Does Cytomegalovirus Infection of the Human Eye Contribute to the Development of Age-related Macular Degeneration (AMD)?

Ming Zhang, MD, PhD
Augusta University Research Institute, Inc. (Augusta, GA)
Year Awarded:
2019
Grant Duration:
July 1, 2019 to June 30, 2021
Disease:
Macular Degeneration
Award Amount:
$200,000
Grant Reference ID:
M2019035
Award Type:
Standard
Award Region:
US Southeastern
Ming Zhang, MD, PhD

The Role of Cytomegalovirus in the Development of Neovascular Age-related Macular Degeneration (AMD)

Summary

Age-related macular degeneration (AMD) is a leading cause of vision loss among people age 50 and older. Cytomegalovirus (CMV), a very common virus staying in the bodies of over half of Americans, is associated with the development of many long-term diseases. The purpose of this application is to investigate if CMV stays in the human eyes and how virus reactivation in the eye contributes to the development of AMD. This study also explores strategies to inhibit virus reactivation and alleviate development of AMD induced by CMV reactivation in the eye. 

Details

The goal of my project is to determine if and how cytomegalovirus (CMV), a very common virus staying in the bodies of over half of Americans, causes the development of neovascular age-related macular degeneration (AMD). 

CMV is usually acquired during early life and often persists in a latent state for the life of the individual. More than 12% of 1 year old U.S. infants have been infected with CMV.  By using a mouse model, our recent studies have revealed for the first time that acquiring systemic CMV infection during early life is associated with widespread viral latency at several sites including the eye. Importantly, pathology typical of AMD developed in eyes of these mice at several months post infection. In specific aim 1 of this project, we will investigate if the human eye is a site of CMV latency. In addition, we will determine if CMV latency in the choroid of human eye is associated with production of inflammatory factors which favor the development of neovascular AMD.  In specific aim 2 of this project, we will continue to use our animal model to investigate the mechanism by which latent CMV infection in the choroid causes the development of AMD, and also explores strategies to inhibit virus reactivation and alleviate development of AMD induced by CMV reactivation in the eye.

Our project is the first to explore a possible viral etiology for AMD as a result of latent CMV infection of the human eye. The results of our studies will further understanding of the pathogenesis of AMD in human patients and may ultimately be translated to new therapies to alleviate in situ inflammation and prevent development of AMD induced by latent infections. 

About the Researcher

I am an assistant professor and a retinal virologist in Medical College of Georgia at Augusta University working on projects using mouse models and retinal culture models related to the pathogenesis of cytomegalovirus (CMV) ocular infections for many years. One of my research project focuses on identify factors and pathways participating in tissue damage and  cell death, leading to the impairment of vision during CMV retinitis, a disease which occurs predominantly in infants with congenital CMV infection or in people whose immune system has been compromised (15-40% of those with AIDS). Recently, we have developed an in vivo mouse model of systemic neonatal CMV infection. By using this model, we will identify the mechanism whereby CMV latent infection in the choroid accelerates the development of neovascular AMD.

Personal Story

I am a native of China and worked in China for several years as pediatrician, who specialized in pediatric infectious diseases before I immigrated to the U.S. and later became an assistant research scientist in the Medical College of Georgia at Augusta University. Indisputably my past experiences have inspired my scientific interests in CMV eye infections.  While I worked as a pediatrician in China I came across numerous children, whom were born with congenital CMV infection, which included my best friend’s daughter, who unfortunately experienced vision loss and cognitive delay caused by the virus.  Support from BrightFocus is invaluable to my research program. Funding from BrightFocus allows my research group to test the novel research idea that the human eye is a site of CMV latency, which could promote development of AMD.  The data acquired from this study should provide a basis to obtain prolonged government support to fully investigate the role of ocular HCMV latency in AMD patients and attempt to identify the mechanism by which latent virus infection in the choroid/RPE contributes to neovascular AMD.

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