How herpes and other dormant viruses 'reactivate' explained in new study
Scientists have found that interactions between different viruses can trigger dormant viruses to reactivate and cause disease. The researchers believe this explains why cases of herpes can sometimes return after the virus has long lain dormant in a host.
Most people in the US get oral herpes - or herpes simplex virus type 1 - by the age of 20. Following the first infection - usually after 1 or 2 weeks - the virus will become dormant in the facial nerve tissues.
Occasionally, however, the virus may reactivate and cause milder cold sore symptoms.
"Probably 95% of us have been infected with at least one herpes virus, but many people never have a problem with it," says study co-author Rolf Renne, PhD, a professor of molecular genetics and microbiology in the University of Florida (UF) College of Medicine and a member of the UF Genetics Institute and the UF Health Cancer Center.
"The question has been: what happens to reactivate these viruses to cause disease?"
The researchers found that interferon gamma kept the herpes virus dormant, but when the immune system responded to a helminth infection, the virus would reactivate.
In co-operation with researchers from Washington University in St. Louis, MO, Renne and his UF colleagues investigated how human herpes virus 8 - a herpes virus linked to the Kaposi's sarcoma cancer - reactivates. They publish their findings in the journal Science.
Working first with a mouse model, and then replicating their findings in human subjects, the team found that after initial infection, the protein interferon gamma kept the virus dormant in the body.
However, the effect of the interferon gamma was cancelled out following an infection from a helminth worm - a common parasite in sub-Saharan Africa, where Kaposi's sarcoma is also common.
The researchers observed that another protein called interleukin 4 was released by the immune system to deal with the helminth, but this blocked the interferon gamma function and also activated the replication function of the herpes virus.
Replication of the virus causes new cells to be infected, increasing the chances that a cancerous tumor will form.
Senior author Dr. Herbert W. Virgin IV, of Washington University, says:
"The fact that the virus can 'sense' the immune reaction to a worm and respond by reactivating is a remarkable example of co-evolution.
We think other interactions between multiple infectious agents and the immune system will be discovered over time that we will view as similarly sophisticated or maybe even devious. Understanding these interactions will help us survive in a complex microbial world."
Earlier this week, Medical News Today reported on research from scientists at the University of Montreal in Canada who suggest that a small molecule found in the urine of pregnant women blocks the growth of Kaposi's sarcoma, as well as a variety of other cancers. The molecule is a metabolite that is a product of the pregnancy hormone human chorionic gonadotropin.
In 2013, we also reported on a study that suggested a type of nanoparticle could be used to deliver vaccines that protect against HIV, human papilloma virus and herpes, as well as flu and other respiratory diseases.
Written by David McNamee
Copyright: Medical News Today
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