cell stress
[URL="http://www.medicalnewstoday.com/releases/237205.php"][U]MNT[/U][/URL]: [QUOTE]His team discovered that inflammation and a specific type of cell stress are closely linked and lead to neurodegeneration and inflammation which cause cells to lose their protective coating - a process known as demyelination. [/QUOTE]
[QUOTE]The team's research also revealed that this specific type of cell stress, called the unfolded protein response, may be caused by an ancient virus that was introduced into the DNA of early humans. This particular cell stress is found at high levels in MS brain lesions.
"We all have this ancient virus in our DNA, but for some reason it is excessively turned on in MS," says Power. "We are doing more research investigating this link." [/QUOTE]
[URL="http://www.medicalnewstoday.com/releases/237205.php"][U]MNT[/U][/URL]: [QUOTE]His team discovered that inflammation and a specific type of cell stress are closely linked and lead to neurodegeneration and inflammation which cause cells to lose their protective coating - a process known as demyelination. [/QUOTE]
[QUOTE]The team's research also revealed that this specific type of cell stress, called the unfolded protein response, may be caused by an ancient virus that was introduced into the DNA of early humans. This particular cell stress is found at high levels in MS brain lesions.
"We all have this ancient virus in our DNA, but for some reason it is excessively turned on in MS," says Power. "We are doing more research investigating this link." [/QUOTE]
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Marsei
Retrvirus: The Insanity Virus
Retrvirus: The Insanity Virus
[URL="http://discovermagazine.com/2010/jun/03 ... :int=0&-C="][U]The Insanity Virus[/U][/URL]
[QUOTE]Sixty million years ago, a lemurlike animal—an early ancestor of humans and monkeys—contracted an infection. It may not have made the lemur ill, but the retrovirus spread into the animal’s testes (or perhaps its ovaries), and once there, it struck the jackpot: It slipped inside one of the rare germ line cells that produce sperm and eggs. When the lemur reproduced, that retrovirus rode into the next generation aboard the lucky sperm and then moved on from generation to generation, nestled in the DNA. “It’s a rare, random event,” says Robert Belshaw, an evolutionary biologist at the University of Oxford in England. “Over the last 100 million years, there have been only maybe 50 times when a retrovirus has gotten into our genome and proliferated.”
But such genetic intrusions stick around a very long time, so humans are chockablock full of these embedded, or endogenous, retroviruses. Our DNA carries dozens of copies of Perron’s virus, now called human endogenous retrovirus W, or HERV-W, at specific addresses on chromosomes 6 and 7.[/QUOTE]
[QUOTE]We lug around 100,000 retro*virus sequences inside us; all told, genetic parasites related to viruses account for more than 40 percent of all human DNA. Our body works hard to silence its viral stowaways by tying up those stretches of DNA in tight stacks of proteins, but sometimes they slip out. Now and then endogenous retroviruses switch on and start manufacturing proteins. They assemble themselves like Lego blocks into bulbous retroviral particles, which ooze from the cells producing them.
Endogenous retroviruses were long considered genetic fossils, incapable of doing anything interesting. But since Perron’s revelation, at least a dozen studies have found that HERV-W is active in people with MS.[/QUOTE]
[QUOTE]Through this research, a rough account is emerging of how HERV-W could trigger diseases like schizophrenia, bipolar disorder, and MS. Although the body works hard to keep its ERVs under tight control, infections around the time of birth destabilize this tense standoff. Scribbled onto the marker board in Yolken’s office is a list of infections that are now known to awaken HERV-W—including herpes, toxoplasma, cytomegalovirus, and a dozen others. The HERV-W viruses that pour into the newborn’s blood and brain fluid during these infections contain proteins that may enrage the infant immune system. White blood cells vomit forth inflammatory molecules called cytokines, attracting more immune cells like riot police to a prison break. The scene turns toxic.
