XMRV infection rate points to cofactor not sole cause

[Wonko]

have you considered applying the same arguement to any other viruses? and the impact this may have oh your hypothesis

eg almost any virus can be mutated and deactivated by the hosts defenses - therefore it doesnt cause any disease process or infection?

in a lot of ilnesses/deseases it's the host own defenses that cause most symptoms - and given there is an autoimmune component to ME anyway............

so relevance may be an issue here (at least IMO)

 

[Fejal]

Immunity is short lived so after the virus is deactivated the immune response eventually goes down to zero so there's no reason for there to be an autoimmune reaction unless a self sustaining co-infection hopped on board while the immunity was compromised.

Also the odds of random mutations giving the same illness are so small they might as well be zero.

This is why XMRV is a waste of our time except to recognize it as a trigger.

 

[Wonko]

ermm..ever heard of arthritis?

arent you in your last sentence actually agreeing withe thw WPI position - that a probable senario is that XMRV introduces a weakness in the hosts immune system which other pathogens then exploit - note that this doesnt mean that XMRV isnt responsible for the condition we know and love - as without it the conifections would be easiy cleared - a similar effect tho not the same mechanism as HIV/AIDS

 

[Fejal]

Do you understand the difference between a trigger and a sustaining pathogen? Triggers are time limited. You can treat them after they've infected the person but all that will do is prevent the initial onset of the coinfections by reducing the time window available to the pathogen. It won't cure anyone whose already infected-which is the main goal for most CFS patients.

I am extremely glad the body can recover from the XMRV retrovirus. If it couldn't we would be looking at a much bleaker situation. Co-infections are curable if they are properly diagnosed and treated.

All this buzz about XMRV is really misinforming most people as to the role this virus plays in CFS.

 

[Wonko]

hold on - hold on - I know that one...............

 

[Wonko]

however there is one small problem here - okay more than one but here's the first one I can think of (lol) - MLV's have been detected after at least 15 years infection - so whilst your arguement seems to be that the body can mutate and clear them to oblivion (so a descrete something else must be the cause of ME) this is demostratably not the case - or are infections which last 15 years normal in healthy people......

btw I am not a medical professional and am as defined by the NHS quite mad because I believe I have a medical condition which doesnt realy exist - in my insanity it's much easier to ascribe my imagined illness to a series of letters which I dont really understand the meaning or implications of

any assistance you as a medical professional can provide me with to cure my rampant insanity and malingering would be appreciated by Her Majesties Government and the Big Society as a whole (ie the people who pay for me to lie around whining)

 

[Fejal]

You changed the subject Wonko. We're talking about XMRV not MLV. MLV is itself a mutation of XMRV and might have been one of the few bugs that survived the mutation process. If it is self sustaining then yes there is probably a cohort of patients with very broken immune systems who need specific treatment for MLV. These patients should be identifiable because their symptoms would not increase in response to L-form bacterial therapeutic probes.

However, XMRV patients should rejoice because the odds are they don't fall into this category. If MLV is really the key to CFS in MLV infected patients they have my condolensces as It could take decades before an effective treatment is available. It seems humanity has a few more terrible plagues to get rid of before we can relax.

 

[Wonko]

or another way of lookign at it (a more accurate way afaik) is XMRV's are a mutation of an MLV (or group thereof) - it's a subgrouping of MLV's according to my , admittedly limited, understanding

specifically (again accordign to my limited understanding) XMRV's are a group of MLV's that mice (most mice) are now immune to by virtue of a cell wall mutation that blocks access to the virus - afaik all the mice which didnt possess this mutation died out - which is odd if cells which XMRV's can enter are so good at mutating them out of existence

but as I said I know next to nothing about any of this - and I really hope your right - it's just it doesnt look that way to this ignorant lunatic atm

This is why XMRV is a waste of our time except to recognize it as a trigger.

Who's time would that be then? I have nothing but time, no resources or energy to do anything productive with it - but plenty of time

 

[xrayspex]

LMAO
leprechauns and mojo love it

well alrighty then, I will just go back on dr. crooks yeast diet, worked so well 15 years ago

 

[heapsreal]

if l form bacteria are the treatment point of those with xmrv, why arent those on long term antibiotics actually recovering, i know some cfsers get improvement with abx but very few recover.

