epigenetics

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Study: New Way To Hold Back Herpes, Keep Virus Latent

Fluorescent staining shows areas of the cornea affected by herpes virus that infected a man's eyes. (Photo: Wikipedia)

Fluorescent staining shows areas of the cornea affected by herpes virus that infected a man’s eyes. (Source: Wikipedia)

Chances are, you’ve got herpes, I’ve got herpes, we’ve all got herpes.

Studies find that by age 60, virtually all adults carry herpes simplex virus 1 — best known for seeping cold sores but also potentially blinding when it hits the eyes. Herpes simplex virus 2, the sexually transmitted disease, infects more than a quarter of people by their forties, the CDC says.

While anti-viral medications can help, there is no cure for herpes viruses. Their wily ways of going latent between recurrences, hiding out in viral reservoirs in our bodies, make them supremely hard to eradicate.

So it’s welcome news that a study just out in the journal Science Translational Medicine describes a whole new strategy for beating down herpes viruses and keeping them down — at least in mice, rabbits and guinea pigs.

Far fewer of the mice died or had virus spreading throughout their bodies.

It’s a tactic that researchers say may also hold promise for attacking HIV, another virus whose habit of hiding out makes it hard to kill, and the herpes zoster virus that causes excruciating shingles.

The new method hinges on epigenetics — specifically, protein “packages” that determine how genes are turned off and on.

For a herpes virus to go from a latent state to an active state, it needs to unpackage or unbundle its genes so they can be “turned on” and begin to replicate and spread. But, the researchers found, if they block an enzyme called LSD1, those genes tend to stay bundled up and inactive.

It’s as if the viral DNA encoding the genes needed to reactivate the virus naturally carries a “Don’t open me!” sign on it, says the paper’s senior author, Dr. Thomas M. Kristie. The LSD1 enzyme can remove that sign. But block the enzyme and the “Don’t open me!” sign stays up. Continue reading

What Happens Early In The Brains Of People Who Get Alzheimer’s Late?

Alexis McKenzie, right, executive director of The Methodist Home of the District of Columbia Forest Side, an Alzheimer’s assisted-living facility, puts her hand on the arm of resident Catherine Peake, in Washington, Feb. 6, 2012. (Charles Dharapak/AP)

Alexis McKenzie, right, executive director of The Methodist Home of the District of Columbia Forest Side, an Alzheimer’s assisted-living facility, puts her hand on the arm of resident Catherine Peake, in Washington, Feb. 6, 2012. (Charles Dharapak/AP)

As we reported on Here & Now, this week brought news of a promising advance on Alzheimer’s disease: A study in the journal Nature that helps illuminate what goes wrong early on in the brains of people who get late-onset Alzheimer’s, the most common form. The researchers aimed to connect the dots between the gene APOE4, the strongest known genetic risk factor, and development of the actual disease.

Please read the Here & Now report for more detail, but for the bigger picture, here are some clear insights from Dr. Robert C. Green, a medical geneticist at Brigham and Women’s Hospital and Harvard Medical School. (To sum up in an adjective: Here & Now host Robin Young asked me if this was “great” news on Alzheimer’s; I only felt comfortable going as far as “promising.” Dr. Green takes it all the way to “exciting.”) His points:

It’s the kind of breakthrough we need to help us be smarter about the drugs that we take to multi-million-dollar clinical trials.

“What I think is the really exciting part of it is that, for nearly 20 years, we’ve known that APOE was a robust risk factor for Alzheimer’s disease, but we really didn’t  know why. And this paper is actually the first paper that begins to offer an answer as to why APOE4 is a risk factor at a molecular level. 

The way they did it is quite remarkable: They did it with gene expression profiles, a hot new area, and they found that certain genes were turned up or down by the APOE4,  and they were genes that appeared to regulate the production of the bad amyloid protein associated with Alzheimer’s disease. So the APOE4 didn’t directly influence the production of the amyloids; it seemed to regulate up or down these signaling genes, sort of like a cascade effect, to regulate some of the amyloid up and down. Continue reading