In one experiment, Perron isolated HERV-W virus from people with MS and injected it into mice. The mice became clumsy, then paralyzed, then died of brain hemorrhages. But if Perron depleted the mice of immune cells known as T cells, the animals survived their encounter with HERV-W. It was an extreme experiment, but to Perron it made an important point. Whether people develop MS or schizophrenia may depend on how their immune system responds to HERV-W, he says. In MS the immune system directly attacks and kills brain cells, causing paralysis. In schizophrenia it may be that inflammation damages neurons indirectly by overstimulating them.[/QUOTE]
[QUOTE]The first, pivotal infection by toxoplasmosis or influenza (and subsequent flaring up of HERV-W) might happen shortly before or after birth. That would explain the birth-month effect: Flu infections happen more often in winter. The initial infection could then set off a lifelong pattern in which later infections reawaken HERV-W, causing more inflammation and eventually symptoms.[/QUOTE]
[QUOTE]Gene studies have failed to provide simple explanations for ailments like schizophrenia and MS. Torrey’s theory may explain why. Genes may come into play only in conjunction with certain environmental kicks. Our genome’s thousands of parasites might provide part of that kick.
“The ‘genes’ that can respond to environmental triggers or toxic pathogens are the dark side of the genome,” Perron says. Retroviruses, including HIV, are known to be awakened by inflammation—possibly the result of infection, cigarette smoke, or pollutants in drinking water. [/QUOTE]
[QUOTE]Perron has founded a biotech start-up —GeNeuro, in Geneva, Switzerland—to develop treatments targeting HERV-W. The company has created an antibody that neutralizes a primary viral protein, and it works in lab mice with MS. “We have terrific effects,” Perron says. “In animals that have demyelinating brain lesions induced by these HERV envelope proteins, we see a dramatic stop to this process when we inject this antibody.” He is scheduled to begin a Phase 1 clinical trial in people with MS near the end of this year. A clinical trial with schizophrenics might follow in 2011.[/QUOTE]
[URL="http://discovermagazine.com/2010/jun/03 ... :int=0&-C="][U]The Insanity Virus[/U][/URL]
[QUOTE]Sixty million years ago, a lemurlike animal—an early ancestor of humans and monkeys—contracted an infection. It may not have made the lemur ill, but the retrovirus spread into the animal’s testes (or perhaps its ovaries), and once there, it struck the jackpot: It slipped inside one of the rare germ line cells that produce sperm and eggs. When the lemur reproduced, that retrovirus rode into the next generation aboard the lucky sperm and then moved on from generation to generation, nestled in the DNA. “It’s a rare, random event,” says Robert Belshaw, an evolutionary biologist at the University of Oxford in England. “Over the last 100 million years, there have been only maybe 50 times when a retrovirus has gotten into our genome and proliferated.”
But such genetic intrusions stick around a very long time, so humans are chockablock full of these embedded, or endogenous, retroviruses. Our DNA carries dozens of copies of Perron’s virus, now called human endogenous retrovirus W, or HERV-W, at specific addresses on chromosomes 6 and 7.[/QUOTE]
[QUOTE]We lug around 100,000 retro*virus sequences inside us; all told, genetic parasites related to viruses account for more than 40 percent of all human DNA. Our body works hard to silence its viral stowaways by tying up those stretches of DNA in tight stacks of proteins, but sometimes they slip out. Now and then endogenous retroviruses switch on and start manufacturing proteins. They assemble themselves like Lego blocks into bulbous retroviral particles, which ooze from the cells producing them.
Endogenous retroviruses were long considered genetic fossils, incapable of doing anything interesting. But since Perron’s revelation, at least a dozen studies have found that HERV-W is active in people with MS.[/QUOTE]
[QUOTE]Through this research, a rough account is emerging of how HERV-W could trigger diseases like schizophrenia, bipolar disorder, and MS. Although the body works hard to keep its ERVs under tight control, infections around the time of birth destabilize this tense standoff. Scribbled onto the marker board in Yolken’s office is a list of infections that are now known to awaken HERV-W—including herpes, toxoplasma, cytomegalovirus, and a dozen others. The HERV-W viruses that pour into the newborn’s blood and brain fluid during these infections contain proteins that may enrage the infant immune system. White blood cells vomit forth inflammatory molecules called cytokines, attracting more immune cells like riot police to a prison break. The scene turns toxic.