 

[Fejal]

That's really a separate issue. L-forms live inside white blood cells which they block from mounting an effective immune response. Traditional medicine approaches with antibiotics are said to not be that effective because:

1) The bacteria are inside the cells so the concentration of abx is too low to knock them out.
2) Unless the immune function is restored the cells just reinfect as soon as the abx is stopped.
3) Normal doses of abx are too high because the bacteria are so pervasive, so you have to kill it in a manageable way.

Right now I'm experimenting with coconut oil in conjunction with the BALI protocol. Medium Chain Fatty Acids are strongly antibiotic and are said to be used by nursing mothers to protect infants from infections. Given my compromised immunity this is exactly what I need. It has been tricky because it causes gastritis side effects but is remedied with lecithin granules. The bacteria express in a three day cycle so some days manifest more symptomatology than others. Hopefully this will work. I'm also trying to get labs to confirm the species as bartinella spp.

 

[heapsreal]

Im not trying to sound negative but trying to understand your approach, if traditional antibiotics dont work, how does coconut oil/medium chain triglyerides work any better if using them for its antibiotic affect. My understanding with abx is that by using them you stop them from infecting other cells when they are released from inside white blood cells and into general circulation, in a way keeping them dormant. Eventually white blood cells die off as they only have a life cycle of so long, i think this is the reason given for using abx long term. Can i also ask how you are tested for l-form bacteria eg blood test and is it easy to obtain.

The BALI approach, correct me if im wrong, is an improved version of the marshall protocol, so does this version try to switch on the immune system to find these l-form infected white cells. The marshall protocol supposedly did this by lowering our vit d levels which then altered our vit d receptors which then helped our immune system to find these bacteria hiding in our white cells, benicar was used to help control herx reactions and possibly something else but cant recall. Can u explain how the bali approach differs??

cheers!!!

 

[Fejal]

Hello heapsreal:

BALI approach differs from the Marshall Protocol approach in many ways:

• It rejects the theory that bacterial L-forms are ever present and instead sees them as pathogens who typically can only infect a host when a virus or other factor lowers immunity enough for them to colonize enough to sustain a complete block of immunity. If the trigger is not temporary then additional treatment must be provided to either eliminate the trigger or provide some kind of immunological restoring work around treatment in order for BALI to be effective.
• It does not put patients into an inflammatory state through omega 3 fatty acid deprivation.
• It uses supplementation responses and lab testing to positively identify which specific pathological organisms have infected the host, which are then targeted for elimination with specific supplements, lifestyle changes, superfoods and drugs.
• It uses intentional dietary and lifestyle change to induce hyovitaminosis D; this along with benecar prescription is used to restore a blocked vitamin D receptor immune pathway.
• It uses supplementation to enhance detoxification to reduce the severity of herxheimer and inflammatory reactions.
• Response time is much faster.

Regarding the mechanism for coconut oil killing bacteria, Yang showed bacteria do absorb and try to use it for energy so it must somehow poison their cellular metabolism.(1) Gill-Varina demonstrated that it is toxic to chick mitochondria.(2) Given the similarity between L-forms and mitochondria it is reasonable to assume that the bacteria are trying to use the MCFAs for cellular activities but are not adapted to do this without being killed while humans are protected by virtue of genetic evolution of liver detoxification pathways (which is specifically enhanced on BALI). Regardless of this effect, I am wary of keeping people on coconut oil MCFAs long term; but in the short term, given the safety record with mother's breast milk, I think it's pretty safe provided people aren't deprived of omega 3 and omega 6 fatty acids.

So while the exact mechanisms are yet to be revealed, the clinical outlook is encouraging. Hopefully it will work.

REFERENCES

1. Yang, D. The Antimicrobial Activity of Liposomal Lauric Acids Against Propionibacterium acnesBiomaterials. 2009 October ; 30(30): 6035–6040. doi:10.1016/j.biomaterials.2009.07.033. Author's Manuscript available online.
2. Gill-Varina, A. Supplementation of coconut oil from different sources to the diet induces cellular damage and rapid changes in fatty acid composition of chick liver and hepatic mitochondria.Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1997 Jul;117(3):243-50.)