Might CCSVI be caused by a VIRUS?
Posted: Sun Nov 29, 2009 11:25 pm
Hello from a newbie!
Several blogs on Dr Zamboni's stunning breakthrough have alluded to a thought-provoking and important (potential) paradox: a) Why is MS more prevalent in colder climates (eg. Canada)? b) How do we reconcile this with Zamboni’s finding of structural changes in veins?
Here is my kick at the can – mostly a collection of (potentially connected) observations and hypotheses:
1) Higher latitudes have less sun;
2) Less sun = less vitamin D
3) Susceptibility to certain viruses is believed to be affected by low vitamin D levels
4) Some viruses cause inflammation of blood vessels (vasculitis), particularly the inner lining or endothelium, narrowing the opening (lumen) of the blood vessel through swelling, vasospasm, immune complex deposition, etc.
5) Changes to the endothelium (lining) of blood vessels can affect “stickiness” of the vessel – potential for blockage?
6) Compromised blood flow might be like a snowball effect – think of river deltas, where “stuff” is deposited at the edges, as flow reduces
7) Is the problem in the veins, or in the valves of the veins? Consider that other auto-immune problems with oft-suspected viral involvement also have known valve problems (eg. Rheumatoid arthritis and heart valves – i.e. the mitral valve). Can auto-immune dysfunction in MS affect the valves in veins?
And FYI – hot new research (still to be replicated) from the esteemed journal Science - a retrovirus named “XMRV” was recently linked with chronic fatigue syndrome, malignant prostate cancer, and – you guessed it – atypical MS. Retroviruses are known to potentiate other infections (think HIV – patients often die of other opportunistic viruses). Has the MS community dug deeply enough into the viral angle?
In other words, the CAUSE of MS might not be narrowing of the veins exiting the brain, resulting in reduced flow, and iron deposition in the brain. That might be the RESULT of a viral infection, in turn resulting in inflammation of those exit veins, and blockage. And a viral infection might in turn be the result of a myriad of genetic/environmental/host factors.
In other words, all the causes of MS might ultimately be proven to be right, in their own way. It’s an “and/and” proposition. MS might be the result of Chronic cerebrospinal venous insufficiency AND auto-immune dysfunction AND viral infection AND genetic factors AND…
I’m a rehab medicine professional, physically, if not intellectually sidelined by CFIDS/ME (Chronic Fatigue Immune Disorder Syndrome). But if I were a molecular biologist, virologist, vascular specialist, or pathologist, I’d want to look even further upstream, with the question in mind: “WHY ARE THESE VEINS BLOCKED”? I’d want to look pronto at biopsy/autopsy specimens of those blocked veins. Do immunohistochemical analysis to look for auto-antibodies against vascular endothelium. Do aggressive viral assays (eg. PCR) to search for an underlying virus – or retrovirus.
This might bridge those two seemingly disparate findings: latitude-related MS incidence, and physical changes in blood vessels.
I'm speaking from the perspective of a CFIDS/ME patient with an 11 year case of chronic parvovirus B19 (PVB19). PVB19 is known to cause endothelial inflammation, hence my stroke-like symptoms, atypical angina (coronary artery vasospasm) - and my positive heart biopsy for PVB19, antibodies against endothelium/myocardium, +ve PCR etc. I can't help wondering if the broader MS population turns out to have XMRV too - or another as-yet undetected virus. I can't help wonder whether a virus might be the smoking gun that connects MS with vasculitis - and potentially even with CFIDS/ME.
Those of us in the CFIDS/ME community are also waiting with bated breath for more info on the XMRV retrovirus - specifically for replication of this groundbreaking research. It would certainly explain why I can't fight off this chronic parvovirus infection - an infection most of us get, and just shrug off as a "flu"!. After all, that's what retroviruses do - they potentiate opportunistic infections.
Bottom line, I can't help wondering why some MS patients relapse after the Liberation procedure. Is there an underlying virus-induced vasculitis that re-blocks the veins? And if you identify and deal with the virus (if there is one), might that eliminate the need for repeat procedures?
