Monday, 15 October 2012

Unrelated Blogger Comments-October

Sometimes you what to say something that is unrelated to the threads. This is a spot for You. Previous comments can be got at on the posts on the right of the main page.


Anonymous said...
RE: ccsvi I have a friend who underwent PTA in June last year. She has poor mobility and the procedure did nothing for this. BUT it did instantly stop her MS fatigue which had been even more of a problem than her walking. She tells me it disappeared 'as if by magic' and has not returned. If it's a placebo effect, it's pretty amazing! What do you think the explanation is?
MouseDoctor said...
I am very happy that the fatigue has gone. I can not explain it, because I do not know what the root of fatigue is.

Maybe it is caused by mediators such as through made by immune cells.

As I have said before if effects are so instantaneous then it should be easy to show so trials sound give instant read outs.


61 comments:

  1. I know that ECTRIMS 2012 is just around the corner. Any feel for what we can expect i.e. breakthroughs, neuro-protection research, repair research. Or will it be the same-old, same-old e.g. infterferon v copaxone? Are you presenting any research?

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  2. If you want an early flavour of what ECTRIMS 2012 has to offer. You can search the contents

    http://registration.akm.ch/einsicht.php?XNKONGRESS_ID=171&XNSPRACHE_ID=2

    Remember it is usually same old same old with a bit of new stuff each year. I suspect you know most of what is round the corner.




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  3. There are a few interesting looking presentations. Lots of BG12 MRI data which looks promising as showing a degree of neuroprotection. There are also some (autologous) stem cell trial results being shared which should be of interest. I'd hope we'll at least hear on the grapevine how the Alemtuzumab extension is going (now year 6 and hopefully many are still stable).

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  4. Prof G refers in another post to NED (or NEDA) as (apparent on all current measures) complete remission of MS in patients. For newly diagnosed 'average' patients (i.e. not highly active/aggressive) is this a realistic treatment aim based on drugs currently or about to available (leaving aside funding, NICE issues etc)? Is our current/soon to be available array of MS drugs from IFN right up to HSCT now at such a level that this is realistic? My view is my neurologist should be able to recommend treatments to achieve this and if MRI/clinical measures show it has not been achieved (allowing for the time it takes for different DMDs to take effect) I should then be offered a different option (and not necessarily escalating - I'd personally jump right in with Lemtrada as it will then be). Until I achieve NEDA then we must keep trying new strategies - only stopping when my risk appetite is exceeded. Is this a fair approach or is it expecting too much?

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  5. Time for neuros to put patients first. What does the patient want? To limit damage = disease free status. Surely neuros should prescribe the best available treatments. You're the doctors - don't let the men in grey suits tell you how to treat.

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  6. Anon 9.29:: Your neuro can always prescribe anything if YOU are willing to pay for it. Look at Prof G's latest presentation on NICE guidelines for the NHS. Your neuro can't make trhe NHS pay for something that is outside the guidelines

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  7. You're the doctors - don't let the men in grey suits tell you how to treat.


    The men in the grey suits are the doctors. I call it neurology grey:-)
    Next time you see a neuro (male) see if they are wearing grey

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  8. News today centres on research in Australia using PI3K (which is already used in other autoimmune diseases). Any observations on the work MouseDoc?

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  9. Yes I saw it, it is yet another example of a drug that inhibits the development of EAE.

    Comerford I, Litchfield W, Kara E, McColl SR. PIKγ Drives Priming and Survival of Autoreactive CD4(+) T Cells during Experimental Autoimmune Encephalomyelitis.
    PLoS One. 2012;7(9):e45095. Epub 2012 Sep 13.

    Plos is open access so you can read the paper

    I have had the same or better data with quite a large number of drugs in my past. So it is one more of the potential treatments for RRMSers.

    I decided not to do a post on it as it yet another of the "cures of the week". I could pick a few of these each week. Do you think I should do a feature?

    With these early studies I can get accused of being jaded, because I see holes that I would like to be filled. I could enthuse about drug. The effect looks pretty solid.

    I would have liked the model to be more robust as the placebo scores were modest. It is always easier to stop weak disease.

