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Originally Posted by Science Mom
The RA27/3 vaccine strain shares 98% homology at the nucleotide level with the progenitor wild-type virus (BLAST) and there is a 31 amino acid alteration.
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Humans share more than 98% of their genome with chimpanzees. Does that mean humans and chimps are not different. So... 31 amino acid alterations... Is that supposed to be a lot or a little. To me that means there are a potential of 31 different phenotypic changes between the wild-type and vaccine viruses. How many have been characterized? You must already be well aware that a single amino acid substitution in a single gene can cause a significant phenotypic change (it's actually been documented for the measles vaccine virus). But the point here is rudimentary: you can't use congenital rubella statistics for the wild-type virus to substantiate safety claims for the vaccine virus.
The phenotypic differences between the two viruses have not been characterized.
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Originally Posted by Science Mom
The immune response to the vaccine is very similar to natural infection although a lowered quantity of antibody responses. So if you wish to call this a different virus, I won't argue semantics on this one.
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It's definitely not semantics. This belies the very heart of your argument: you attempted to treat the wild-type virus as indistinguishable from the vaccine virus so that you could present CRS/wild-type data to assume the safety of the vaccine virus. I don't disagree with you on the grounds of semantics, I disagree with you because the differences between the wild-type and vaccine viruses can not be dismissed as you've done. While the genotypic differences may have been 'counted', the phenotypic differences (the actual effects of the gene alterations) are almost entirely uncharacterized. Therefore you can not possibly know that the vaccine virus does not contain some mutation that alters its neuropathology.
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Originally Posted by Science Mom
As far as some attenuated viruses causally associated with neurotropism e.g. Urabe mumps strain and meningitis well that was established and that strain was withdrawn from many markets.
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Okay, you cited the Urabe example - Great! You've clearly demonstrated that you understand attenuation can lead to increased neuropathology. So what are you arguing with me for? The point was not how often it happens, the point was that it
can! happen. And that means it can happen for rubella, too. Maybe you want to argue with me about whether it did happen. Well, it can't be ruled out. And that's really all I was trying to say.
And I should point out that the Urable example doesn't scratch the surface of what research has been done on this topic. Measles is by far the best documented with well over a hundred papers researching it or discussing it.
But getting bogged down in the specifics of the neuropathology of measles, mumps or even rubella virus is not very useful. The point is that vaccine attenuation means attenuation of acute clinical symptoms only. It does not mean that all characteristics of the virus are attenuated. I originally brought this up as a counterfact to the statement that attenuation makes the virus mild. So there is absolutely no need to get bogged down in the minutiae of specific examples where attenuation increased neuropathology. It can happen. You've admitted that by offering your own example.
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Originally Posted by Science Mom
The rubella vaccine has been in use for nearly 40 years now; what are the structural changes of the immundominant regions do you propose have occurred that could attribute rubella vaccine with regressive autism?
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This question does not make sense to me. You're trying to tell me that in order to attribute autism to a 40-year old vaccine, I must detail the structural changes of the immunodominant regions. Okay, first off, I haven't attributed regressive autism to the rubella vaccine - what I'm saying is that
you can not rule it out. That moots the entire question but I'll continue. Secondly, changes to a virus do not have to occur in the immunodominant regions for there to be a change in neuropathology. This is basic stuff and should hopefully not lead to further digressions. Thirdly, structural changes do not need to be quantified in order to identify changes in neuropathology. In fact that's almost never the way it happens. You do not need to know the tertiary structure of a protein (viral or otherwise) to determine if it exerts an effect, e.g. binds to something. I honestly hope that this will not devolve into further tangential debate. Because none of that is even relevant. The artificial hurdle that you constructed for me to jump over only gets in the way of the legitimate point that you were actually making: the vaccine has been around for 40 years so for the vaccine to now be causing an epidemic of autism, there must be interceding variables that have prevailed on the vaccine in the last 40 years to produce such an effect. Obviously the variables do not need to be located in the tertiary protein structure of the immunodominant region of the rubella vaccine virus.
Anyway, there
are some differences between rubella vaccination 40 years ago and rubella vaccination today. There are many. Some of them may indeed impinge on immunodominant viral structures. Some of them affect the pathology of the virus without even changing the viral genome. But regardless, the vaccine can not be absolved simply because it's been around for 40 years - many variables pertaining to rubella vaccination have occurred or been introduced in the last four decades. And I don't need to prove that those variables do cause neuropathological changes leading to autism. The relevant issue is that these variables can change neuropathology and that a possible change in neuropathology has not been ruled out. You can argue the probability but not the possibility. Additionally, neuropathology of the rubella vaccine virus can not be ruled out on the basis of wild-type data on CRS.
I apologize for the length of this post. I felt that your response to my criticism expanded the argument into areas that were not particularly relevant. I attempted here to cauterize the loose ends and corral the argument back toward the original points that were made - or at least to articulate myself better.