*15th July* Dr Lucinda Bateman & Vincent Racaniello - Webinar!
- Thread starter VillageLife
- Start date
FOr thos in the USA you can call in to listen over your phone: 312-878-0218 Access Code: 643-221-242
I'm listening, and the audio is clear and free of distraction.
You'll be asked for a pin number, but are given the option of going through without one.
I'm listening, and the audio is clear and free of distraction.
You'll be asked for a pin number, but are given the option of going through without one.
Cool, Big pharma will teach current clinicians about what CFS is and how to treat it, when we get that far.
I got the feeling Vincent new a lot more then he was aloud to say!
and I think dr Bateman was really positive and excited!!
and I think dr Bateman was really positive and excited!!
I agree, she said better to be a tortoise than a hare. I took that to mean that rushed studies will be shown to be faulty and perhaps the likes of her own and the Alter study will win the day.
And I got a big stack of ironing done while listening and sitting down. A productive afternoon in all.
I hope Dr Bateman gets back to us with the answers to some questions posted as her connection failed.
Paddy x
And I got a big stack of ironing done while listening and sitting down. A productive afternoon in all.
I hope Dr Bateman gets back to us with the answers to some questions posted as her connection failed.
Paddy x
I got the feeling Vincent new a lot more then he was aloud to say!
and I think dr Bateman was really positive and excited!!
and I think dr Bateman was really positive and excited!!
For those who missed it - there were a lot of technical problems (so you didn't miss that much!) - the one golden egg - Lucinda Bateman's positivity about the study she is just finalising - look forward to this being released - but she bascially said - that there are positive things to look forward to - and no news is good news! I was very very encouraged by her words. Everything in her tone, choice of words etc (I think) suggested that she believes XMRV is playing a big role in this disease.
I think I've got a crush on doctor Bateman. Too bad she couldn't answer the patient questions (hope they will appear soon) but I loved her 'turn the negatives into positive' angle. It wasn't hollow optimism, to me it made a lot of sense and it gave me a lot of hope. Wasbeer loves Lucinda :Retro tongue:
LOVE dr Bateman !!!! One thing that I heard that worries me.
Dr. Racaniello talked about HTLV. I believe he said that it was like XMRV with very few copies in the blood, difficult to detect, and that it spreads in the body similar to XMRV (not positive about the spreading but it sounded similar). He then went on to say that there are no anti-retrovirals that work angainst HTLV. The anti-retrovirals that work against HIV work because it is reproducing like mad.
I think he also said that the way HTLV causes disease has to do with what cells or organs are next to infected cells. So even if they can eradicate the HTLV, the disease process will not be stopped.
Maybe this was my pessimistic understanding.
In my mind I had it all worked out in a very simple manner. I would be tested and find I have XMRV. I would take ARVs (maybe current ones or maybe ones that will be developed later). I would then be better.
Now i am not so sure.
Lynn
That really hit home that we are making a big leap
Dr. Racaniello talked about HTLV. I believe he said that it was like XMRV with very few copies in the blood, difficult to detect, and that it spreads in the body similar to XMRV (not positive about the spreading but it sounded similar). He then went on to say that there are no anti-retrovirals that work angainst HTLV. The anti-retrovirals that work against HIV work because it is reproducing like mad.
I think he also said that the way HTLV causes disease has to do with what cells or organs are next to infected cells. So even if they can eradicate the HTLV, the disease process will not be stopped.
Maybe this was my pessimistic understanding.
In my mind I had it all worked out in a very simple manner. I would be tested and find I have XMRV. I would take ARVs (maybe current ones or maybe ones that will be developed later). I would then be better.
Now i am not so sure.
Lynn
That really hit home that we are making a big leap
Lynn it will not be anything like that simple. Sorry but it's maybe a good time for everybody to address that issue. If I'm following the Dr.'s Ruscetti correctly here are some things that might be useful to know to date.
Let me preempt this with a caveat that I'm in over my head on this but since speculation can be fun and there is that desire to push things forward one way or another I just keep poking around in this stuff and the stuff below is what I've come up with. Take it with a grain of salt.