    The researcher is quoted on MSRC that they think it is at least 5 years from being a drug I would say that this is a naive view it will usually take longer.

    "It was preventive and also we could reverse the disease ..Progression breakthrough" This is a terminology has become common and I don't like it because it (a) implies going back to start, this is never shown. It is a case of inhibiting the disease going forward. There is a difference (b) something about progressive MS when it is about RRMS

    I did have a look in the patent database and their are a few companies that have drugs against this target. They will be the ones who could be really excited

    I would also need to do homework. The specificity of biology is often on the cell surface and the messengers in the cell from these receptors are common to many pathways. It is conservatism in biology. So you need to find out what PI3K gamma does for other cells as the side-effect profile could be marked PI3K is a molecule used in cell proliferation etc etc.

    http://en.wikipedia.org/wiki/Phosphoinositide_3-kinase

    PS it could be the best thing since sliced bread.....too early to say

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  10. Thanks MouseDoc.

    I entirely appreciate what you mean about "cures of the week" - but we only need one or two of the more exciting ones to turn out to be right and then MS could be transformed, so it's helpful to have a view on which have real potential and which are just pure EAE spin!

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  11. Do we have a sense of what drives mild vs severe MS (RRMS) other than frequency of replase/location of lesions?

    For example, amongst MSers I know there is one lady who has very frequent relapses (and commensurate lesions) but each one is incredibly mild. Another has maybe one every other year but it is always severe. So, the former might have a bit of eye pain whereas the latter will lose all vision etc. The former never has enhancing lesions and the latter always does. Is there something around the strength of the immune response? i.e. in some people the immune system is only slightly 'out of whack' and so has a 'nibble' at the myelin (and a low level of inflammatory response) whereas others it is much stronger and destroys it much more comprehensively (and high inflammatory response)? Equally, presumably the former would respond better to immunmodulation DMT (i.e. not as much is needed to get back to a balanced immune response)? Do we see that in trials - better response by degree of relapse severity or EDSS - ignoring time since onset of MS? Is there ever such a cross-section study carried out within the major DMT trials? eg in the BG-12 trials has there been a comparison of response by degree of disability? Sorry - lots of questions but I think it is an interesting area!

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  12. Minocycline...

    Has had a brief mention on here from time to time but not a lot. I've just read a paper: http://www.ncbi.nlm.nih.gov/pubmed/21565409 extolling it's "anti-inflammatory, neurprotective and immunomodulatory effects". Not many trials have been done, a few are underway so it's clearly relatively unproven. However, as someone not currently on a DMT (still trying to decide which one/waiting for BG12 and/or Lemtraded to be approved) would Minocycline represent a reasonable, safe, potentially effective 'holding' therapy to minimise any damage whilst making longer term DMT decisions? I'd assume even a (relatively forward thinking) GP could prescribe Minocycline off-label.

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  13. Re 'cure of the week' - I'm not interested in anything that is more than a few years away from human trials or where we are not even sure if human trials will ever happen

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  14. I have found some intersting things about Chinol and Inositol.
    But it seems that these traces stopped somewhere in the late 70's to the early 80's.

    E.g.:

    http://archneur.jamanetwork.com/article.aspx?articleid=576694

    Could you tell me your opinion about these two alcohols?
    And are there any actual studies going on?

    Thanks!

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  15. Talking about cure of the week, what's this about PEDF repairing myelin on the MSRC website today?

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  16. Great to meet Stephanie Millward today. Truly inspirational and reminds us all why we do what we do.
    Those medals are heavy!!
    Let's hope that she gets more funds to continue with her outstanding swimming career.

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  17. Here here MouseDoctor2.

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  18. How about this cure of the week: 'multistem'? A stem cell treatment by a company called Athersys that claims to have both immunomodulatory and remyelinating properties in EAE. Mousedoc?

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  19. "I entirely appreciate what you mean about "cures of the week" so it's helpful to have a view on which have real potential and which are just pure EAE spin!"

    Easiest to assume they are all pure EAE spin and then wait until they surface in human studies. I will report from time to time, usually if I see them in the media.

