However, until now, no one even understood how herpes simplex 1 maintained its latent state.
That's all changed, thanks to the painstaking research conducted at Duke. According to Umbach, scientists had long noted that during latency, herpes simplex 1 produces only one tiny product, dubbed "latency associated transcript RNA" (LAT RNA).
These bits of genetic material didn't seem to have any useful function. However, after careful research, the Duke team found that this gene "is processed into smaller parts called microRNAs, and those microRNAs are actually used to target the genes that are required for active replication," Umbach said.
In other words, over weeks or even years, dormant herpes simplex 1 quietly generates just enough LAT RNA to act as a kind of "damper" on the genetic switch that would normally push it into full activation.
"So, the genes for active replication stay asleep -- until this gene is interrupted somehow," Umbach said.
This, then, appears to be the elusive mechanism by which herpes simplex 1 stays dormant and evades drug therapy.
The next step, according to Umbach, is to find an agent that blocks LAT RNA, thereby waking up the entire population of virus at once.
She said her team is already experimenting with an experimental drug that appears to do just that. Once this agent is inside the host nerve cell, "it binds to the microRNAs and inhibits their function," she explained. The virus is then allowed to activate. "Then one of the drugs like acyclovir should be able to handle the infection," Umbach said.
That strategy appears to be working in the test tube at least. "There are animal trials under way, and we are looking into clinical trials for humans. But it will be a while before we can get there," Umbach cautioned.
Another expert was also guardedly optimistic.
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