Interview met Harald zur Hausen
[URL="https://www.eoswetenschap.eu/voeding/me ... e-sclerose"][U]Melk[/U][/URL] veroorzaakt multiple sclerose
[QUOTE]Het gaat om een samenspel van viraal DNA in melk, het herpesvirus en een tekort aan vitamine D. Dat ontdekte Nobelprijswinnaar Harald zur Hausen. Hij onderzocht koemelk en merkte dat die vol zit met DNA dat niet van de koe zelf afkomstig is, maar vermoedelijk van virussen waarmee de dieren ooit besmet raakten. Als wij melk drinken, raken ook wij besmet met dat viraal DNA. Dat kan op zich geen kwaad. Behalve als je ooit ook besmet raakte met het herpesvirus en als je ook nog eens een tekort hebt aan vitamine D.[/QUOTE]
[QUOTE]Zowel het herpesvirus als het viraal DNA dat we als baby via koemelk binnenkrijgen, infecteert onze hersencellen. Een vitamine D-tekort leidt tot extra productie van de groeifactor TGF-β, die de sluimerende herpesvirussen opnieuw actief maakt.
Daardoor gaat het viraal DNA uit runderen zich sterk vermenigvuldigen en infecteert het nabijgelegen cellen. Het immuunsysteem treedt op tegen deze infectie: er ontstaan ontstekingshaarden die typisch zijn voor multiple sclerose, waarbij de getroffen zenuwcellen uiteindelijk vernietigd worden. [/QUOTE]
[QUOTE]Moeten we voortaan koemelk laten staan? ‘Daarvoor is het voor de meesten onder ons te laat’, zegt Harald zur Hausen in een interview in Eos Psyche&Brein. ‘Als kind hebben we allemaal melk gedronken. De infectie gebeurt in een heel vroege levensfase, vermoedelijk tijdens de eerste twee jaren van ons leven. Ik adviseer wel om baby’s lang borstvoeding te geven. Vooral tijdens het eerste levensjaar heeft moedermelk een beschermend effect. Daarna kan een kind zelf antilichamen aanmaken, waardoor een besmetting met viraal DNA uit melk waarschijnlijk niet meer zo gevaarlijk is.’[/QUOTE]
Virussen
-
MarcC
beetje een verkooppraatje van GeNeuro, maar eind dit jaar de fase 2B - studieresultaten van GNbAC1, dat veranderingen in het menselijke DNA neutraliseert, veroorzaakt door Human Endogenous Retrovirus.
[url=https://www.geneuro.com/data/documents/ ... y-2017.pdf]ontwikkeling GNbAC1 voor MS[/url]
Zou dit het dan zijn? Wie weet.
groetjes, Marc
[url=https://www.geneuro.com/data/documents/ ... y-2017.pdf]ontwikkeling GNbAC1 voor MS[/url]
Zou dit het dan zijn? Wie weet.
groetjes, Marc
-
Leonard
op pg 6 staat:
HERV genes encode proteins, notably as a result of a
viral infection
mijn thesis van vorig jaar zegt hetzelfde en was gebaseerd op andere bronnen (moet ik nazoeken):
At that point, herpes viruses including the Varicella Zoster Virus (VZV) and the Epstein-Barr Virus (EBV) may trigger large scale HERV activation in a triangular arrangement with the genome
Naast deze ontwikkeling zijn er ook andere ontwikkelingen van compounds die alle autoimmuniteit stopzetten. Alles bij elkaar hoopvol, maar wanneer????
HERV genes encode proteins, notably as a result of a
viral infection
mijn thesis van vorig jaar zegt hetzelfde en was gebaseerd op andere bronnen (moet ik nazoeken):
At that point, herpes viruses including the Varicella Zoster Virus (VZV) and the Epstein-Barr Virus (EBV) may trigger large scale HERV activation in a triangular arrangement with the genome
Naast deze ontwikkeling zijn er ook andere ontwikkelingen van compounds die alle autoimmuniteit stopzetten. Alles bij elkaar hoopvol, maar wanneer????
-
MarcC
Hoopvolle zaken en ontwikkelingen genoeg, maar het duurt allemaal zoooo lang.
Wat dacht je van deze ontwikkeling: [url=http://www.ms-uk.org/could-lifnano-be-n ... -ms-050617]LIFNano[/url]
Nog hoopvoller, maar ook "futuristischer". Hierbij is een nog langere weg te gaan, en ons geduld wordt nog langer op de proef gesteld. Maar er is wel geld aangetrokken vanuit de farmacie (Merck), als die winstpotentieel zien, dan kan het wel eens snel gaan.
