I wasn't referring to Ms. Umbach

I was referring to Maggie Fox, the Health and Science Editor who wrote the article that appeared online.

Here's the abstract of the article.

"Nature. 2008 Jul 2.
MicroRNAs expressed by herpes simplex virus 1 during latent infection regulate viral mRNAs.
Umbach JL, Kramer MF, Jurak I, Karnowski HW, Coen DM, Cullen BR.

Department of Molecular Genetics and Microbiology and Center for Virology, Duke University Medical Center, Durham, North Caroline 27710, USA.

Herpesviruses are characterized by their ability to maintain life-long latent infections in their animal hosts. However, the mechanisms that allow establishment and maintenance of the latent state remain poorly understood. Herpes simplex virus 1 (HSV-1) establishes latency in neurons of sensory ganglia, where the only abundant viral gene product is a non-coding RNA, the latency associated transcript (LAT). Here we show that LAT functions as a primary microRNA (miRNA) precursor that encodes four distinct miRNAs in HSV-1 infected cells. One of these miRNAs, miR-H2-3p, is transcribed in an antisense orientation to ICP0-a viral immediate-early transcriptional activator that is important for productive HSV-1 replication and thought to have a role in reactivation from latency. We show that miR-H2-3p is able to reduce ICP0 protein expression, but does not significantly affect ICP0 messenger RNA levels. We also identified a fifth HSV-1 miRNA in latently infected trigeminal ganglia, miR-H6, which derives from a previously unknown transcript distinct from LAT. miR-H6 shows extended seed complementarity to the mRNA encoding a second HSV-1 transcription factor, ICP4, and inhibits expression of ICP4, which is required for expression of most HSV-1 genes during productive infection. These results may explain the reported ability of LAT to promote latency. Thus, HSV-1 expresses at least two primary miRNA precursors in latently infected neurons that may facilitate the establishment and maintenance of viral latency by post-transcriptionally regulating viral gene expression.

PMID: 18596690"

There's no mention of getting the latent viral dna out of the cell. There is mention of microRNA preventing productive infection by keeping certain genes inactive. Allowing those genes to become active results in replication and production of new, whole viruses, and those leave the cell. The original copy stays put. They have not discovered a way to get that out.

As far as my being a pessimist... I'd rather think of myself as an optimist. Having herpes doesn't have to be the end of anything. It hasn't been for me. I have a loving wife, children, a job, friends, etc. For the vast majority of people, it's an occasional skin irritation. What's bad is the unfair stigma associated with it in ignorant people's minds. I think that's where a lot of work should be done. Nobody needs a PhD in microbiology to help fight the stigma. We can all work on that one.

That said, research into the nature of herpes is very important and I'm not at all saying that my opinion is that there will never be a cure, but if one appears, it's a long way down the road from now. I actively support research would definitely welcome new treatments. I'm enough of a realist not to get caught up in the hype about a miracle "cure".