Something to think about…
Congratulations to your community on this riveting CCSVI finding, and know that other patient groups are wishing you WELL! Oh, and “YES” to a Nobel for Dr Zamboni. I’ll eat my hat if his results aren’t replicated. [/i]
Several blogs on Dr Zamboni's stunning breakthrough have alluded to a thought-provoking and important (potential) paradox: a) Why is MS more prevalent in colder climates (eg. Canada)? b) How do we reconcile this with Zamboni’s finding of structural changes in veins?
Here is my kick at the can – mostly a collection of (potentially connected) observations and hypotheses:
1) Higher latitudes have less sun;
2) Less sun = less vitamin D
3) Susceptibility to certain viruses is believed to be affected by low vitamin D levels
4) Some viruses cause inflammation of blood vessels (vasculitis), particularly the inner lining or endothelium, narrowing the opening (lumen) of the blood vessel through swelling, vasospasm, immune complex deposition, etc.
5) Changes to the endothelium (lining) of blood vessels can affect “stickiness” of the vessel – potential for blockage?
6) Compromised blood flow might be like a snowball effect – think of river deltas, where “stuff” is deposited at the edges, as flow reduces
7) Is the problem in the veins, or in the valves of the veins? Consider that other auto-immune problems with oft-suspected viral involvement also have known valve problems (eg. Rheumatoid arthritis and heart valves – i.e. the mitral valve). Can auto-immune dysfunction in MS affect the valves in veins?
And FYI – hot new research (still to be replicated) from the esteemed journal Science - a retrovirus named “XMRV” was recently linked with chronic fatigue syndrome, malignant prostate cancer, and – you guessed it – atypical MS. Retroviruses are known to potentiate other infections (think HIV – patients often die of other opportunistic viruses). Has the MS community dug deeply enough into the viral angle?
In other words, the CAUSE of MS might not be narrowing of the veins exiting the brain, resulting in reduced flow, and iron deposition in the brain. That might be the RESULT of a viral infection, in turn resulting in inflammation of those exit veins, and blockage. And a viral infection might in turn be the result of a myriad of genetic/environmental/host factors.
In other words, all the causes of MS might ultimately be proven to be right, in their own way. It’s an “and/and” proposition. MS might be the result of Chronic cerebrospinal venous insufficiency AND auto-immune dysfunction AND viral infection AND genetic factors AND…
I’m a rehab medicine professional, physically, if not intellectually sidelined by CFIDS/ME (Chronic Fatigue Immune Disorder Syndrome). But if I were a molecular biologist, virologist, vascular specialist, or pathologist, I’d want to look even further upstream, with the question in mind: “WHY ARE THESE VEINS BLOCKED”? I’d want to look pronto at biopsy/autopsy specimens of those blocked veins. Do immunohistochemical analysis to look for auto-antibodies against vascular endothelium. Do aggressive viral assays (eg. PCR) to search for an underlying virus – or retrovirus.
This might bridge those two seemingly disparate findings: latitude-related MS incidence, and physical changes in blood vessels.
I'm speaking from the perspective of a CFIDS/ME patient with an 11 year case of chronic parvovirus B19 (PVB19). PVB19 is known to cause endothelial inflammation, hence my stroke-like symptoms, atypical angina (coronary artery vasospasm) - and my positive heart biopsy for PVB19, antibodies against endothelium/myocardium, +ve PCR etc. I can't help wondering if the broader MS population turns out to have XMRV too - or another as-yet undetected virus. I can't help wonder whether a virus might be the smoking gun that connects MS with vasculitis - and potentially even with CFIDS/ME.
Those of us in the CFIDS/ME community are also waiting with bated breath for more info on the XMRV retrovirus - specifically for replication of this groundbreaking research. It would certainly explain why I can't fight off this chronic parvovirus infection - an infection most of us get, and just shrug off as a "flu"!. After all, that's what retroviruses do - they potentiate opportunistic infections.
Bottom line, I can't help wondering why some MS patients relapse after the Liberation procedure. Is there an underlying virus-induced vasculitis that re-blocks the veins? And if you identify and deal with the virus (if there is one), might that eliminate the need for repeat procedures?
Something to think about…
Congratulations to your community on this riveting CCSVI finding, and know that other patient groups are wishing you WELL! Oh, and “YES” to a Nobel for Dr Zamboni. I’ll eat my hat if his results aren’t replicated. [/i]