A world-leading team of viral and transplant immunologists have prevented reactivation of Human Cytomegalovirus (CMV) in mouse models by injecting th with their own antibodies. Typically dormant, the virus can be triggered in compromised immune systs.LEI Head of Experimental Immunology Professor Mariapia Degli-Esposti, who led the research in conjunction with QIMR Berghofer in Brisbane and the Fred Hutchinson Cancer Research Center in Seattle, told Insight CMV could be life-threatening and is thought to potentially contribute to ocular complications in transplant patients.“It is hoped that this will provide a therapeutic strategy for transplant patients not only because of the extre effectiveness in preventing reactivation, but also because this approach has a very low risk profile,” Degli-Esposti said.{{quote-A:R-W:400-I:2-Q:“It is hoped that this will provide a therapeutic strategy for transplant patients not only because of the extre effectiveness in preventing reactivation, but also because this approach has a very low risk profile.” -who:Professor Mariapia Degli-Esposti, LEI}}Around 80% of the world’s population are infected with CMV, but the virus usually rained inoperative in healthy people. However, it is known to ‘reactivate’ in up to 66% of post-transplantation patients due to their severely weakened immune systs. Up to 10% of those will develop life-threatening end-organ virally-mediated disease.Previous studies by LEI researchers have also shown CMV could exacerbate Sjogren’s syndrome, which is a related complication of ocular graft-versus-host-disease (GVHD). Although it rains unclear, it is possible CMV may contribute to some of the pathologies observed in patients with ocular GVHD.Degli-Esposti and her team discovered that injecting mice with their own anti-viral antibodies – a form of serotherapy – protected th from CMV reactivation. Traditional methods have focussed on controlling the virus, whereas this method is aimed at prevention.“Viruses are clever and keep adapting and changing. These slightly different viral strains trick the immune syst and bypass the critical defence check-points,” Degli-Esposti said.“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 probl and in these pioneering mouse studies conferred great protection from CMV reactivation.”Degli-Esposti added: “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.”