Wat dacht je van deze ontwikkeling: [url=http://www.ms-uk.org/could-lifnano-be-n ... -ms-050617]LIFNano[/url]
Nog hoopvoller, maar ook "futuristischer". Hierbij is een nog langere weg te gaan, en ons geduld wordt nog langer op de proef gesteld. Maar er is wel geld aangetrokken vanuit de farmacie (Merck), als die winstpotentieel zien, dan kan het wel eens snel gaan.
-
Marsei
#PlainEnglish: Targeting the “virus factory” to stop MS activity
#PlainEnglish: Targeting the “virus factory” to stop MS activity
#PlainEnglish: Targeting the “[URL="http://multiple-sclerosis-research.blog ... op-ms.html"][U]virus factory[/U][/URL]” to stop MS activity
#PlainEnglish: Targeting the “[URL="http://multiple-sclerosis-research.blog ... op-ms.html"][U]virus factory[/U][/URL]” to stop MS activity
-
Leonard
[QUOTE=Marsei;1084228]#PlainEnglish: Targeting the “[URL="http://multiple-sclerosis-research.blog ... op-ms.html"][U]virus factory[/U][/URL]” to stop MS activity[/QUOTE]
deze BartsMS Blog is maar deel van het hele verhaal.
het herpes virus is honderden miljoenen jaren met ons geco-evolueerd.
verschillende stammen zijn betrokken bij MS; sommige doen iets met T cellen, sommige met B cellen, sommige met cellen in het genome.
er ontstaat een zeer geconvolueerd plaatje.
verdere details hier: [url]http://www.thisisms.com/forum/general-d ... ml#p248066[/url]
ik ben er van overtuigd dat dit het verhaal is.
de farma - bedrijven die verantwoording schuldig zijn aan hun aandeelhouders - kan ik niet kwalijk nemen dat ze achter de winst aangaan.
de politiek doet niks en verschuilt zich achter de academische wereld.
de academische wereld en onze eigen MS verenigingen zijn vervuild en denken niet verder dan hun neus lang is.
ik maak me er zo kwaad over..
deze BartsMS Blog is maar deel van het hele verhaal.
het herpes virus is honderden miljoenen jaren met ons geco-evolueerd.
verschillende stammen zijn betrokken bij MS; sommige doen iets met T cellen, sommige met B cellen, sommige met cellen in het genome.
er ontstaat een zeer geconvolueerd plaatje.
verdere details hier: [url]http://www.thisisms.com/forum/general-d ... ml#p248066[/url]
ik ben er van overtuigd dat dit het verhaal is.
de farma - bedrijven die verantwoording schuldig zijn aan hun aandeelhouders - kan ik niet kwalijk nemen dat ze achter de winst aangaan.
de politiek doet niks en verschuilt zich achter de academische wereld.
de academische wereld en onze eigen MS verenigingen zijn vervuild en denken niet verder dan hun neus lang is.
ik maak me er zo kwaad over..
-
Marsei
-
Marsei
T Cells Targeting Epstein-Barr Virus -- A New Treatment for MS?
T Cells Targeting Epstein-Barr Virus -- A New Treatment for MS?
[URL="http://www.medscape.com/viewarticle/879140"][U]T Cells Targeting Epstein-Barr Virus[/U][/URL] -- A New Treatment for MS?
[QUOTE]A new approach to the treatment of multiple sclerosis (MS) — use of T cells sensitized to the Epstein-Barr virus — has shown encouraging results in a preliminary study.
The study, presented at the American Academy of Neurology 2017 Annual Meeting (AAN) as part of the Emerging Science Poster Session, was led by Michael Pender, MD, University of Queensland, Brisbane, Australia.
The researchers believe Epstein-Barr virus plays a causative role in the development of MS by infecting B cells and inducing them to attack the brain and spinal cord. By sensitizing a patient's T cells to the virus — an approach known as adoptive immunotherapy — the T cells are enabled to keep the infected B cells under control, resulting in improvements in MS.
