Genetics can have a big impact on immune responses, making some individuals more suspectible to infections than others. In the world of small mammals, the virus LCMV-Clone 13 establishes a chronic infection in one mouse strain without too much damage. Yet in another mouse strain, the same virus activates a host T cell response that reacts so vigorously against virally-infected tissues that it kills the animal. Such deaths are often characterised by haemorrhagic fevers, where blood vessels start to leak, the body loses its ability to form blood clots and organs start to fail. Pathogens such as Lassa fever virus, Ebola virus and Dengue virus can cause haemorrhagic fever in humans, and represent a serious health threat.
Now, a team of scientists at the Scripps Institute in California, USA, have found that the immune cascade that leads to virus-induced haemorrhagic fever requires the activation of type I interferon signalling in non-haematopoietic cells. They found that simply administering antibodies that block type I interferon receptors could protect susceptible infected mice from developing serious pathological conditions, even though virus still persisted long after the antibody treatment had finished.
This could represent a basic but incredibly effective approach for preventing deaths due to haemorrhagic viral disease. The one caveat is that the type I interferon blockade must be administered relatively soon after infection, since treatment efficacy declines over time, with 100% efficacy at 24 hours, 30% at 60 hours and 0% at 72 hours post-infection.
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Repost from the Stojdl Lab blog.