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What I learnt from talking with Rolf Zinkernagel
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Prof Trevor Marshall
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 Posted: Fri Jul 28th, 2006 12:12

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Prof Rolf Zinkernagel, 1996 Nobel Laureate, gave the keynote at the DMM2006 conference at the Karolinska Institute last May.

The theme of his keynote was: 'you guys/gals forget about autoimmunity - these diseases are due to pathogens' (my paraphrase, of course)

I was so delighted to have the conference kick off in that way that I didn't go straight to the library and pull the text of the paper he was discussing. During the conference I had a number of detailed conversations with him about his work, trying to understand what importance it had to the "Marshall Pathogenesis." I knew it must be important but wasn't sure why:X

Back in California I pulled the paper, and printed the key diagram, which he had caricatured on the whiteboard during his presentation - Figure 8. Here is just the graphics from that figure:



Look. I am a slow learner. I admit it. I am going to hide behind the excuse that I am "thorough":):):)

What Rolf's team had done was to take mice in the first few days after they were born, before their immune systems were producing T-lymphocytes, and inject a virus into their brains. Because their immune systems were unable to fight the virus, or make antibodies to it, the virus persisted in the brains. When those mice were challenged by infection with the same virus later in life they couldn't fight it, and they died (see the sad picture on the top line there...)

The top graph line shows the dotted black line rising at about day 7, when the T-lymphocytes started to be manufactured by the mice immune system.

When other mice were not challenged with the virus until they were grown, and had normally functioning immune systems, they fought the virus, and lived (graph line 2).

So what has this all got to do with the 'Marshall Pathogenesis,' and persistent bacterial infections? Well it has taken me 2 months to realize that here is one mechanism by which babies could be infected at birth.

The human adaptive immune system takes even longer to become fully functional, although the mother is supposed to pass some immune function to the infant by breast feeding.

Worse, if the baby was being bottle-fed (in the 1950's onwards) Nestle was fortifying that milk with Vitamin D, perverting innate immunity. Therefore only adaptive immunity could protect the infant, and the T-lymphocytes associated with adaptive immunity don't appear until weeks after birth (mice live and die at an accelerated rate compared with humans).

Breast fed-babies would eventually get supplemented baby-food as well. But when? Before or after immunity had been acquired? How much sunshine would the infants get? Hmm...

Now if certain bacterial species were able to persistently infect the neo-natal brain in the same way as Rolf's CMV did, then it could be expected that those folk might well experience a greater degree of difficulty clearing a challenge later in life, just like the mice did... Hmmm...

Eureka!...

So we don't need to postulate placental transmission of the pathogens, just normal spread between the family members (and pets) during those first few weeks of life... Ah, that's much more sensible... and there we have the familial aggregation... ("Please pass the baby for a cuddle, Mom")

..Trevor..

ps: Not everybody reacts violently to insect bites.. only a minority.. Only about 5% of tickbite events progress to chronic Lyme... Hmmm...

pps: you don't really want to know this, but hospitals here in California have started to give Hepatitis B immunization to new-borns, even before they are discharged from the maternity ward:X

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 Posted: Fri Jul 28th, 2006 12:41

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Trevor,

Wow... that is a real eye opener. :shock:

I was bottle fed and Mom was only allowed to breast feed my older sister one day, then told she couldn't breast feed due to having a different Rh blood factor than us.  Mom's Rh is negative while mine and sis' are positive.  

I wonder how much help that one day gave sis' immune system over mine.  I always seemed to be more sickly than my sis.   

It'll be interesting to see how mine and sis' children do healthwise, being breast fed babies. :cool:

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 Posted: Fri Jul 28th, 2006 12:43

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Trevor-

Why would the mouse survive the virus injection in the first few days but the same virus kill the mouse later in life? In neither case does the innate immune system function so why the differing outcomes?

JCB



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Prof Trevor Marshall
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 Posted: Fri Jul 28th, 2006 12:49

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JCB:
They used a lower dose at birth, not enough to kill, only enough to 'plant' the virus.
They also used different (although related) species of virus.

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 Posted: Fri Jul 28th, 2006 13:26

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In reference to the Hep B immunization, here on the East Coast, the birth mother has to sign permission for the shot.  The permission slip is brought in during labor or shortly after giving birth and most of the young mothers don't know enough not to sign.  And why does a newborn need Hep B?  They're not sexually active or have STD, etc.  That shot is terrible for a newborn!!!  So many unknowns associated with it.  This is just my opinion.