In the current study, six patients with progressive MS have so far been treated with autologous Epstein-Barr–specific T cells, and three patients have shown marked benefits, including a large reduction in fatigue and improvements in visual acuity, manual dexterity, lower-limb weakness, and involuntary spasms, the researchers report.[/QUOTE]
[URL="http://www.medscape.com/viewarticle/879140"][U]T Cells Targeting Epstein-Barr Virus[/U][/URL] -- A New Treatment for MS?
[QUOTE]A new approach to the treatment of multiple sclerosis (MS) — use of T cells sensitized to the Epstein-Barr virus — has shown encouraging results in a preliminary study.
The study, presented at the American Academy of Neurology 2017 Annual Meeting (AAN) as part of the Emerging Science Poster Session, was led by Michael Pender, MD, University of Queensland, Brisbane, Australia.
The researchers believe Epstein-Barr virus plays a causative role in the development of MS by infecting B cells and inducing them to attack the brain and spinal cord. By sensitizing a patient's T cells to the virus — an approach known as adoptive immunotherapy — the T cells are enabled to keep the infected B cells under control, resulting in improvements in MS.
In the current study, six patients with progressive MS have so far been treated with autologous Epstein-Barr–specific T cells, and three patients have shown marked benefits, including a large reduction in fatigue and improvements in visual acuity, manual dexterity, lower-limb weakness, and involuntary spasms, the researchers report.[/QUOTE]
-
MarcC
-
Marsei
Hidden herpes virus may play key role in MS, other brain disorders
Hidden herpes virus may play key role in MS, other brain disorders
[URL="https://www.sciencedaily.com/releases/2 ... 122959.htm"][U]Hidden herpes virus[/U][/URL] may play key role in MS, other brain disorders
[QUOTE][I]The ubiquitous human herpesvirus 6 (HHV-6) may play a critical role in impeding the brain's ability to repair itself in diseases like multiple sclerosis. The findings, which appear in the journal Scientific Reports, may help explain the differences in severity in symptoms that many people with the disease experience.[/I]
"While latent HHV-6 -- which can be found in cells throughout the brain -- has been associated with demyelinating disorders like multiple sclerosis it has not been clear what role, if any, it plays in these diseases," said Margot Mayer-Proschel, Ph.D., an associate professor at the University of Rochester Medical Center Department of Biomedical Genetics and co-author of the study. "These findings show that, while in the process of hiding from the immune system, the virus produces a protein that has the potential to impair the normal ability of cells in the brain to repair damaged myelin."
It is estimated that more than 80 percent of people have been exposed to HHV6 at some point during their early childhood. HHV-6 is the most common human herpesvirus and infections that occur during childhood often go unnoticed but the virus can cause roseola, which is characterized by a fever and rash in infants. A much smaller number -- one percent of people -have congenital HHV6 where a single copy of the virus is acquired through either the father's sperm or mother's egg and is passed on to the developing child.
While the immune system fights off the most active forms of the infection, the virus never truly leaves our bodies and can reactivate later in life. The herpesvirus 6 accomplishes this form of latency by integrating itself into our genetic code and thus hiding in cells and evading the immune system.
One of the first studies to show an association between latent HHV-6 infection and demyelinating disorders was conducted in 2003 by URMC researchers David Mock, M.D., who is a co-author of the current study, Andrew Goodman, M.D. and others. They noted that HHV6 genetic code could be found in the brain cells of individuals with severe forms of multiple sclerosis.
Viruses have long been suspected to contribute to multiple sclerosis, a disorder in which the body's own immune system attacks and destroys myelin -- the fatty tissue that insulates the connections between nerve cells. However, while the 2003 study indicated that the herpes virus played some role in multiple sclerosis, it has subsequently become clear that the virus is unlikely to trigger the disease.
The Rochester researchers in the current paper took a new approach and asked instead whether the virus could have an impact on a critical support cell found in the brain called oligodendrocyte progenitor cells (OPCs). These cells play an important role in maintaining the brain's supply of myelin. When myelin is lost to disease, age, or injury, OPCs are activated, migrate to where they are needed, and mature into myelin-producing cells which repair the damage.
The researchers examined the impact of the latent HHV-6 on the activity of human OPCs, which was possible through the work of Chris Proschel, a co-author of the manuscript with expertise in the generation of human OPCs. One of the ways the virus stays hidden in cells is by expressing a protein called U94 that helps it keep its place in the human DNA and remain undetected from the immune system. By studying human cells and transplanting human OPCs into animal models, the team discovered that when U94 was expressed in OPCs, the cells stopped migrating to where they were needed.
