The cold sore virus is mysterious and confounding even to those sufferers who are likely to understand its makeup and pathology. For example, the way the virus lurks waiting to break out when you are under stress or at a low ebb, leaving you to reach out for your cold sore cream at a time when you'd rather be getting on with something else.
It is this characteristic of the cold sore virus, the way it hibernates in the body, that has also long perplexed scientists. However, now researchers at Harvard Medical School have demonstrated how the Herpes Simplex Virus 1 manipulates a host protein called CTCF in order to sleep quietly before breaking out, usually at the most inopportune moment possible.
The research, which subjected mice to the cold sore virus, found that CTCF plays a key role in regulating its activation-dormancy cycle by allowing it to set-up latent infections in sensory neurons, ready to be reawakened at any moment. Crucially, the scientists found that by altering the CTCF protein, they were able to reduce the virus's ability to activate.
Although the research gives renewed hope to sufferers that scientists are on track in their mission to find a cold sore cure, it also sheds some light on the incredible survival skills of the virus. Because it can hide during latent periods, it is able to keep away from the immune system, priming it for the next outbreak.
"Our findings shed light on one of the more confounding behaviours of the herpes simplex virus – its ability to transition between a silent and active infection, a state of so-called poised latency, which allows it to be quiet yet remain on standby," commented David Knipe, one of the key researchers and the Higgins Professor of Microbiology and Molecular Genetics at Harvard Medical School's Department of Microbiology and Immunobiology.
The ultimate hope from this research is that further work might yield a way for scientists to target CTCF binding sites so that they can reduce the cold sore virus's ability to wake from dormancy. They now have proof that the CTCF protein regulates infection cycles, they just don't have a way of effectively addressing this in humans, at least not yet. In the meantime, we'll have to continue watching what we eat, washing our hands regularly and, when necessary, applying the cold sore cream we know to work best.
