Updating the Hygiene Hypothesis

From  The New York Times  on June 3rd, 2016 – Educate Your Immune System

Summary:

This article summarizes recent research done on the development of autoimmune diseases (Type I diabetes, celiac disease, severe allergies, etc.) in children who grew up in different microbial environments – represented by households in Finland, Estonia, and the Karelia region of Russia. Studies found that, when factors such as diet and breastfeeding were controlled for, toddlers  who grew up in Finland were four times as likely as those in Karelia to develop precursors for Type I diabetes, and the two groups had very few similarities between their microbiomes. Karelia is a significantly poorer area than most of Finland, and many households drink untreated well water, so researchers hypothesized that early exposure to microbes from the environment “taught” the toddlers’ immune systems how to respond appropriately to common environmental pathogens, and so they developed fewer autoimmune issues.

Connections:

We’ve discussed acquired immunity in class, but this area of research takes it a bit farther, and suggests that our microbiomes and  when we are exposed to certain microbes may play a larger role in our immune development than previously thought. Other studies mentioned in this article found that children who were exposed to certain pathogens at a young age were much less likely to develop autoimmune diseases than those that first encountered the same pathogens as teenagers or adults. This updates the hygiene hypothesis (which I think we discussed briefly?), which essentially says that people exposed to fewer kinds of microbes during their development tend to be sicker than those that were exposed to a wider variety of microbes.

Critical Analysis:

I appreciated  the angle this article took, describing autoimmune diseases and decreased exposure to diverse microbial communities as an issue of the 21st century. The author did an excellent job of defining terms and ideas that may be foreign to the lay reader, and I think this article is accessible to a wide range of audiences. However, the article implicitly assumed that the relationship between early microbial exposure and autoimmune disease was proven, and I don’t think any of the studies examined in the piece proved a causal relationship. Popular science writing needs to be careful not to assume causation when it has not been proven!

Questions:

How might we (ethically) prove a link between childhood microbial exposure and autoimmune disease?

A2: Microbes in the News

Antibody helps detect protein implicated in Alzheimer’s, other diseases

https://www.eurekalert.org/pub_releases/2017-04/wuso-ahd041417.php

Summary: The article discusses research looking to find less invasive ways to identify and then track the progress of neurodegenerative diseases like Alzheimer’s. They have accomplished the first step by crafting an antibody which binds to the protein tau, which is present in tangles when damage to the brain is occurring. The antibody allows tau to stay present in the blood and accumulate long enough to be observable via blood tests.

Connection: The article discusses the use of an human antibody, but in a way we didn’t really cover in class. The antibody is not used as a flag for the destruction of a microbe or “not-self” entity in the body, but rather keep an entity around long enough to track its concentrations.

Critical Analysis:  This article does an excellent job of explaining the issues related to diagnosing neurodegenerative diseases, as well as the way in which the protein tau is associated and was identified as a potential measurable product for blood tests. Though the study has only done limited preliminary human trials, they were able to magnify the presence of tau in the blood of individuals with known neurodegenerative diseases. I believe the article did a great job of translating the innovative way in which scientists approach problems like that of diagnostics, and the interdisciplinary cooperation and literacy that is at the command of these researchers to accomplish what was discussed.

Question:  Would this antibody have the ability to track damage as it accumulates in individuals like football players, perhaps as a longitudinal study to gain more data and a predictive model for brain damage?

Microbes in the News Assignment: Post #2

Article and link: “New HIV reservoir discovered: Findings reveal a second target for cure research’, Science Daily (it should be noted that the article on Science Daily sites the University of North Carolina Health Care as their source and mentions that the original findings were published in Nature Medicine on this same date), April 17, 2017.

 

https://www.sciencedaily.com/releases/2017/04/170417114806.htm

 

Summary: This article describes scientists’ recent discovery that there is another cell within the human body which can act as a reservoir for HIV in addition to T cells: the macrophage. This discovery that macrophages are susceptible to infection by HIV is very important to current research focusing on the treatment of AIDS: this tells researchers that a successful treatment or cure would have to be effective in ridding the virus from both T cells and macrophages. One investigation found that viral replication within macrophages is effectively repressed when antiretroviral therapy is administered; however, the study also found that this effect is only temporary. Following treatment conclusion, macrophages still act as reservoirs for the virus and therefore remain capable of reinfecting the host. More research must be conducted in order to find the most effective way to resolve HIV infection of macrophage cells.

 

Connections: This relates to information we have discussed over the course of the semester in that it discusses a virus, HIV, and also cells involved in the immune response (T cells and macrophages). It also relates to the resolution of disease through treatment and also the ways in which viral cells can find ways to persist inside a host even following treatment; both of these are subjects which were briefly touched on in class this semester.

 

Critical analysis: I found it interesting to learn that HIV can also afflict host macrophage cells in addition to the host’s T cells. It has been known for some time that HIV targets T cells, but I had not heard of any other types of cells being specifically targeted by the virus. I also found it interesting that the antiretroviral therapy typically used in treating HIV infections in T cells does not work effectively on macrophages. I expect that the story is scientifically accurate as I have not seen indications to the contrary. I also did not find anything confusing in the article that would need to be corrected.  I believe that they did a good job in relating this news; it seemed as though they kept their audience in mind, and focused on relating the pertinent details and implications of this discovery without making the article too technical for those who may not have the background to understand a technical explanation.
Question: What are the most significant differences in terms of structure between T cells and macrophages which would cause antiretroviral therapeutic (ART) agents to be effective on T cells but ineffective in macrophages? Which ART’s were tested on the macrophages? What is their mechanism of action? Are scientists already aware of the specific reason that the ART does not work on macrophages?

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?