What is still not fully understood is the relationship between the extent of the viral infection in the brain and the severity of diseases like multiple sclerosis and other demyelinating diseases such as leukodystrophies and Vanishing White Matter disease. For example, do the number of infected cells need to reach a certain threshold before OPC function is impeded? Are individuals who have congenital HHV6 more vulnerable to severe forms of these diseases?
"More research is needed to understand by which mechanisms the virus impedes the function of OPCs and what impact this has on the progression of these diseases," said Mayer-Proschel. "But it is clear that HHV6, while not necessarily the cause of demyelinating diseases, is limiting the ability of the brain to repair damage to myelin thereby potentially accelerating the progression of these diseases."[/QUOTE]
[URL="https://www.sciencedaily.com/releases/2 ... 122959.htm"][U]Hidden herpes virus[/U][/URL] may play key role in MS, other brain disorders
[QUOTE][I]The ubiquitous human herpesvirus 6 (HHV-6) may play a critical role in impeding the brain's ability to repair itself in diseases like multiple sclerosis. The findings, which appear in the journal Scientific Reports, may help explain the differences in severity in symptoms that many people with the disease experience.[/I]
"While latent HHV-6 -- which can be found in cells throughout the brain -- has been associated with demyelinating disorders like multiple sclerosis it has not been clear what role, if any, it plays in these diseases," said Margot Mayer-Proschel, Ph.D., an associate professor at the University of Rochester Medical Center Department of Biomedical Genetics and co-author of the study. "These findings show that, while in the process of hiding from the immune system, the virus produces a protein that has the potential to impair the normal ability of cells in the brain to repair damaged myelin."
It is estimated that more than 80 percent of people have been exposed to HHV6 at some point during their early childhood. HHV-6 is the most common human herpesvirus and infections that occur during childhood often go unnoticed but the virus can cause roseola, which is characterized by a fever and rash in infants. A much smaller number -- one percent of people -have congenital HHV6 where a single copy of the virus is acquired through either the father's sperm or mother's egg and is passed on to the developing child.
While the immune system fights off the most active forms of the infection, the virus never truly leaves our bodies and can reactivate later in life. The herpesvirus 6 accomplishes this form of latency by integrating itself into our genetic code and thus hiding in cells and evading the immune system.
One of the first studies to show an association between latent HHV-6 infection and demyelinating disorders was conducted in 2003 by URMC researchers David Mock, M.D., who is a co-author of the current study, Andrew Goodman, M.D. and others. They noted that HHV6 genetic code could be found in the brain cells of individuals with severe forms of multiple sclerosis.
Viruses have long been suspected to contribute to multiple sclerosis, a disorder in which the body's own immune system attacks and destroys myelin -- the fatty tissue that insulates the connections between nerve cells. However, while the 2003 study indicated that the herpes virus played some role in multiple sclerosis, it has subsequently become clear that the virus is unlikely to trigger the disease.
The Rochester researchers in the current paper took a new approach and asked instead whether the virus could have an impact on a critical support cell found in the brain called oligodendrocyte progenitor cells (OPCs). These cells play an important role in maintaining the brain's supply of myelin. When myelin is lost to disease, age, or injury, OPCs are activated, migrate to where they are needed, and mature into myelin-producing cells which repair the damage.
The researchers examined the impact of the latent HHV-6 on the activity of human OPCs, which was possible through the work of Chris Proschel, a co-author of the manuscript with expertise in the generation of human OPCs. One of the ways the virus stays hidden in cells is by expressing a protein called U94 that helps it keep its place in the human DNA and remain undetected from the immune system. By studying human cells and transplanting human OPCs into animal models, the team discovered that when U94 was expressed in OPCs, the cells stopped migrating to where they were needed.
What is still not fully understood is the relationship between the extent of the viral infection in the brain and the severity of diseases like multiple sclerosis and other demyelinating diseases such as leukodystrophies and Vanishing White Matter disease. For example, do the number of infected cells need to reach a certain threshold before OPC function is impeded? Are individuals who have congenital HHV6 more vulnerable to severe forms of these diseases?
"More research is needed to understand by which mechanisms the virus impedes the function of OPCs and what impact this has on the progression of these diseases," said Mayer-Proschel. "But it is clear that HHV6, while not necessarily the cause of demyelinating diseases, is limiting the ability of the brain to repair damage to myelin thereby potentially accelerating the progression of these diseases."[/QUOTE]