    The pure immune modulators are going to stuggle to do better than current or soon to be current drugs, so the ethics of testing them is going to be the issue.

    I will post every now and then depending on what else is in the news, if there is less on MS you may get one. However we will try focus on things that are in the not too distant future.

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  20. Do we have a sense of what drives mild vs severe disease.

    Still lots of unknowns, I'll leave this to Prof G as his pulse is more on the effects of treatment

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  21. Minocycline

    One can make arguments for use of minocycline as well as other agents, but the question were is the evidence base in humans..that is what is lacking.

    Until that is present I am sure Prog G can not make any recommendations.

    I certainly would not base my plans on the EAE literature, as some of it is almost certainly flawed because of unreported toxicity

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  22. I have found some intersting things about Chinol and Inositol.

    The only alcohols I can comment on is ethanol and no I do not drink real-ale:-)

    sorry I don't know there were some spectral studies on inositol I think the question is what does it represent-monitor?

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  23. Multistem'?

    I cannot comment on this except to say it is a company press release. These are usually advertising to help raise funds. This company has the backing of fastforward from the NMSS USA and let us hope it goes somewhere.

    This press release is to report that the company are presenting at a meeting, which I am not attending and so have no access to the data.

    I have heard claims of stem cells
    having both immunomodulatory and remyelinating properties in EAE. Unless we see the data we cannot comment on whether it is impressive or not.

    Check out recent post

    http://multiple-sclerosis-research.blogspot.co.uk/2012/09/neural-stem-cells-will-be-no-use-as.html

    So what is the experimental design.

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  24. Waiting for Profs G & B to give their opinions on Ben Goldacre's new Ted talk

    You can see it here
    http://www.badscience.net/2012/09/i-did-a-talk-at-ted-about-drug-companies-and-hidden-data/

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  25. Ted Talk-Yep there is a load of rubbish published in so called quality journals.

    If you want more read Bens new book..Bad Pharma

    Maybe MS pharma need to watch out in case they get Goldacred!!!
    Are they squeeky clean?

    Do they publish all trials?

    The science community, pharma and Journal editors need to pull their fingers out to stop all this toothless rhetoric. Does this happen? Yes it does we have a paper submitted on this very aspect

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  26. Whenever I talk to people about RRMS I say that most neurologists nowadays believe that early aggressive treatment is the way forward- but is this right? A lady with PPMS commented on the MS and depression blog that more seasoned neurologists she knew didn't believe in it than did, and that an esteemed neurologist at her hospital felt early aggressive treatment did nothing of any significance. Is there any consensus in the world of neurology?

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  27. Anonymous 10.10
    Many neurologists are more conservative than others. I would suggest that younger ones with a more open mind (such as Prof G) would agree that the earlier and more aggressive the treatment, the better the chances of an improved long-term outcome, which seems to be borne out by the data from trials.
    Sadly it seems to be the luck of the draw what sort of neurologist you get. Hopefully soon the consensus will be established that early treatment is the way to go.

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  28. It seems to me that early is beyond question the right way to go. The real question is how aggressive? I'm newly diagnosed and have virtually zero symptoms and have never had any objectively measurable deficit (as opposed to some annoying subjective signs). My EDSS is therefore zero and has never gone above zero. I have a pretty high risk profile - if I thought it was the right thing to do I'd go straight to Alemtuzumab, for example. My neurologist is keen for me to wait and go onto BG12 once licensed (I know I'd have to pay for this privately for the time being). Does early BG12 count as early aggressive or would Prof G say that is early but not aggressive enough to have a material long-term impact? I'm willing to jump straight to a more aggressive treatment. I guess my question is does BG12 accord with early, aggressive or it is too 'mild'? Prof G?

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  29. Not sure early BG12 counts as "aggressive" but it is my opinion (I'm not a clinician) that early administration of neuroprotectants in combination with effective DMTs will make a real difference with regard to progression.
    Hopefully we will be seeing many more neuroprotective therapies entering the arena over the next few years.

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  30. Dear Anon 11:29
    I am not sure that Prof G can comment on this one. He may disagree.

    Looking at influence on relapse rates in phase III trials there are a number of drugs with similar profiles, so they are agressive as each other.

