A new XMRV Workshop has taken place today in Vall Hebron Hospital in Barcelona. We have had five lectures, all of them full of the history of all the papers that have been published since Dr. Judy Mikovits’s paper came out in September 2009. But each speaker has also given a summary of what are they working on.
Dr. José Alegre opened the session and was the first to speak. He is one of the most well known specialists in CFS, and as soon as the Science paper was published, he immediately tried to involve a group of Biologists from his Hospital in this research. One of the things mentioned by Dr. Alegre was the fact that pregnant women seem to have a remission of their symptoms during their pregnancy and a relapse right after they give birth, which points out a hormonal component in this illness. He also mentioned that it would be interesting to research the genome of post polio patients given that they have similar fatigue symptoms as CFS patients, and in that way it could be understood for both conditions.
Dr. Cecilia Cabrera from IrsiCaixa talked for an hour. Dr. Cabrera discussed that the structure of XMRV was simpler that HIV, and so far, only 3 genes had been identified: gag, pal and M. She mentioned the great importance of Dr. Ila Singh’s study with animals, and all they have learned about XMRV. Then she said that they have tested 11 patients and done 4 controls, that they have identified sequences of XMRV (not polytrophic virus) in B cells of CFS patients and controls, and that they are developing models of infection in human tissues in vitro, and in this way was able to study the viral pathogenicity. In their studies they had observed that XMRV was being restricted by the APO-B system, and also that the lymphoid tissue could act as a reservoir.
Dr. Cabrera also motioned that there is a common effort overseas to find a common assay to allow everybody to detect XMRV in the same way, and this is being developed by the SRWG (Scientific Research Working Group) which is conformed by the Blood Working Group, Retrovirologist teams, CFS researchers and Federal Agencies.
Dr. José Montoya of Stanford University was next. He started explaining that six years ago he met his first CFS patient, and since then he has visited more than 450. He is sure that you can develop CFS after a viral infection, and he believes that 11 % of patients that suffer EBV, Q fever, Ross River virus, etc, can end up with a CFS. About Dr. Judy Mikovit’s paper he remarked that since it was published everybody is turning to CFS with the intention to find out all they can because they have completely changed their opinion.
In a random, double-blind, placebo-controlled study they have found that there was a clinical improvement in patients who were taking valganciclovir for a period of more than six months, compared with placebo. CFS patients met Fukuda’s international criteria and had high antibody data against HHV-6 and EBV. Several immunological markers changed significantly in the treated patients that were not seen in patients taking placebo. This study will be submitted for publication this month, and provides evidence that CFS is a real illness that can be caused by an infectious agent that can be treated with prolonged antiviral intervention. They are also working on the hypothesis that besides the antiviral mechanism there could also be an immune modulator component in the good results.
The dramatic improvement of these patients was both cognitive and physical. Also worth to mention that the medication did not work in every case, and they are working on markers that could help ascertain the suitability of the medication each individual patient. Among the markers monocytes are a good candidate given that in the study they came down significantly and then normalized in the patients where the drug did work. The cytokine profile of the patients also played a role in following the good effects of this medication, specifically:IL5, IL17F, ENA78, EOTAXIN, IP10… Additionally, Dr. Montoya mentioned that HHV6 plays a unique role because it integrated in the chromosome of CFS patients, which is simply not normal in a virus.
Dr. Montoya remarked that the Early Antigen was used to prevent the relapses in naso-pharyngeal cancer, and in CFS patients is very elevated even after 20 years of the acute infection, which is simply not normal. Therefore this is a marker He uses for patients selection in the study.
Dra. Carmen Mendoza from Hospital Carlos III of Madrid did not talked much on XMRV, but instead on HIV. Off the record She mentioned that they have found 0% of XMRV in their lab, and in my view She was a bit lost on the latest advances on XMRV research, as She was still talking about geographical distribution and contamination as potential reasons not to find XMRV in Europe, We had to remind her that XMRV has been found in Spain, Italy, Holland, Norway, UK…It was a bit discouraging to find out that the “extra effort” that Carlos III plans to do is to send to Abbot Labs in the US, the blood of the patients that already they declared “negative” to perform a serological test, that on the other hand has already been criticized of not being accurate out of the animal model, this means in humans. Therefore we do not expect Carlos III to advance on the XMRV research, and postulates to be the Spanish publicly financed entity that slows down the research process with meaningless negative studies.
Dr. Jordi Petriz, of the Vall Hebron Hospital. He told us that the aim of his research with Dr. Alegre was the development of a diagnosis tool for the disease based on the functional response of the cells of CFS patients. It was also mentioned that the interferon response was key to allow XMRV to do damage in the health of CFS patients.
They will use, functional flow cytometry, a very sophisticated technology on the whole blood of people with CFS infected with XMRV, and compare the results with appropriate controls, in the hope of finding a pattern and goal differential characteristic of CFS. These techniques will also allow the analysis of the lymphocytes in the study of CFS patient’s immune system. He has also widely described the study that is focused on neutrophil oxidative metabolism and how this may affect their function. As they plan to study the membrane structure of CFS patients, it was suggested to him in the Q&A to have a look on the paper published on Mitochondrial dysfunction a bacterial translocation by Sarah Mhyll and Kenny De Meirleir.
Our conclusion is that all of them have mentioned the importance of an animal model to study the pathogenesis of XMRV. It’s also very important to have accepted tools to work with, and this means the urgent need of a universal kit. They are all working in the same direction, they are sharing lots of data, samples, etc, and they all agreed with the great complicity between the different groups, which they had not observed so far, for the other diseases they have worked on. Good long term perspectives.