First up I don't think we need to be too concerned with any information in the Sandra Ruscetti video file since it's all on her NCI web site. (grins)
The first part of the research mission statement is pretty clear.
Research
The focus of our research is devoted to understanding the molecular basis for the pathogenesis of retrovirus-induced diseases. We have been studying retroviruses that cause leukemia or neurological disease in rodents to obtain basic information on how molecular changes in normal cells can result in pathological consequences. Our current studies are focused on determining whether similar mechanisms may be utilized by the human retrovirus XMRV to cause cancer and neuroimmune diseases in man. Overall, we hope to use the information gained from our studies to design and test rational strategies to counteract the retrovirus-induced molecular events that are responsible for these diseases.
Pasted from <http://ccr.cancer.gov/staff/staff.asp?profileid=5518>
The thing I noticed most during the video and in looking at the wording is that Ruscetti is looking at models for both cancer and neuroimmune although on the neuroimmune front she is using the PVC-211 mouse model which is a neurological degenerative illness. After listening to and looking up more information on the PVC-211 model I sat down and had a really good cry. I'm personally hoping that we don't have anything like that particular model!
Model 1 the SFFV model
The cancer model is pretty straight forward. It goes like more or less like this.
1- The found that the envelope or capsid portion of the XMRV virus has a "deletion" in it much the same as the SFFV MLV that they had been studying. This means that it can stick to another virus or absorb another virus if and only if that virus has Long Term Repeating Sequences that match the deletion portion.
2- This allows XMRV to hook other viruses either in the cell or going into the cell. I'm not well educated enough to discern which viruses it is most likely to hook but I get the impression that the scientist involved have a good ideal and that somehow or another there maybe other MLV's involved. But that's about as good as I can make out and that includes information from Dusty Millers recent paper as well.
3- That XMRV the pure form of the virus is present in low copy numbers because most of the virus is transformed into a "recombinate" virus type. Miller's work shows that when XMRV is paired with an Onco(cancer causing) gene from a different virus in this case from Firosarcoma that it will combine and produce more cancer causing cells that are different from the original. (This might explain why Elaine DeFrites had problems isolating the virus and why the primer pairs needed to detect the virus didn't always work. If DeFrites was looking at a recombinate viral form then it would change from geographic area to geographic area and would be impossible to actually isolate since it was NOT a pure RNA strand.)
4- That it is highly infectious because it uses an XPR1 receptor. This doesn't mean infectious between persons but rather infectious within the host's cells. XPR1 is the key to open over 80% of all human cells. So XMRV may not turn out to be the puppet master but rather the key master. Combining with a host of other viruses and providing them the opportunity to enter into cells that they wouldn't normally be able to get into.
5- That XMRV has a very high fidelity rate or that it reproduces each copy of itself exactly. This is unusual in viruses that normally change rapidly in order to stay ahead of the host's immune response. In this case XMRV uses it's perfect copies to attract an attach to other viruses. The attached viruses provide cover for the XMRV and the XMRV provides a key to the cell the other virus needs to get into.
So I think the take home message may be something along these lines. The XMRV is a key to over 80% of the cells in the human body. It reproduces exact copies of itself because it is not a virus that needs to change in order to survive, instead it uses parts of other viruses possibly more than one in order to create a range of quasi species that are able to pass undetected by the host's immune system. Since XMRV has the ability to incorporate more than one type of virus into it's genome it can cause more than one type of cancer and more than one type of disease but it is limited to those viruses that will fit into the deletion sequence that is part of the envelope gene of the XMRV virus.
This would explain why CFS patients have a range of "primary" antibody responses that differ. For instance my antibody response is for EBV which may be what my XMRV is bound to, meaning my body senses that the EBV is their but can't do anything about it no matter how much antibody it throws at it because it is protected by its recombination with XMRV. Someone else may have a "primary" antibody response for HHV-6.
