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A vaccine against the disease associated with a virus carried by migrating wildebeest
7/3/13

The chance vaccine

For more than ten years, the study of this singular virus fascinates Benjamin Dewals who is now a Researcher Associate at the FNRS in the Immunology and Vaccinology Unit of the Faculty of Veterinary Medicine of the University of Liege. When he began his doctoral thesis on this subject in 2002, his objective was to uncover all the secrets of this pathology. He did such a good job that he succeeded in discovering a vaccine! “The laws of chance”, he says modestly with a smile.

His discovery is far from modest, in fact. Alain Vanderplasschen, who supervised his research, makes the following prediction. “Benjamin’s discovery will be recorded in virology reference books. His work is very impressive. He was not content to achieve his goals by using techniques that were developed by others. He had to devise his own tools to achieve results. Certain subjects that directly concern humans (cancer, asthma, etc.) often resonate more with the wider public…” The scientific investigations of the Veterinary Department attracted the attention of the American Journal PNAS (Proceedings of the National Academy of Sciences), which devoted ten pages to them in their May edition (1).

The alcelaphine herpesvirus is far from being a new discovery. “I heard about it for the first time in 1986”, recalls Alain Vanderplasschen. If the virus has caused a stir among specialists for a long time, it is because its singularity is quite rare. There is only one other virus that adapts perfectly to its reservoir host but can cause devastating symptoms in other species: Aujesky’s disease, which is harmless in pigs, causes rapid encephalitis in some carnivores and ruminants.

An epidemiological dead end

However, the AlHV-1 virus possesses a specificity: its latency. At the commencement of their study, Benjamin Dewals and the team from Liege noticed an astonishing characteristic thanks to experiments carried out on rabbits. “Once the animal is infected, it dies, but is incapable of transmitting the virus to another animal. It is an epidemiological dead end. This drew our attention because we observed a lymphoproliferation, a proliferation of lymphocytes. The viral load in terms of DNA increases exponentially. We then asked ourselves whether the growing infection we saw was not due to a latent infection”, he explains.

Infection by alcelaphine herpesvirus 1, therefore, only becomes transformed into malignant catarrhal fever after a certain time lapse. But before it manifests itself, it causes a frenzied production of leucocytes. In other words, the virus does not replicate itself, unlike infected cells which spread. “It infects the animal, remains quiet for a few weeks and then, suddenly, we notice an explosion of viral DNA which is not even associated with viral replication!” Explains Alain Vanderplasschen.

This assessment went against the majority of theories that had been put forward up to that point. Most scientists generally affirmed that very few cells were infected. Some of them even went as far as to theorize that only one cell in 10,000 or 100,000 was infected. Benjamin Dewals was able to demonstrate that the opposite was true.

(1) Palmeira L., Sorel O., B.G.Dewals et al., An essential role for γ-herpesvirus latency-associated nuclear antigen homolog in an acute lymphoproliferative disease of cattle, PNAS, May 2013, Vol. 110, n°21

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