A new XMRV Workshop has taken place today in Vall Hebron Hospital in Barcelona. We have had five lectures, all of them full of the history of all the papers that have been published since Dr. Judy Mikovits’s paper came out in September 2009. But each speaker has also given a summary of what are they working on.
Dr. José Alegre opened the session and was the first to speak. He is one of the most well known specialists in CFS, and as soon as the Science paper was published, he immediately tried to involve a group of Biologists from his Hospital in this research. One of the things mentioned by Dr. Alegre was the fact that pregnant women seem to have a remission of their symptoms during their pregnancy and a relapse right after they give birth, which points out a hormonal component in this illness. He also mentioned that it would be interesting to research the genome of post polio patients given that they have similar fatigue symptoms as CFS patients, and in that way it could be understood for both conditions.
Dr. Cecilia Cabrera from IrsiCaixa talked for an hour. Dr. Cabrera discussed that the structure of XMRV was simpler that HIV, and so far, only 3 genes had been identified: gag, pal and M. She mentioned the great importance of Dr. Ila Singh’s study with animals, and all they have learned about XMRV. Then she said that they have tested 11 patients and done 4 controls, that they have identified sequences of XMRV (not polytrophic virus) in B cells of CFS patients and controls, and that they are developing models of infection in human tissues in vitro, and in this way was able to study the viral pathogenicity. In their studies they had observed that XMRV was being restricted by the APO-B system, and also that the lymphoid tissue could act as a reservoir.
Dr. Cabrera also motioned that there is a common effort overseas to find a common assay to allow everybody to detect XMRV in the same way, and this is being developed by the SRWG (Scientific Research Working Group) which is conformed by the Blood Working Group, Retrovirologist teams, CFS researchers and Federal Agencies.
Dr. José Montoya of Stanford University was next. He started explaining that six years ago he met his first CFS patient, and since then he has visited more than 450. He is sure that you can develop CFS after a viral infection, and he believes that 11 % of patients that suffer EBV, Q fever, Ross River virus, etc, can end up with a CFS. About Dr. Judy Mikovit’s paper he remarked that since it was published everybody is turning to CFS with the intention to find out all they can because they have completely changed their opinion.
In a random, double-blind, placebo-controlled study they have found that there was a clinical improvement in patients who were taking valganciclovir for a period of more than six months, compared with placebo. CFS patients met Fukuda’s international criteria and had high antibody data against HHV-6 and EBV. Several immunological markers changed significantly in the treated patients that were not seen in patients taking placebo. This study will be submitted for publication this month, and provides evidence that CFS is a real illness that can be caused by an infectious agent that can be treated with prolonged antiviral intervention. They are also working on the hypothesis that besides the antiviral mechanism there could also be an immune modulator component in the good results.
The dramatic improvement of these patients was both cognitive and physical. Also worth to mention that the medication did not work in every case, and they are working on markers that could help ascertain the suitability of the medication each individual patient. Among the markers monocytes are a good candidate given that in the study they came down significantly and then normalized in the patients where the drug did work. The cytokine profile of the patients also played a role in following the good effects of this medication, specifically:IL5, IL17F, ENA78, EOTAXIN, IP10… Additionally, Dr. Montoya mentioned that HHV6 plays a unique role because it integrated in the chromosome of CFS patients, which is simply not normal in a virus.
Dr. Montoya remarked that the Early Antigen was used to prevent the relapses in naso-pharyngeal cancer, and in CFS patients is very elevated even after 20 years of the acute infection, which is simply not normal. Therefore this is a marker He uses for patients selection in the study.
Dra. Carmen Mendoza from Hospital Carlos III of Madrid did not talked much on XMRV, but instead on HIV. Off the record She mentioned that they have found 0% of XMRV in their lab, and in my view She was a bit lost on the latest advances on XMRV research, as She was still talking about geographical distribution and contamination as potential reasons not to find XMRV in Europe, We had to remind her that XMRV has been found in Spain, Italy, Holland, Norway, UK…It was a bit discouraging to find out that the “extra effort” that Carlos III plans to do is to send to Abbot Labs in the US, the blood of the patients that already they declared “negative” to perform a serological test, that on the other hand has already been criticized of not being accurate out of the animal model, this means in humans. Therefore we do not expect Carlos III to advance on the XMRV research, and postulates to be the Spanish publicly financed entity that slows down the research process with meaningless negative studies.
Dr. Jordi Petriz, of the Vall Hebron Hospital. He told us that the aim of his research with Dr. Alegre was the development of a diagnosis tool for the disease based on the functional response of the cells of CFS patients. It was also mentioned that the interferon response was key to allow XMRV to do damage in the health of CFS patients.
They will use, functional flow cytometry, a very sophisticated technology on the whole blood of people with CFS infected with XMRV, and compare the results with appropriate controls, in the hope of finding a pattern and goal differential characteristic of CFS. These techniques will also allow the analysis of the lymphocytes in the study of CFS patient’s immune system. He has also widely described the study that is focused on neutrophil oxidative metabolism and how this may affect their function. As they plan to study the membrane structure of CFS patients, it was suggested to him in the Q&A to have a look on the paper published on Mitochondrial dysfunction a bacterial translocation by Sarah Mhyll and Kenny De Meirleir.
Our conclusion is that all of them have mentioned the importance of an animal model to study the pathogenesis of XMRV. It’s also very important to have accepted tools to work with, and this means the urgent need of a universal kit. They are all working in the same direction, they are sharing lots of data, samples, etc, and they all agreed with the great complicity between the different groups, which they had not observed so far, for the other diseases they have worked on. Good long term perspectives.