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 Posted: Fri Jul 28th, 2006 13:32

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Trevor,
It seems like the paper also proposes that the prior infection increases the inflammatory response to the related virus (via the cytotoxic T cells arising from the early infection), and the increased inflammation can cause inflammatory damage (a hypothesis somewhat in line with the autoimmune view, but with the idea of the long term presence of a microbial trigger).  Is that correct?

It seems to me that the infant would also acquire infections just by sharing the same blood supply with the mother, wouldn't it?  Or is there a problem with that aspect of transmission?

Joyce Waterhouse



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 Posted: Fri Jul 28th, 2006 13:41

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Dr Trevor Marshall wrote: When the same mice were not challenged with the virus until they were grown, and had normally functioning immune systems, they fought the virus, and lived (graph line 2).

Trevor, this is not exactly clear to me. You say: the same mice. Do you mean the ones infected in the first few days after they were born?

Thanks, Frans

From Trevor: Fixed Frans, thanks:)

Last edited on Fri Jul 28th, 2006 13:44 by Prof Trevor Marshall



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 Posted: Fri Jul 28th, 2006 13:42

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Joyce,
Whenever I try to advance the concept that pathogens can be acquired through the placental barrier I hit a lot of resistance, even though I have seen studies showing Mycobacterium tuberculosis transmission via that pathway, and also transmission in sperm (thereby presumably straight into the embryo).

It is certainly easy to see how a wide range of (eg, air-borne or skin-borne) pathogens could be transfered in the first few weeks of life, while acquired immunity is still being built up.

Additionally, this is a persuasive demonstration that a (supposedly pathogenic) virus can persist in the brain throughout life, which, in itself, is a radical departure from conventional thinking. I don't think anybody has given enough thought to persistence, let alone what happens in the first few days and weeks of life.

I think Rolf's attempt to show that the cytotoxic T-cells might be more active is because he didn't have the missing piece of the puzzle (L-forms), we had that...

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 Posted: Fri Jul 28th, 2006 13:59

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Trevor,

I was working on an analogy these last days to explain how the innate immunesystem differs from the acquired one.

To make it extremely short at this time I would make the analogy of building a house (growth of embryo to baby to (even older) child).

When one builds a house, normally there is an overseer making sure that all the materials are in proper order. Eg no rot in the wood or concrete used.

This overseer is the immunesystem.

The problem is that when the overseer trusts the one who is delivering the materials (the mother), but that person is really trying to rip you and your overseer off, you might end up with materials that are rotten to the core.

In this instance it is the virus/L-form that is in the materials that stem from the mother (or, as you point out above, anyone (in the family) who takes the child on her/his lap).

Now, when we keep on using the same overseer for the rest of our lives, the building (the body) will fall apart, since he (the immune system) is convinced the materials used are ok (not infected).

What the MP in fact does, is appoint another overseer who starts inspecting the materials used and finds them faulty (immunesystem starts recognizing the pathogens) and he starts to replace them (herx).

Is this about the drift of what you are saying? I know it is oversimplifying things, but still works for me as an analogy  :D

Sincerely, Frans



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 Posted: Fri Jul 28th, 2006 14:03

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Frans,
I think the MP is like a new boss for the overseer, who retrains him/her to recognize what rot really looks like:)

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 Posted: Fri Jul 28th, 2006 14:04

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You are right, of course, never heard of transplanting a whole immunesystem....

Frans



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 Posted: Fri Jul 28th, 2006 14:17

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Trevor, there is something I don't understand.

When these mice were infected in the first few days, why didn't innate immunity take care of the pathogens.

If innate immunity develops later on, why didn't the innate immunity of these mice get rid of the pathogens after it was fully functional.

How do the pathogens shield themselves from innate immunity in these mice is the right question I guess.

Frans



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 Posted: Fri Jul 28th, 2006 14:23

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Frans, that is the $64,000 question which Rolf's group was posing. They were showing that persistent infection is possible, and how to recreate it in the lab. At least, I think that was what they set out to do. Or maybe it just happened that way, because they were also clearly focused on proving that autoimmunity is not the immune system attacking "self."

