It is possible to bring herpes simplex virus-1 (HSV-1) out of its hiding place inside the body and render it vulnerable to drugs, a virologist at Duke University in Durham, North Carolina, has revealed.
Bryan Cullen said that his team had found clues to how a gene called LAT, switched on by the herpes virus, works.
AdvertisementDescribing HSV-1 as a docile beast, the researcher pointed out that it could snooze inside a person's neurons, secluded from drugs and the immune system.
He said that scientists had for long suspected that LAT was the key to herpes' ability to remain dormant inside nerve cells, but no-one knew how it did so.
To unravel this mystery, the researchers infected mice with HSV-1, and waited for the virus to retreat to nerve cells and go silent.
The group later scoured the cells for traces of sliced RNA that matched that from LAT.
Cullen revealed that the team found several microRNAs, a recently-discovered kind of molecule that cells use to dial down the levels of proteins.
While four microRNAs came from cut-up LAT, the fifth came from a previously unknown chunk of RNA, which suggests LAT was not the only viral DNA molecule involved in latency.
Many microRNAs play a role in maladies such as cancer and heart disease, and some viruses even make microRNAs to stymie cell defences.
The researchers, however, observed that HSV-1's microRNAs latched onto viral mRNA molecules, and blocked cells from cranking out two virus proteins (ICP0 and ICP4) essential for escaping dormancy.
Cullen is of the opinion that viruses may be coaxed out of hiding by blocking such microRNAs, and then to treat patients with drugs that stamp out herpes in epithelial cells, such as acyclovir.
"Every virus that pops out gets killed," New Scientist magazine quoted Cullen as saying in a study report published in the journal Nature.
However, Patricia Spear, a virologist at Northwestern University in Evanston, Illinois, thinks that this approach may prove troublesome because waking a virus seems to sacrifice the infected nerve cell
"You would be inducing replication of virus in the neuron and the question is how many neurons you want to kill off," she says.
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