    At present neither Alemtuzumab or BG-12 are licenced, how long will it be before they are licenced?I do not know because I am not on the commitees deciding. Either could fall because of some unknown Hiccup.

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  31. BG12 is due to be approved in the US on 28th December. It is extremely unlikely that it will not be. Alemtuzumab is more controversial for well-known reasons. To be early, agressive as Prof G believes to be the way forwards for RRMS does it need to be one of Tysabri, Fingolimod or Alemtuzumab or could BG12 be 'sufficient' in terms of its impact? I don't want to take BG12 then develop SPMS in 15 years only to discover I should have gone for a 'harder' therapy instead right from the beginning - if that makes sense? Or is MouseDoctor2 suggestion BG12 in combination with something else would be better (I believe it is being trialled in combo with IFN and GA at present)?

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  32. BG12 may be neuroprotective, but it might have to be given in very big doses to achieve this- see the blog of 2nd Oct. about BG12. Maybe ECTRIMS will give us more information. And do you really think you'd be able to conform to the protocol of 2 pills and an injection every day?

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  33. Re: "It seems to me that early is beyond question the right way to go."

    This is not for everyone; those of you with mild disease (non-disabling relapses and fully recovery with a very low lesion load on MRI) may opt for something milder. It all depends on how risk adverse you are re treatments. In addition, the local authorities will not pay for some drugs unless you fail first-line therapies. So the decision is being made for you.

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  34. "BG12 may be neuroprotective, but it might have to be given in very big doses to achieve this- see the blog of 2nd Oct".

    Maybe not. I can see a way that the dose does not have to be that high based on biology of MS. This is because the way that some drugs do not get in the brain may be missing in MS. However I would like to see the data that my hunch is correct.

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  35. The post may prod pharma into showing some answers to the questions, if they do not have the answers they need to do some homework

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  36. I don't know how previous discussions of BG-12 have passed me by - it would be great if it proves to be neuroprotective at acceptable doses and cost. Prof G, hopefully you'll let us know what you hear at ECTRIMS. BTW Is there someone employed full time to make up all these MS related acronyms?!

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  37. There is a search feature, that you can try

    Neuroprotection

    http://multiple-sclerosis-research.blogspot.co.uk/2012/01/research-bg12-targeting-nrf2-to-help.html

    I bet there is a an advertising company comming up with the acronyms and the weird names of the compounds..maybe just call them "Bloody expensive" :-)

    Maybe you guys can come up with an
    Anacoym forProf G repeated lumbar puncture trial to treat progression?

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  38. Hmm, will give it some thought...

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  39. You asked "Whats happening with Anti-LINGO-1" Well according to the news report about BIOGEN IDEC posted by reader today

    Proof of concept studies in optic neuritis are expected to start in the fourth quarter of this year, and during the second half of 2013 for MS.

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  40. A friend of mine is one month post dx of mono. Since I am probably already infected w/ EBV due to MS, can I get infected again and/or could more exposure impact my disease?

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  41. Hope your friend gets better from mono, Once infected you stay infected and we are all virtually infected. So I would not worry

    The exposure that we think could impact on disease is the exposure from within. The aim of the Charcot project is to attack EBV in MSers not their friends.

    I am not a real Doc or EBV expert, but if I am wrong I am sure Prof G will pipe up after his glass of Champagne, that's if he can get one.

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  42. Genzyme are touting a 'next generation' Lemtrada about to enter the clinic. Anyone know more about this? As a big fan of the potential of Alemtuzumab this is quite exciting. The question is - wait for this new, presumably more effective, safer drug or crack on with taking Lentrada as soon as its possible to do so? I'm surprised they've announced this - its a bit like announcing iPhone 5 before you've started selling 4 - people might hold off and wait for the improved model... Especially when iPhone 4 could equal death from ITP or renal failure from Goodpastures... Any thoughts or insider info on this chaps

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  43. Genzyme are touting a 'next generation' Lemtrada

    Can you send us a link to a source of information? I have not heard anything, Maybe ProF G has.

