Common virus may be celiac disease culprit

—  Article and link:

“Common virus may be celiac disease culprit’

Science News Magazine

6 April 2017

https://www.sciencenews.org/article/common-virus-may-be-celiac-disease-culprit?mode=topic&context=87&tgt=nr

—  Summary:   A study in mice suggests a reovirus (a common virus responsible for upper respiratory infections and fever in children) could cause celiac disease by blocking the immune systems regulatory response. If the first time gluten is consumed by a child while infected by a reovirus, the immune system will mount an attack against the food particle. This would cause the damage to the intestines when gluten is consumed by someone with celiac disease.

—  Connections:   We have learned about the immune system and what triggers it. There is normally a regulatory response to prevent food particles from being attacked and in this case the immune system thinks that gluten is an invader when it was originally present with a reovirus.

—  Critical analysis:   It is great that we are finally beginning to understand the underlying cause of celiac disease. We had always thought it was an immune response but why the immune system attacked gluten specifically was always a mystery. This article seems factual since it does not make any definite claims; it is only reporting what the peer reviewed paper said. It does a great job breaking down the science so that anyone can understand it and it gives you enough information to make conclusions for yourself.

—  Question:

I would like to know: how can viruses stimulate the activity of an enzyme? This is discussed in the article but not really explained. We have learned that viruses inject genetic material, so does the virus code for a protein that interacts with the enzyme or does the genetic material alone bind to the enzyme?

1 Comment for “Common virus may be celiac disease culprit”

mevelasco

says:

I agree with your critical analysis. All the article is saying is that this may be an explanation for celiacs. This article gives good reason to put further research into studying human microbiome interactions and how they relate to disease. As for stimulating the activity of an enzyme, i can imagine for some cases, slight alterations in the genetic code code cause deformities in normally coded proteins. If this protein is normally inhibited, maybe a mutation in the coding prevents the enzyme from binding from the inhibiting molecule?

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