In one experiment, Perron isolated HERV-W virus from people with MS and injected it into mice. The mice became clumsy, then paralyzed, then died of brain hemorrhages. But if Perron depleted the mice of immune cells known as T cells, the animals survived their encounter with HERV-W. It was an extreme experiment, but to Perron it made an important point. Whether people develop MS or schizophrenia may depend on how their immune system responds to HERV-W, he says. In MS the immune system directly attacks and kills brain cells, causing paralysis. In schizophrenia it may be that inflammation damages neurons indirectly by overstimulating them.[/QUOTE]
[QUOTE]The first, pivotal infection by toxoplasmosis or influenza (and subsequent flaring up of HERV-W) might happen shortly before or after birth. That would explain the birth-month effect: Flu infections happen more often in winter. The initial infection could then set off a lifelong pattern in which later infections reawaken HERV-W, causing more inflammation and eventually symptoms.[/QUOTE]
[QUOTE]Gene studies have failed to provide simple explanations for ailments like schizophrenia and MS. Torrey’s theory may explain why. Genes may come into play only in conjunction with certain environmental kicks. Our genome’s thousands of parasites might provide part of that kick.
“The ‘genes’ that can respond to environmental triggers or toxic pathogens are the dark side of the genome,” Perron says. Retroviruses, including HIV, are known to be awakened by inflammation—possibly the result of infection, cigarette smoke, or pollutants in drinking water. [/QUOTE]
[QUOTE]Perron has founded a biotech start-up —GeNeuro, in Geneva, Switzerland—to develop treatments targeting HERV-W. The company has created an antibody that neutralizes a primary viral protein, and it works in lab mice with MS. “We have terrific effects,” Perron says. “In animals that have demyelinating brain lesions induced by these HERV envelope proteins, we see a dramatic stop to this process when we inject this antibody.” He is scheduled to begin a Phase 1 clinical trial in people with MS near the end of this year. A clinical trial with schizophrenics might follow in 2011.[/QUOTE]
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Marsei
Multiple sclerosis-associated retrovirus and progressive disability of MS
Multiple sclerosis-associated retrovirus and progressive disability of MS
Multiple sclerosis-associated [URL="http://msj.sagepub.com/content/16/10/1248.abstract"][U]retrovirus[/U][/URL] and progressive disability of multiple sclerosis
[QUOTE]Retrovirus-like particles containing the multiple sclerosis-associated retrovirus RNA, significantly found in the cerebrospinal fluid of patients with multiple sclerosis, have been preliminarily associated with a short-term poor clinical and radiological prognosis of the disease. We asked whether these prognostic indications are still measurable after a long-term clinical evaluation (10 years). Our 10-year blind observational study confirms that the presence of multiple sclerosis-associated retrovirus in the cerebrospinal fluid of early multiple sclerosis patients is associated with a significantly greater rate of relapse-unrelated unremitting disability and secondary progression of the disease.[/QUOTE]
Multiple sclerosis-associated [URL="http://msj.sagepub.com/content/16/10/1248.abstract"][U]retrovirus[/U][/URL] and progressive disability of multiple sclerosis
[QUOTE]Retrovirus-like particles containing the multiple sclerosis-associated retrovirus RNA, significantly found in the cerebrospinal fluid of patients with multiple sclerosis, have been preliminarily associated with a short-term poor clinical and radiological prognosis of the disease. We asked whether these prognostic indications are still measurable after a long-term clinical evaluation (10 years). Our 10-year blind observational study confirms that the presence of multiple sclerosis-associated retrovirus in the cerebrospinal fluid of early multiple sclerosis patients is associated with a significantly greater rate of relapse-unrelated unremitting disability and secondary progression of the disease.[/QUOTE]
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Marsei
Endogenous Retroviral Genes, Herpes Viruses and Gender in MS
Endogenous Retroviral Genes, Herpes Viruses and Gender in MS
Endogenous [URL="http://www.unitedspinal.org/msscene/200 ... der-in-ms/"][U]Retroviral Genes[/U][/URL], Herpes Viruses and Gender in MS
[QUOTE]The group reviewed the pieces of a puzzle and now offer a consistent picture for the cause of MS. Interestingly, at the gene-environment interface, this picture also includes gender-related specificities through the potential interplay with endogenous retrovirus type W copies present on the [B]X chromosome[/B].[/QUOTE]
Endogenous [URL="http://www.unitedspinal.org/msscene/200 ... der-in-ms/"][U]Retroviral Genes[/U][/URL], Herpes Viruses and Gender in MS
[QUOTE]The group reviewed the pieces of a puzzle and now offer a consistent picture for the cause of MS. Interestingly, at the gene-environment interface, this picture also includes gender-related specificities through the potential interplay with endogenous retrovirus type W copies present on the [B]X chromosome[/B].[/QUOTE]