    Lemtrada is the next generation of Alemtuzumab i.e it is alemtuzumab repacked with a different amount of antibody and according to the grapevine a different cost.

    If there was a me too we would surely know about it by now as it would have to be in trial now.

    I like you analogy with the phones


    about to enter the clinic

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  44. Hi MD,

    See below - any thoughts?

    http://mobile.businessweek.com/news/2012-10-12/sanofi-aims-to-add-second-generation-lemtrada-to-pipeline

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  45. I am non the wiser from seeing this so I am not sure what a second generation lemtrada, maybe the drug they bought to stick on the shelf so that nonone else would develop the pill that would compete with Lemtrada.

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  46. Mouse - thanks for holding the fort.

    When Prof G has sobered up, could he list six key things covered at Ectrims.

    Make him lots of black coffees when he returns to work and don't let him operate any machinery.

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  47. Shift.ms is a part of ths blog, right?

    Why are all the short movies they make so institutionally racist? We never see anyone othe than white middle-class characters in them. Do white middle-class people have a monoply on MS?

    Tell them to change their ways. It's meant to be a charity that represents all walks of MS, not just one particular.

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  48. Shift.ms is a part of ths blog, right?

    Wrong.. Shift.ms is not part of the blog They are their own entity with their own remit.

    Ours is on research.

    Theirs is about creating an MS communality focussing on young MSer and doing stuff that others do not do.

    We know the founders very well and have worked closely with them on different projects and one of the webmasters Beki was based in Barts.

    I think it is very unfair and wrong to accuse them of institutional racism concerning their movies and their action

    Why are all the short movies they make so institutionally racist? We never see anyone other than white middle-class characters in them.

    The demographic of MS is that there are more white MSers than others but there are only two main characters Dave and Karen.

    If watch the films Karen worked in a Greasy spoon (That is a Cafe) and Dave in a Bar......very middle class...not. Later, he was running a club and Karen was making T shirts....Is that not following an ambition?

    Ambition should have no class..my dad was a postman and mum a school cleaner/cook after my dad died when I was eleven

    Now to racism and shift you are wrong. Indeed when Shift MS were making us meet MSers as part of their educational remit they invited black, white, brown people and in fact when we had to do talks with MS, we were grilled by someone of Asian origin who was invited by Shift to do this.

    If you care to look at the home page of www.shift.ms and I can see Trishna's top tips and that links to Asian MS, GLAMS (lesbians, gay men, bisexuals and transsexuals)

    Shift MS is essentially run by the people who use it and there are no bars to joining







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  49. Sorry Dad was a postmouse and mum a cleaner yep not all mice are dirty:-)

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  50. When Prof G has sobered up,

    I suspect is not black coffee that he needs but a retread on his tongue and and a fresh pair of ear drums after the endless series of meeting he had.

    As a roving reporter...I think we can all agree this time he was a bit crap. Just....too busy.

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  51. "Sorry Dad was a postmouse and mum a cleaner yep not all mice are dirty:-)"

    MouseDoc you're just a sweet fella really :-)

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  52. Anon said 10.27

    "I thought this was particularly interesting at ECTRIMS:......

    It's a massive registry of MSers.... You can go online put in your own EDSS scores at various durations and find out what percentile of severity you....This tool has its limitation but it is interesting in an attempt to provide some basis for prognosis in MS".

    If this is an MSer I apologise for curtailing this post. Please come back and let us know, but use of the word Quartile and percentile is
    not an everyday term, non scientists use. Furthermore there is more information here than is in the abstract. So you are either an academic MSer or someone plugging the data base in Australia.


    If answer is yes to the latter suggestion please have the courtesy to ask us to post a link to this site. It may not be refused. You can write to Prof G.


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  53. Hi MouseDoc,

    It was my post - and I've nothing to do with the people who run the site I promise (which I don't think is profit-making so I'm not sure they'd want to surreptitiously post under a pseudonym!!). I'm just an MSer - and not an academic as such (although I have science A-levels - is percentile and quartile really so academic?!)! Anyway, sorry for posting the link - I just thought it was really interesting (both as a prognostic tool and also showing a milder natural history than some older studies). Anyway, I'll ask next time before posting a link!

