During their studies, the Scripps team, led by Elina Zuniga, found that the virus disabled the natural response of the host's immune system by binding with the plamacytoid dendritic cells, which are key triggers for the production of Type 1 interferons. These interferons play an important part in starting other chain reactions, that eventually lead to the massive production of lymphocytes and innate killer cells, which can successfully prevent a great many infections from setting in.
"It's the first demonstration that a virus causes suppression of the interferon response in vivo. This model explains how a secondary infection can be caused by a normal virus infection and this provides the guide for what to do and where to look in human diseases, which are of course more difficult." said Michael Oldstone, senior study author and Scripps research professor.
The authors noticed that the herpes virus had a very high incidence rate in mice that were infected with the lymphocytic choriomeningitis virus, which led them to believe that the first only takes advantage of the "gap" in the immune system to infect the host. Under normal conditions, it would be eliminated by the highly-adaptive T lymphocytes. But because the blood elements are not produced, due to the fact that the interferons are bound with the suppressive virus, the herpes virus is free to replicate at will.
By understanding the exact way in which immunosuppressive viruses bind to designated "defense" cells in the body, scientists hope to someday be able to develop novel treatments against human diseases such as AIDS and measles. Their guess so far is that these types of viruses bind to the cells in the immune system and somehow hide their presence, which leads the host body to believe that nothing is wrong. Eliminating this advantage the virus has could lead to successful immune response to infections.