How herpes and other dormant viruses ‘reactivate’ explained in new study

illustration-of-herpes-zoster-virus 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.

In total, there are eight herpes viruses that can affect humans. Some versions of the virus can cause chickenpox, mononucleosis and cancer.

“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?”

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.

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