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 Posted: Fri Jul 28th, 2006 19:42

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To those of you who are concerned about newborn vaccinations, you should know that parents can postpone the baby's vaccinations. The policy to vaccinate in the hospital was put in place to increase compliance because many parents do not return for clinic visits in a timely manner. Check on the hospital policy before the birth to avoid hassles if a doctor's signed permission is needed.

If parents decide to vaccinate, they can delay the start until the baby is older and also space them out. Not getting more than one vaccination at a time will allow the baby's immune system to cope with the challenge.

Best,

Meg

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 Posted: Fri Jul 28th, 2006 20:36

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Meg, this is exactly what my daughter is now doing with her two.  The oldest who received the shot at birth and is now 4 years old is just overcoming speech and language delay.  Some say is related to the Hep B vaccine before he was even a day old.  Others don't know.  The great news is that he's almost completely back on track in all areas of his precious life.

The youngest did not receive the shot, only because my daughter's pediatrician read her the riot act about the oldest one getting it at birth, and all the cons associated thereto.  She is fine, thank God.  Both children receive one shot at a time, even now, mercury free.  It costs more because she (daughter) has more copays, but it's your child's life at stake here.  If there's a reaction, we know immediately what it's from.  There's no guessing games going on.  There's always so much to learn--at any age.



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 Posted: Fri Jul 28th, 2006 20:36

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We were fortunate in having a doctor for our babies who thought it was too much for an infant to get so many vaccinations so early in life.  He just pushed the time table forward, and spaced things out. We had no trouble with having the appropriate vaccinations in time for school attendance.

In terms of breast-fed infants being exposed to vitamin D - friends from Brazil whose brunette daughters were born in Denmark were told that they needed to give their babies vitamin D supplements as they would not get enough vitamin D from the sun in Denmark.  Breast-fed babies in other places were probably also prescribed vitamin D supplements.

I'm surprised that people still think that the placenta will protect against disease transmission.  Babies are certainly born HIV positive, for example, and can also suffer from the mother's case of rubella.

Margo



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 Posted: Fri Jul 28th, 2006 20:42

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Toni D,
Children with learning, attention and relationship difficulties are responding well to the MP. Remember that these Th1 diseases aggregate in the family, especially down the maternal line. Take a look at the parent's forum and see how young Matt, and also Margo's daughter, have overcome their difficulties.

ps: I am not convinced that mercury is the problem. Remember the paper by the scientist who discovered L-forms in 1934: "Filterable Forms of Bacteria."
http://www.marshallprotocol.com/forum39/6844.html
What she meant is that the L-forms are so small they go right through the filters used to ensure purity in pharmaceutical manufacturing. I think you get the picture...

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 Posted: Fri Jul 28th, 2006 21:13

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Thank you, Dr. Marshall.  I went to the site, but will have to print it out to read.  My eyes are doing better reading on paper, as opposed to the screen, about right now.  Can then use my magnifying glass;).



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 Posted: Sat Jul 29th, 2006 04:23

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Trevor,

As I understand it, they found that after introducing the virus just after birth, the virus only persisted in the brain, but was eridicated by innate immunity in the other parts of the body.

This seems to me as if the viruses have a preference for certain cells (maybe even bodyparts) which very much reminds me of bacteria who have a preference for certain human cells (bodyparts).

I know you think that the different th1-diseases differ, amongst others, because the different bacteria involved have a liking for different cells/tissues.

Taking this further, it would be of great importance for prof. Z in future experimants, to use other species of viruses or rather, bacteria, to see if they survive in the same way as the virus in this paper of prof. Z.

Furthermore, on cell-level, one should investigate which molecules of the pathogens and the host (human) interact in such a way that they, synergistically (together), evade the innate immune response.

Can you explain how the immunesystem recognizes intracellular infection? I mean what happens if a muscle-cell gets infected. How does the immunesystem 'see' that invader?

Do even 'normal' cells have the ability to show pathogenic proteins/molecules on their surface?

It seems to me that that might be a weak spot.

Sincerely, Frans



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 Posted: Sat Jul 29th, 2006 07:38

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Each family of cells is specialized by not only what is inside its membrane, but the particular set of receptors in its membrane. I think the complexity is probably too great to quantify the cells operation, but not too much to get a broad overview of what is happening.

I wouldn't attempt to guess why the neo-natal mice can't clear the CMV from their brains. But it certainly is a big signpost for us on our quest for an understanding of the precise manner in which Th1 disease manifests itself in so many different ways.


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