Different recombinations are going to produce slightly different disease patterns, hence the troubling subsets of patients.
Let me preempt this with a caveat that I'm in over my head on this but since speculation can be fun and there is that desire to push things forward one way or another I just keep poking around in this stuff and the stuff below is what I've come up with. Take it with a grain of salt.
First up I don't think we need to be too concerned with any information in the Sandra Ruscetti video file since it's all on her NCI web site. (grins)
The first part of the research mission statement is pretty clear.
Research
The focus of our research is devoted to understanding the molecular basis for the pathogenesis of retrovirus-induced diseases. We have been studying retroviruses that cause leukemia or neurological disease in rodents to obtain basic information on how molecular changes in normal cells can result in pathological consequences. Our current studies are focused on determining whether similar mechanisms may be utilized by the human retrovirus XMRV to cause cancer and neuroimmune diseases in man. Overall, we hope to use the information gained from our studies to design and test rational strategies to counteract the retrovirus-induced molecular events that are responsible for these diseases.
Pasted from <http://ccr.cancer.gov/staff/staff.asp?profileid=5518>
The thing I noticed most during the video and in looking at the wording is that Ruscetti is looking at models for both cancer and neuroimmune although on the neuroimmune front she is using the PVC-211 mouse model which is a neurological degenerative illness. After listening to and looking up more information on the PVC-211 model I sat down and had a really good cry. I'm personally hoping that we don't have anything like that particular model!
Model 1 the SFFV model
The cancer model is pretty straight forward. It goes like more or less like this.
1- The found that the envelope or capsid portion of the XMRV virus has a "deletion" in it much the same as the SFFV MLV that they had been studying. This means that it can stick to another virus or absorb another virus if and only if that virus has Long Term Repeating Sequences that match the deletion portion.
2- This allows XMRV to hook other viruses either in the cell or going into the cell. I'm not well educated enough to discern which viruses it is most likely to hook but I get the impression that the scientist involved have a good ideal and that somehow or another there maybe other MLV's involved. But that's about as good as I can make out and that includes information from Dusty Millers recent paper as well.
3- That XMRV the pure form of the virus is present in low copy numbers because most of the virus is transformed into a "recombinate" virus type. Miller's work shows that when XMRV is paired with an Onco(cancer causing) gene from a different virus in this case from Firosarcoma that it will combine and produce more cancer causing cells that are different from the original. (This might explain why Elaine DeFrites had problems isolating the virus and why the primer pairs needed to detect the virus didn't always work. If DeFrites was looking at a recombinate viral form then it would change from geographic area to geographic area and would be impossible to actually isolate since it was NOT a pure RNA strand.)
4- That it is highly infectious because it uses an XPR1 receptor. This doesn't mean infectious between persons but rather infectious within the host's cells. XPR1 is the key to open over 80% of all human cells. So XMRV may not turn out to be the puppet master but rather the key master. Combining with a host of other viruses and providing them the opportunity to enter into cells that they wouldn't normally be able to get into.
5- That XMRV has a very high fidelity rate or that it reproduces each copy of itself exactly. This is unusual in viruses that normally change rapidly in order to stay ahead of the host's immune response. In this case XMRV uses it's perfect copies to attract an attach to other viruses. The attached viruses provide cover for the XMRV and the XMRV provides a key to the cell the other virus needs to get into.
So I think the take home message may be something along these lines. The XMRV is a key to over 80% of the cells in the human body. It reproduces exact copies of itself because it is not a virus that needs to change in order to survive, instead it uses parts of other viruses possibly more than one in order to create a range of quasi species that are able to pass undetected by the host's immune system. Since XMRV has the ability to incorporate more than one type of virus into it's genome it can cause more than one type of cancer and more than one type of disease but it is limited to those viruses that will fit into the deletion sequence that is part of the envelope gene of the XMRV virus.
This would explain why CFS patients have a range of "primary" antibody responses that differ. For instance my antibody response is for EBV which may be what my XMRV is bound to, meaning my body senses that the EBV is their but can't do anything about it no matter how much antibody it throws at it because it is protected by its recombination with XMRV. Someone else may have a "primary" antibody response for HHV-6.
