Scientists Make Herpes Breakthrough
ROBERT SIEGEL, host:
Most people in this country are infected by herpes viruses, and they may not know it. That's because the virus has a remarkable property, it can lie dormant for years and then suddenly flare up. How herpes manages this hibernation and reawakening is been a mystery.
But now, as NPR's Joe Palca reports, scientists think they may have figured it out.
JOE PALCA: There are many different types of herpes virus. Herpes simplex virus type 1 causes cold sores, herpes simplex virus type 2 causes genital sores, and a third herpes virus causes chickenpox in children and shingles in adults.
Bryan Cullen studies the cold sore variety of herpes. Cullen is at Duke University in Durham, North Carolina. He says people usually become infected with this herpes virus early in life.
Professor BRYAN CULLEN (Molecular Genetics and Microbiology, Duke University): You get infected when you're a kid and the virus actually stays with you until you die.
PALCA: Cullen says the virus typically enters the body through the mouth or lips, but then it goes to infect nerve cells called neurons.
Prof. CULLEN: When herpes simplex virus infects the neuron, it actually goes to the nucleus and it just sits there.
PALCA: And it can just sit there in what's called the latent state for decades.
Prof. CULLEN: And during that time, what it makes is this one, RNA molecule called the Latency Associated Transcript or LAT.
PALCA: This strand of genetic material called LAT breaks down into a lot of tiny fragments called microRNAs. These microRNA molecules can switch off genes. Cullen says in the case of herpes infection, the genes switched off by the microRNAs are the very genes that caused the virus to replicate. So normally, the microRNAs keep the virus dormant.
It's only when replication genes get specially revved up, usually because of some external stress, that the microRNAs are overwhelmed. The virus explodes from its resting state and the symptoms of the herpes infection reappear. Cullen says it's interesting to think about what would happen if you switched off the microRNAs. By his theory, without them, the virus would be replicating all the time.
Prof. CULLEN: Now, that arguably is a bad thing. But it turns out that we have really good drugs that kill productively replicating herpes simplex viruses that are approved drugs that are commercially available.
PALCA: So switching off the microRNAs might actually be a good thing. The drugs can't kill the virus when it's dormant.
Prof. CULLEN: The concept would be that you might be able to activate the virus, drive it into productive replication, treat with one of these drugs, and kill the virus as soon as it pops its heads out.
PALCA: All that is for the future. For the moment, scientists will want to confirm Cullen's work to make sure it holds up. There have been a lot of rival theories about how the herpes virus can remain dormant in cells for decades.
But Patricia Spear says the theory of Cullen and his colleagues involving microRNAs will attract a lot of attention from people in the field - many, no doubt, trying to prove it wrong. Spear is a herpes expert at Northwestern University in Evanston, Illinois.
Dr. PATRICIA SPEAR (Microbiology, Northwestern University): They've presented a plausible way for this to happen.
PALCA: So I guess what you would be saying then is it's not like every lab studying latency in herpes virus is going to pack up and say, well, our work is done.
Dr. SPEAR: No. No way.
(Soundbite of laughter)
Dr. SPEAR: This has been a very contentious field and this is new information. It's exciting information and it undoubtedly is a part of the story. But just, we caution, it's not the whole story.
PALCA: That's usually the way it is in science.
Joe Palca, NPR News, Washington.
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