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  54. Thanks for coming back, I have had a bit of time to look over the website and as you say it is run by academics and not pharma. I will do a post as not everyone reads the comments and maybe try and do this with other registers

    With regard to links it is not an issue but I try and check them out, when I have time, otherwise we put in links to a mumbai escort agency, penile implants, stem cells agencies etc. etc.

    I am a bit sensitive to this at the moment as MSers are not our only readers and people e.g. pharma and other companies do seed in feeds which may help benefit them.

    We prefer to know it when we are being manipulated.

    Thanks for the vocab lesson I will feel no worry in throwing in quartile from now on.

    Best wishes

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  55. Dear Anon 6:57 I forwarded your original comment to prof G and he has done a post already for tomorrow.

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  56. Anon 6.57 original post

    I thought this was particularly interesting at ECTRIMS:

    http://registration.akm.ch/einsicht.php?XNABSTRACT_ID=155973&XNSPRACHE_ID=2&
    XNKONGRESS_ID=171&XNMASKEN_ID=900

    It's a massive registry of MSers and EDSS scores/disease duration.
    You can go online (https://www.msbase.org/msbase/en/msbase/mscurves)
    put in your own EDSS scores at various durations and find out what
    percentile of severity you are in against this database.
    Interestingly, the median time to EDSS 3.5 (the point at which ambulation is
    impacted) is 20 years in RRMS - longer than some studies but in line with
    more recent population studies. At the same point the 75th centile is still
    just under EDSS 6 meaning 3 in 4 are still able to walk without assistance
    at 20 years (albeit for limited distances in many cases). The 25% percentile
    of RRMS/SPMS is less than EDSS2 at 20 years, meaning 1 in 4 of this registry
    have particularly benign disease.

    No doubt this tool has its limitation but it is interesting in an attempt to
    provide some basis for prognosis in MS.

    PROF G has made a post on this

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  57. I saw this at the bottom of the CCSVI post this morning

    "These are all important questions that need an answer!"

    So I read some of the comments and it read at the bottom.

    "New comments have been disabled for this post by the administrator"

    The irony made me chuckle :-)

    Regards as always.

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  58. @Andy Clarke: What are you talking about? I was able to make a new comment to the post, As did someone else before me. But I could understand why Team G had to disable the comments. There were vicious attacks not only towards the members of Team G, but also towards MSers who weren't true believers. Sadly, some people cannot stand having their ideology questioned without abandoning all civility.

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  59. Maria
    You have identified the problem re CCSVI. If we activate comments then we get swamped by VV et al or get abuse. Trying to respond to him/her is like wrestling with a blancmange! On the other hand there are others who don't have a fixed agenda who would like to comment.
    As so often it's a case of damned if you do, damned if you don't.
    On balance I'm in favour of leaving comments on but if the blog shows signs of being hijacked by the CCSVI lobby (as has ruined other MS sites) then we would have to consider turning comments off again on this topic only.
    We'll see how it goes.
    Don't worry about the abuse, it's water off a ducks back! If people have to resort to abuse then they have already lost the argument.
    All the best MD2.

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  60. Hi Maria,
    I see it must have been opened back up again, supposedly so some answers can be proffered ?
    I'm all for healthy debate and I must have missed the abusive comments. Without hyjacking this thread, I see this argument rolling on for a number of years yet and eventually the playground antics will stop and research studies will reveal answers not yet seen.

    From a Mouse to a Duck ? now there's an area for funding.
    Regards as always.

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  61. Reply
    Gavin GiovannoniMonday, July 16, 2012 8:20:00 PM

    Re: "Is there a more dangerous virus in some patients?"

    Yes, it is a mutant virus that causes the PML. We have been able to detect or monitor the mutant in MSers on Natalizumab.

    "I have heard that in some hospitals look at the virus level, assigning a risk level of 1, 2, 3 as a function of the amount of virus."

    No sure about this. There is some theoretical data that suggest if your titre of antibodies against the virus go sup this increases your risk. Not enough numbers to confirm of refute this.
    .....wonder if you could provide any more info on possibility of finding out if one has the mutant virus

    ReplyDelete

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