GALVESTON, Texas When a virus infects a person, it triggers a series of biochemical reactions in immune-system cells that literally may have life or death consequences.
Usually, the result is an effective immune response, leading to the elimination of the virus and the infected persons recovery. But in the case of some of the worlds deadliest pathogens including the Ebola, Marburg and Lassa fever viruses, as well as the influenza virus strain responsible for the 1918 flu pandemic the immune system itself actually becomes the most dangerous element of the disease. All too often, a sudden immune overreaction sends the infected person into a shock-like state from which he or she may never recover.
Now, researchers at the University of Texas Medical Branch at Galveston (UTMB) believe theyve found a way to spot the biochemical profile of an inappropriate immune response to viral infection an important step toward developing new therapies that may head off or stop an otherwise fatal immune system meltdown.
In a paper published in the February 14 issue of the Journal of Virology, highlighted in the journals Spotlight section and available now online, the scientists describe using a newly developed protein-scanning chip and a uniquely capable computer database to examine the activation and deactivation of more than a thousand proteins in cells from guinea pigs infected with two different strains of Pichinde virus. Guinea pigs infected with one of the Pichinde strains experience no ill effects, while those infected with the other strain develop symptoms similar to those seen in humans infected by the much more dangerous Lassa virus, which can cause an acute hemorrhagic fever and kills about 5,000 people a year in West Africa. (During some Lassa fever epidemics, as many as 50 percent of those diagnosed with the disease have died from it.)
With these two forms of the virus and this new technology, we were able to compare pathog
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Contact: Jim Kelly
jpkelly@utmb.edu
409-772-8791
University of Texas Medical Branch at Galveston
14-Feb-2007