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ZENODO
Report . 2017
License: CC BY
Data sources: Datacite
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ZENODO
Report . 2017
License: CC BY
Data sources: Datacite
https://dx.doi.org/10.5281/zen...
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Role Of Mmr Ii Vaccine Contamination With Gad65 Containing Chick Embryo Cell Culture In The Etiology Of Type 1 Diabetes

descriptionPublicationkeyboard_double_arrow_right Report , Other literature type 22 Jul 2017Publisher:Zenodo
Authors: Arumugham, Vinu;

doi: 10.5281/zenodo.1034771 , 10.5281/zenodo.1034770

Role Of Mmr Ii Vaccine Contamination With Gad65 Containing Chick Embryo Cell Culture In The Etiology Of Type 1 Diabetes

Abstract

Autoimmunity against glutamate decarboxylase (GAD) has been associated with type 1 diabetes. GAD65 is involved in type 1 diabetes. Following an anecdotal report of type 1 diabetes diagnosis a few weeks after measles, mumps and rubella (MMR) vaccine administration, MMR vaccine contents were examined. Major proteins in the vaccine apart from the measles, mumps and rubella live viruses were chicken embryo cell culture proteins. Bioinformatics analysis provide strong evidence that chicken embryo cell culture proteins in the MMR vaccine can cause the development of antibodies against chicken GAD65 which cross-react with human GAD65 protein to cause type 1 diabetes. This is very similar to the Pandemrix vaccine causing narcolepsy.

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selected citations
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This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
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