Using an approach that might also prove successful against HIV, scientists in the US have developed a vaccine for the herpes simplex virus that causes cold sores and genital lesions.

Previous efforts to develop vaccines to protect people from these viruses, which infect more than 80% of the population, have not been successful.

Part of the reason is that, once an individual is infected, the virus retreats inside the nervous system, lurking in just its DNA form beyond the reach of the immune system. From this "latent" state, which persists for a person's lifetime, the virus periodically reactivates, producing infectious skin lesions that can transmit the agent to other individuals.

So the key to effective vaccination is to prevent the virus getting into the nervous system in the first place.

But therein lies the problem, because the very parts of the body that the virus has evolved to infect first, chiefly the mucous membranes of the mouth and genital tract - which are also richly supplied with sensory nerve cells - are normally no-go areas for virus-targeting CD8 T lymphocytes that can provide protection. And so initial vaccination attempts, while very effective at marshalling an immune army, were incapable of deploying the troops to the tissues most in need of defence.

Now two Yale scientists may have found a way to solve the problem. Haina Shin and Akiko Iwasaki, writing in Nature, call their approach "prime and pull".

Put simply, they first vaccinate by administering a weakened form of herpes to the skin. This drives an immune response to the virus, including production of key CD8 virus-combating T cells. They then "pull" these cells to the genital tract by administering, 5 days later, a dose of a pair of chemical "chemokine" signals called CXCL9 and CXCL9. These chemicals are used naturally by the immune system to target cells to tissues.

The result, in groups of experimental mice used by the researchers, was the accumulation of long-lived herpes-recognising memory T cell "sentries" within the genital tracts of the animals.

When these mice were then subsequently exposed, up to 3 months later, with what would otherwise have been a potentially lethal dose of a naturally-occurring herpes simplex virus strain, the animals all survived. Control mice, that had been vaccinated via the skin but had not received the pull signals administered genitally, had mortality rates of almost 50%.

Moreover, checks on the nervous systems of the vaccinated mice showed that, compared with the controls, the levels of virus reaching these sites were orders of magnitude lower.

According to Shin and Iwasaki, "a single topical treatment with the chemokines applied vaginally can provide superior protection against genital herpes by preventing the spread of the infection from the mucosa into neurones."

They also hint at the tantalising possibility that this same strategy might work with HIV too, arresting the virus before it gains access to the immune cells it needs to penetrate in order to initiate an infection...

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