Different recombinations are going to produce slightly different disease patterns, hence the troubling subsets of patients.
Thanks George that was helpful.
So if XMRV recombines with other viruses, does that mean that even if we use antiretrovirals and get a handle on XMRV, we probably still leave the population of aberrant viruses unchecked? Would that then leave our symptoms unchanged?
I am totally bummed about this.
Lynn
So if XMRV recombines with other viruses, does that mean that even if we use antiretrovirals and get a handle on XMRV, we probably still leave the population of aberrant viruses unchecked? Would that then leave our symptoms unchanged?
I am totally bummed about this.
Lynn
I'm Gozer, are you the Key Master? (Too cool, 2 Ghostbusters quotes in 1 day.)
Thanks George for your speculation, it's intriguing if somewhat over this little pup's head.
I'm having a hard time with the immune system part of this so bear with me. If understand this (highly questionable), it seems that a proper antibody response would occur but that the immune system fails later.
Am I understanding that your body would mount an EBV (in your example) antibody response (based on recognizing EBV) but that the T (?) cells wouldn't be able to find (or will find or can't kill) the virus because it's in a combined form?
So EBV goes unchecked and takes XMRV along for the ride to open more doors?
Does this have any implications for looking for XMRV antibodies and controlling XMRV? Does it make XMRV antibodies harder to detect?
This would all seem to get really messy with multiple reactivated infections, especially with unknown or novel pathogens in the mix.
Hope that made the smallest amount of sense...
Thanks George for your speculation, it's intriguing if somewhat over this little pup's head.
I'm having a hard time with the immune system part of this so bear with me. If understand this (highly questionable), it seems that a proper antibody response would occur but that the immune system fails later.
Am I understanding that your body would mount an EBV (in your example) antibody response (based on recognizing EBV) but that the T (?) cells wouldn't be able to find (or will find or can't kill) the virus because it's in a combined form?
So EBV goes unchecked and takes XMRV along for the ride to open more doors?
Does this have any implications for looking for XMRV antibodies and controlling XMRV? Does it make XMRV antibodies harder to detect?
This would all seem to get really messy with multiple reactivated infections, especially with unknown or novel pathogens in the mix.
Hope that made the smallest amount of sense...
Total sense Otis. Yeah, that's the impression I get from what I saw and read afterward. But hey it's a bit over my head as well. (grins) I got the impression that there are antibodies to XMRV but like the virus itself they are low count and this is why there is a problem in finding them every time. I know from my own experience that my EBV reactivation titers are consistently between 3800 and 5700 (over 150 is positive, grins) when I have an EBV flare but there is a big fat 9 (well below the 150 threshold) for the actual "capsid" antibody.
In other words my body is not responding to actual EBV although there is some present because you carry silenced EBV with you for life. Rather the "flare" is caused by proteins put out by the "recombined" XMRV/EBV/MLV combo. It lease that's how the SFFV MLV mouse model works. So there are antibody's to XMRV and to which ever "primary" and later "secondary" infections you have had.
This is not going to be an easy ride.
Lynn While different recombinations are going to produce slightly different disease patterns, hence the troubling subsets of patients. It also explains why some people get "better" on their own, why others do well on Anti-virals, why Ampligen sometimes works and folks trying Anti-Retrivirals like Dr. Deckhoff-Jones are seeing improvement. Any of these strategies will treat a portion of the problem and give the body a much needed boost to allow it's own anti-viral pathways to engage the XMRV base problem more effectively. However, not everyone responds to any single treatment protocol because it doesn't address the other potential problems present in the patient.
Now if you cook up a cocktail that address' say two or more of the problems then you're cookin on the front burner with gas. But of course as Mindy Kitei (www.cfscentral.com) points out in her excellent summary of the IRIS problem that will have to be addressed as well in order for a treatment program to work. But I think that there are far more treatment's that will be rapidly available far more quickly than for say HIV or HTLV or any preceding Retrovirus. I think that it's very, very possible that combination treatments that don't require anymore "clinical trials" will be available within three years. That's seven years faster than HIV!
