Interaction with other infections can trigger the herpes virus to reactivate, research shows -
The famous slogan "A diamond is forever", but this sentence could be best for herpes: Unlike most viruses, which succumb to the attack of the immune system, herpes stays in the body forever, lying in wait, sometimes years later reactivating
researchers have long wondered what causes herpes virus -. two strains that are linked to cancer - to reactivate after remaining dormant after initial infection resolves. Now a team of researchers, including two of Florida's University scientists, found that interactions with others later in life these infections can trigger dormant virus to resurface and cause disease.
Understanding more about how specific pathogens interact with each other could help scientists design new and better ways to fight against these infections and the diseases they cause, the researchers write in an article published today (June 26) in the journal science .
"Probably 95 percent of us were infected with at least one herpes virus, but many people never have a problem with it," said co-author Rolf Renne, Ph.D., professor of molecular genetics and microbiology in the UF College of Medicine and a member of the UF genetics Institute and the UF health cancer Centre. There are eight herpes viruses that infect humans, causing diseases that range from cold sores and chickenpox mononucleosis and cancer. "The question was :? What happens to reactivate these viruses to cause disease"
Conducted by researchers at Washington University in St. Louis, the study found that parasitic infections later in life can trigger an immune response that paves the way for the herpes virus to reactivate. In this case, the scientists studied a specific herpes virus linked to a form of cancer called Kaposi's sarcoma virus, human herpesvirus 8.
The researchers found that after the initial infection with the virus, a protein called interferon gamma herpes keeps in check, which is why the virus usually remains dormant in the body. But when the immune system later, responded to infection by a parasitic worm called helminths, another protein called interleukin-4 was released, which not only blocked the gamma interferon from doing its job, but also virus replication directly activated. When the virus replicates, infects new cells, which increases the chances of a cancerous tumor will form, Renne said.
"The fact that the virus can" sense "of the immune response to a worm and respond reactivating is an outstanding example of co-evolution," said senior author Herbert W. Virgin IV , MD, Ph.D., of Washington University in St. Louis. "We believe that other interactions between multiple infectious agents and immune system will be discovered over time that we will see the same sophisticated way or maybe even devious. Understanding these interactions will help us survive in a complex microbial world. "
Washington University in St. Louis researchers made the discovery by first studying a mouse herpes virus. UF researchers were able to replicate these findings in human cells infected with the herpes virus associated with Kaposi's sarcoma.
The parasitic helminth infections frequently occur in developing countries, including sub-Saharan Africa, where Kaposi's sarcoma cases are also particularly common.
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