Australian researchers have found a way to control the virus which causes infection after transplants.

A team of researchers from Western Australia and Queensland has revealed a way to prevent reactivation of a common virus - Human Cytomegalovirus - using a patient’s own antibodies.

They say it could be extremely effective in reducing the impact of this infection in transplant patients.

Around 80 per cent of people worldwide are infected with Human Cytomegalovirus (HCMV), a virus that is seldom a problem as it usually remains dormant in healthy people.

Problems only arise when the immune system is compromised and the virus “reactivates” or comes out of its dormancy.

Cytomegalovirus (CMV) will reactivate in up to two thirds of patients post-transplantation, and up to 10 per cent of those will develop life-threatening end-organ virally-mediated disease.

The team of researchers led by Professor Mariapia Degli-Esposti created a new mouse model to examine the reactivation of CMV during transplantation.

They discovered that antibodies are key to limiting reactivation and injecting mice with their own anti-viral antibodies – a form of serotherapy - protected them from CMV reactivation.

They believe the results will translate to humans in future clinical trials.

“HCMV reactivation is particularly problematic in the setting of transplantation, and affects the successes of both solid organ and stem cell transplants,” Professor Degli-Esposti said.

“Despite much effort being put into improving the control of CMV reactivation in transplantation, we still fall very short of effective treatments and CMV reactivation remains associated with significant sickness and even death.

“We have found that protection from reactivation is achievable using passively acquired antibodies.

“But viruses are clever and keep adapting and changing. These slightly different viral strains trick the immune system and bypass the critical defence check-points.

“Indeed, although we are just beginning to recognise the enormous strain variability that exits for HCMV, we know that people are often infected with more than one HCMV variant. But matching antibodies to the infecting CMV strains bypasses the problem and in these pioneering mouse studies conferred great protection from CMV reactivation.

“It is hoped that this will provide a therapeutic strategy for transplant patients not only because of the extreme effectiveness in preventing reactivation, but also because this approach has a very low risk profile.

“Our research has provided a new strategy to control CMV reactivation and the exciting possibility that we will be able to reduce rates of sickness and death among organ and bone marrow transplant recipients, as well as lower the high costs currently involved in managing this common infection.”