In other words my body is not responding to actual EBV although there is some present because you carry silenced EBV with you for life. Rather the "flare" is caused by proteins put out by the "recombined" XMRV/EBV/MLV combo. It lease that's how the SFFV MLV mouse model works. So there are antibody's to XMRV and to which ever "primary" and later "secondary" infections you have had.
This is not going to be an easy ride.
Lynn While different recombinations are going to produce slightly different disease patterns, hence the troubling subsets of patients. It also explains why some people get "better" on their own, why others do well on Anti-virals, why Ampligen sometimes works and folks trying Anti-Retrivirals like Dr. Deckhoff-Jones are seeing improvement. Any of these strategies will treat a portion of the problem and give the body a much needed boost to allow it's own anti-viral pathways to engage the XMRV base problem more effectively. However, not everyone responds to any single treatment protocol because it doesn't address the other potential problems present in the patient.
Now if you cook up a cocktail that address' say two or more of the problems then you're cookin on the front burner with gas. But of course as Mindy Kitei (www.cfscentral.com) points out in her excellent summary of the IRIS problem that will have to be addressed as well in order for a treatment program to work. But I think that there are far more treatment's that will be rapidly available far more quickly than for say HIV or HTLV or any preceding Retrovirus. I think that it's very, very possible that combination treatments that don't require anymore "clinical trials" will be available within three years. That's seven years faster than HIV!
Rolling on the floor with all paws up. Yep and we all remember how hard Gozer was to kill! (squealing doggie grins and laughs)
I listened to the webinar today and thought I would post my personal notes (subjective and might include innacuracies, of course):
Karin's notes on the XMRV Webinar 7/15/10
1. Prof. Racaniello talked about the current status of XMRV research (bench)
XMRV was discovered in 2006 in prostate cancer tumors. The virus was not detected directly in the tumor, but rather it
was recovered from CULTURED cells transfected with proviral DNA.
Prof. Racaniello then gave a 101 on retroviruses, how they integrate in the cell DNA (provirus), and how they
replicate. He emphasized a very important distinction in the two modes by which retroviruses replicate:
- production of new virions budding from infected cells, which is the primary replication mode of HIV,
- or, direct transfer of the provirus from one cell to another during cell division, which is the promary replication
mode of HTLV-1. In this case, the pathogenic consequence depends where the proviral DNA inserts in the cell's DNA and
how it might turn genes ON and OFF. Production of virions is not necessarily involved.
Prof. Racaniello then talked about what kind of studies need to be done, for instance to determine if XMRV is the
cause of a disease or just a passenger. He stated that case-studies are needed that have the following features:
- multi-city, multi-continent,
- well-defined patient population,
- look into transmission modes,
- determine the seroprevalence in healthy individuals,
- determine what fraction of infected people develop disease,
- use multiple assays simultaneously to determine infection, to avoid false negative/false postives: virus/proviral
DNA/viral proteins/antibodies,
- determine which tissues and cells the virus replicates in,
- is there a specific type of cells infected that could explain disease, as it is the case for CD4+T in AIDS,
- is there a consistent integration site that would explain pathogenesis.
Prof. Racaniello then presented a table listing the studies examining XMRV that have been published so far, and listed
some possible reasons for inconsistence in the results:
- selection of patients,
- geographic differences,
- differences in viral sequences,
- no standardized sensitive methods, this being the main issue in his opinion.
There he mentioned a very important point, in my opinion: THE SCIENCE LOMBARDI PAPER DESCRIBED THAT PCR WAS USED TO
DETECT PROVIRAL DNA IN PBMC. This is the method that most other papers tried to reproduce. THE METHOD OF IN-VITRO
CULTURE OF PBMC TO AMPLIFY XMRV HAS NOT BEEN PUBLISHED YET. This might be reason why other labs have issues
reproducing the Lombardi results.
