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Herpes infection may be symbiotic, help beat back some bacteria

Mice with chronic herpes virus infections can better resist the bacterium that causes plague and a bacterium that causes one kind of food poisoning, researchers report in this week's Nature.

Scientists at Washington University School of Medicine in St. Louis attributed the surprising finding to changes in the immune system triggered by the long-term presence of a latent herpes virus infection. In latent viral infections, the virus is present for the lifetime of the host in a relatively quiescent form that does not cause overt symptoms.

While presenting their results, researchers stressed that they did not want to minimize or in any way disregard the human suffering and health risks caused by disease-causing herpes infections. But they noted that several strains of herpes viruses found in much of the human population remain symptom-free throughout the host's lifetime.

"Our results suggest that we should look at whether humans receive similar advantages from these and other chronic infections that do not cause active disease," says senior author Herbert W. "Skip" Virgin, M.D., Ph.D., head of the Department of Pathology and Immunology. "If so, that has public health implications because we would want to very carefully weigh the risks and benefits of eliminating a virus that our bodies have established a symbiotic relationship with."

Scientists previously used vaccination to eliminate the deadly and highly contagious smallpox virus. Vaccines are currently in use or in clinical trials for several disease-causing strains of herpes.

Human herpes viruses include oral and genital herpes, the chickenpox virus, cytomegalovirus, Epstein-Barr virus and Kaposi's sarcoma-associated herpes virus. During an initial period of acute infection, many of these viruses cause symptoms, such as fever, cold sores or blisters. They then enter periods of latency. Sometimes symptoms never recur; sometimes they flare up periodically before becoming quiescent again
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Contact: Michael C. Purdy
purdym@wustl.edu
314-286-0122
Washington University School of Medicine
16-May-2007


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