A team of
researchers, including a scientist from the Viral Immunology Center at Georgia
State University, have found that a type of herpesvirus infection of the eye is
associated with neovascular age-related macular degeneration (AMD), a disease
that causes blindness in the elderly.
The scientists found that human cytomegalovirus, a
type of herpesvirus, causes the production of vascular endothelial growth
factor, or VEGF, a signal protein that regulates the formation of new blood
vessels.
With the formation of new blood vessels, retinal
tissue destruction occurs, leading to the development of "wet" AMD
and eventually, vision loss and blindness. The results were published in PLoS Pathogens, a
journal of the Public Library of Science.
"Prior to this work, cofactors for the
development of AMD included genetics, a high fat diet and smoking. Now, we are
adding an infections agent as another cofactor," said Richard D. Dix,
professor at the Georgia State Viral Immunology Center's Ocular Virology and
Immunology Laboratory.
The research team includes Dix, Scott W. Cousins,
Diego G. Espinosa-Heidmann, Daniel M. Miller, Simone Pereira-Simon, Eleut P.
Hernandez, Hsin Chien and Courtney Meier-Jewett.
Affiliated research institutions include the Duke
University Eye Center, the Bascom Palmer Eye Institute of the University of
Miami Miller School of Medicine, the Viral Immunology Center at Georgia State,
and the Department of Ophthalmology at the Emory University School of Medicine.
Human cytomegalovirus is a common herpesvirus, said
Dix, who is also an adjunct professor of ophthalmology at the Emory University
School of Medicine. About 80 percent of the population is estimated to have
antibodies for the virus, and it is often acquired during childhood.
If a person has a normal, healthy immune system,
the virus becomes latent in the cells of bone marrow and blood, he said. But in
the elderly, the immune system's function is reduced, the virus proliferates,
and the production of VEGF increases.
Identifying human cytomegalovirus as a cofactor in
the development of AMD opens up new paths for the treatment of AMD, Dix said.
One route could include reducing the viral load – the amount of the human
cytomegalovirus in the blood stream – by treatment with an antiviral drug known
as ganciclovir.
Additional research paths include looking at the
genetics involved in the upregulation of VEGF by human cytomegalovirus.
"If we can knock down a certain gene or genes
of the virus that stimulates VEGF production, we might be able to decrease it
production and minimize AMD," Dix said.
More information: Cousins
SW, Espinosa-Heidmann DG, Miller DM, Pereira-Simon S, Hernandez EP, Chien H,
Meier-Jewett, and Dix RD (2012) Macrophage Activation Associated with Chronic
Murine Cytomegalovirus Infection Results in More Severe Experimental Choroidal
Neovascularization.PLoS Pathog 8(4): e1002671. doi:10.1371/journal.ppat.1002671
Provided by Georgia
State University
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