Prof. Racaniello then explained the differences between HTLV-1 and HIV, noting that both are very different.
HTLV-1:
- transmitted cell to cell, not through free virions like HIV,
- multiplies as the cell divides,
- is detected by looking at antibodies in serum with ELISA,
- virus isolation is not used for diagnosis because there are no free virions,
- no proven antivirals exist to treat it,
- it is unknown whether eliminating the virus would impact the progression of the disease.
HIV:
- millions of viral particles can be detected in a milliliter of blood,
- is treatable by limiting the virus production with antiviral therapies HAART.
Prof. Racaniello then stated that animal models of XMRV will be needed to understand the disease. He mentioned the
rhesus macaques study, that was not published but was presented at a conference earlier this year. The animals had low
viral load in their plasma.
Prof. Racaniello then presented the history of AIDS and HTLV as examples of the amount of time needed from discovery
to treatment:
AIDS was discovered in 1982 and HAART started being implemented in 1995.
HTLV-1 was discovered in 1970 as the cause of ATL, Human T Cell Lymphoma. In 1986, it was also associated to another
disease, myelopathy. Since then, blood has been screened for HTLV.
HTLV-2 was identified in 1985 but so far has not veen associated with any disease.
Both HTLV and HIV are thought to have originated from non-human primates. XMRV likely originated from mice.
(My own note: interesting that so many different human retroviruses appeared in the 70's, and originated from animals
commonly used in laboratories: monkeys and mice.)
Prof. Racaniello finished his persentation with Koch's Postulate: how can it be determined if a given bacteria causes
disease. And how do adapt this postulate to viruses.
Prof. Racaniello's blog can be found on: www.virology.ws
************************************************************************
2. Dr. Bateman talked about the clinical aspects of CFS (bed-side)
She started by stating that when she accepted this webinar invitation several months ago, she was hoping she would be
discussing the latest research done in Utah by Dr. Singh (spelling?). However, publication has been delayed and since
it has not been published yet she cannot say anything. She emphasized though that she was SURE we were going to hear A
LOT from this publication very soon...
She then spent a good part of her talk talking about the good things coming from the XMRV controversy, then was
disconnected.
*************************************************************************
3. Q/A with Prof. Racaniello (Dr. Bateman still disconnected)
- End of Karin's notes -
Karin's notes on the XMRV Webinar 7/15/10
1. Prof. Racaniello talked about the current status of XMRV research (bench)
XMRV was discovered in 2006 in prostate cancer tumors. The virus was not detected directly in the tumor, but rather it
was recovered from CULTURED cells transfected with proviral DNA.
Prof. Racaniello then gave a 101 on retroviruses, how they integrate in the cell DNA (provirus), and how they
replicate. He emphasized a very important distinction in the two modes by which retroviruses replicate:
- production of new virions budding from infected cells, which is the primary replication mode of HIV,
- or, direct transfer of the provirus from one cell to another during cell division, which is the promary replication
mode of HTLV-1. In this case, the pathogenic consequence depends where the proviral DNA inserts in the cell's DNA and
how it might turn genes ON and OFF. Production of virions is not necessarily involved.
Prof. Racaniello then talked about what kind of studies need to be done, for instance to determine if XMRV is the
cause of a disease or just a passenger. He stated that case-studies are needed that have the following features:
- multi-city, multi-continent,
- well-defined patient population,
- look into transmission modes,
- determine the seroprevalence in healthy individuals,
- determine what fraction of infected people develop disease,
- use multiple assays simultaneously to determine infection, to avoid false negative/false postives: virus/proviral
DNA/viral proteins/antibodies,
- determine which tissues and cells the virus replicates in,
- is there a specific type of cells infected that could explain disease, as it is the case for CD4+T in AIDS,
- is there a consistent integration site that would explain pathogenesis.
Prof. Racaniello then presented a table listing the studies examining XMRV that have been published so far, and listed
some possible reasons for inconsistence in the results:
- selection of patients,
- geographic differences,
- differences in viral sequences,
- no standardized sensitive methods, this being the main issue in his opinion.
