Finnish team makes diabetes vaccine breakthrough

[tamarian]

http://yle.fi/uutiset/finnish_team_makes_diabetes_vaccine_breakthrough/6893356

Researchers in Finland could be close to a breakthrough in the search for a vaccine against Type 1 diabetes. Clinical trials could start soon.

A team working at Tampere University has discovered the virus that causes type 1 diabetes. The enterovirus penetrates the pancreas and destroys insulin-producing cells, eventually causing diabetes.

Researchers have looked at more than a hundred different strains of the virus and pinpointed five that could cause diabetes. They believe they could produce a vaccine against those strains.

”We have identified one virus type that carries the biggest risk,” said professor Heikki Hyöty. ”A vaccine could also protect against its close relatives, to give the best possible effect.”

[teaser]

I guess if this works out, maybe we'd have to start calling Type 1 diabetes an immune-disease, rather than auto-immune.

And start wondering about every other "auto-immune" disease out there.

I wonder how common the virus is--virtually everybody might be a carrier, and the damage only done if certain other variables are in place (leaky gut, bottle-fed etc. compromising the immune system).

I also wonder about stuff like this;

The first clue that a skin eruption may be DH is that “it itches like crazy,”; said Zone. “People are digging at themselves.”; As a result, the blisters are almost always broken open by the time a DH sufferer seeks medical help.
The second characteristic sign of DH is its location on the body. Lesions most often appear on the extensor surfaces—the forearms near the elbows, the knees, and the buttocks. The outbreak of lesions also tends to be bilateral, meaning it appears on both sides of the body.
The grouping of the lesions provides a final clue. Although DH is not caused by the herpes virus, its lesions resemble those of herpes, hence the word “herpetiformis.”; In both conditions, lesions form in small groups.

If an otherwise harmless virus caused these lesions--would anyone notice? A disrupted immune system due to leaky gut might cause an inappropriate immune response to our own tissues--but also an inappropriate immune response to otherwise harmless viruses.

[rightnow]

Now we just have to worry about what one more bit of dreck stuffed into the body of an incompletely developed human will have 'in context.'

PJ

[Cleome]

This brings to mind the case of geneticist Dr. Michael Snyder. His genes suggested he was predisposed to T2DM, and during the course of an in-depth study of his integrative Personal “Omics” Profile* he developed T2DM. It was correlated with a viral infection.

For Snyder, one set of measurements was particularly telling. On day 301, about 12 days after a viral infection, his glucose regulation appeared to be abnormal. Shortly thereafter his glucose levels became elevated, prompting him to visit his primary care physician. On day 369, he was diagnosed with type-2 diabetes. . .

Snyder, who has two small children, experienced two viral infections during the course of the study: one with rhinovirus (at day 0), and one with respiratory syncytial virus (beginning at day 289). Each time, his immune system reacted by increasing the blood levels of pro-inflammatory cytokines — secreted proteins that cells use to communicate and coordinate their responses to external events such as an infection. Snyder also exhibited increased levels of auto-antibodies, or antibodies that reacted with his own proteins, after viral infection. Although auto-antibody production can be a normal, temporary reaction to illness, the researchers were interested to note that one in particular targeted an insulin receptor binding protein.

News Article Revolution in personalized medicine: First-ever integrative 'omics' profile lets scientist discover, track his diabetes onset (http://med.stanford.edu/ism/2012/march/snyder.html)

* Genome (DNA) + proteome (all the proteins) + metabolome (metabolites) + transcriptome (RNA transcripts) + autoantibody profiles.

[aj_cohn]

Thank you for bringing this case study to our attention, Cleome. This might be an important mechanism for T2DM onset that no one's had a way to detect before. I'd love to hear of somebody developing an ethical clinical trial (we can't give this virus to people just to see if they develop T2DM, right?) to test this hypothesis.

[Cleome]

I guess if this works out, maybe we'd have to start calling Type 1 diabetes an immune-disease, rather than auto-immune.
Or diabetes in general is an immune-response side effect? I had not heard that T1DM was related to a viral infection, but it is plausible.

-Cleome's musing-

I'm grappling with the real meaning of 'auto-immune'. Why do human immune systems attack their own cells? My immunology is rusty, does this response require that that cells under attack be in some way labelled as foreign, as in containing viral DNA? Sheep in wolves clothing, so to speak.

T1DM: Enterovirus attacks pancreas, the human immune response destroys pancreatic cells that they now recognize as foreign.

T2DM: Immune response to respiratory syncytial virus also targets insulin receptor binding proteins on healthy cells. A decrease in receptor binding proteins (or a decrease in cells with an abundance of these) leads to insulin resistance in general.

Viral (or bacterial?) infections could explain correlations of inflammation and diseases in general. Inflammation is correlated with the cause, and not the cause itself. Similar to the plaque and heart disease, plaque is correlated not causal.

Note to AJ-Cohn: The frontier of 'Omics is fascinating. No doubt we are on the edge of a much better understanding of health and illness.