There he mentioned a very important point, in my opinion: THE SCIENCE LOMBARDI PAPER DESCRIBED THAT PCR WAS USED TO
DETECT PROVIRAL DNA IN PBMC. This is the method that most other papers tried to reproduce. THE METHOD OF IN-VITRO
CULTURE OF PBMC TO AMPLIFY XMRV HAS NOT BEEN PUBLISHED YET. This might be reason why other labs have issues
reproducing the Lombardi results.
Prof. Racaniello then explained the differences between HTLV-1 and HIV, noting that both are very different.
HTLV-1:
- transmitted cell to cell, not through free virions like HIV,
- multiplies as the cell divides,
- is detected by looking at antibodies in serum with ELISA,
- virus isolation is not used for diagnosis because there are no free virions,
- no proven antivirals exist to treat it,
- it is unknown whether eliminating the virus would impact the progression of the disease.
HIV:
- millions of viral particles can be detected in a milliliter of blood,
- is treatable by limiting the virus production with antiviral therapies HAART.
Prof. Racaniello then stated that animal models of XMRV will be needed to understand the disease. He mentioned the
rhesus macaques study, that was not published but was presented at a conference earlier this year. The animals had low
viral load in their plasma.
Prof. Racaniello then presented the history of AIDS and HTLV as examples of the amount of time needed from discovery
to treatment:
AIDS was discovered in 1982 and HAART started being implemented in 1995.
HTLV-1 was discovered in 1970 as the cause of ATL, Human T Cell Lymphoma. In 1986, it was also associated to another
disease, myelopathy. Since then, blood has been screened for HTLV.
HTLV-2 was identified in 1985 but so far has not veen associated with any disease.
Both HTLV and HIV are thought to have originated from non-human primates. XMRV likely originated from mice.
(My own note: interesting that so many different human retroviruses appeared in the 70's, and originated from animals
commonly used in laboratories: monkeys and mice.)
Prof. Racaniello finished his persentation with Koch's Postulate: how can it be determined if a given bacteria causes
disease. And how do adapt this postulate to viruses.
Prof. Racaniello's blog can be found on: www.virology.ws
************************************************************************
2. Dr. Bateman talked about the clinical aspects of CFS (bed-side)
She started by stating that when she accepted this webinar invitation several months ago, she was hoping she would be
discussing the latest research done in Utah by Dr. Singh (spelling?). However, publication has been delayed and since
it has not been published yet she cannot say anything. She emphasized though that she was SURE we were going to hear A
LOT from this publication very soon...
She then spent a good part of her talk talking about the good things coming from the XMRV controversy, then was
disconnected.
*************************************************************************
3. Q/A with Prof. Racaniello (Dr. Bateman still disconnected)
- End of Karin's notes -
Thanks Karin that was a nice summary. Woof, woof lick, grins!
Thankyou George
(And thanks to Otis as well.)
George your long post explained so much:
Most importantly what treatment will look like and a guess on when it might be available
and
an explanation of mechanism and variety of disease presentation.
I know its only speculation at this stage but its drawing a laymans picture of the path out of hell. Its making it real. Just having the label "retrovirus" was helpful but not enough detail (especially 9 months after the Science paper) .
Looking forward to watching the webinar on youtube. (broadcast in the middle of the night my time)
OTH
(And thanks to Otis as well.
)George your long post explained so much:
Most importantly what treatment will look like and a guess on when it might be available
and
an explanation of mechanism and variety of disease presentation.
I know its only speculation at this stage but its drawing a laymans picture of the path out of hell. Its making it real. Just having the label "retrovirus" was helpful but not enough detail (especially 9 months after the Science paper) .
Looking forward to watching the webinar on youtube. (broadcast in the middle of the night my time)
OTH
Way cool OTH, I stuck it on a blog along with my old mouse theory so it will be easier to find. Get some sleep. Woof, woof!