May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Persistent cytomegalovirus infection causes more severe experimental choroidal neovascularization (CNV) in the mouse
Author Affiliations & Notes
  • D.M. Miller
    Ophthalmology, Bascom Palmer Eye Institute, Miami, FL
  • D.G. Espinosa–Heidmann
    Ophthalmology, Bascom Palmer Eye Institute, Miami, FL
  • S. Pereira–Simon
    Ophthalmology, Bascom Palmer Eye Institute, Miami, FL
  • D.D. Sedmak
    Dean, Georgetown University School of Medicine, Washington, DC
  • R.D. Dix
    Ophthalmology, Jones Eye Institute, University of Arkansas College of Medicine, Little Rock, AR
  • S.W. Cousins
    Ophthalmology, Bascom Palmer Eye Institute, Miami, FL
  • Footnotes
    Commercial Relationships  D.M. Miller, None; D.G. Espinosa–Heidmann, None; S. Pereira–Simon, None; D.D. Sedmak, None; R.D. Dix, None; S.W. Cousins, None.
  • Footnotes
    Support  EY/AI–13318
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 490. doi:
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      D.M. Miller, D.G. Espinosa–Heidmann, S. Pereira–Simon, D.D. Sedmak, R.D. Dix, S.W. Cousins; Persistent cytomegalovirus infection causes more severe experimental choroidal neovascularization (CNV) in the mouse . Invest. Ophthalmol. Vis. Sci. 2004;45(13):490.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: We have previously shown that macrophages are important in mouse models of experimental CNV, and that anti–macrophage therapy can limit severity. Second, patients with wet age–related macular degeneration (AMD) appear to have macrophages with higher levels of pro–inflammatory activity. Third, we have found a much higher frequency of elevated cytomegalovirus–specific IgG titers in the serum of patients with wet AMD compared to patients with dry AMD. Therefore, we hypothesize that wet AMD may be associated with macrophage activation in response to persistent infection with cytomegalovirus. We sought to test this idea in a mouse model of experimental CNV. Methods: C57BL/6 mice were injected with UV inactivated virus or infected with non–lethal doses of the Smith strain of murine cytomegalovirus. At various times after infection (6 days, 6 weeks and 12 weeks), laser–induced CNV was performed. CNV severity was determined 4 weeks later by analysis of choroidal flatmount and histopathology. Various tissues were recovered to document the persistent murine cytomegalovirus infection using nested PCR. Results: Mice receiving UV inactivated virus demonstrated typically small CNV (1.8+/–0.3 disc areas). In comparison, all mice infected with live virus demonstrated more severe CNV. The most severe CNV developed in mice with the most chronic infection (12 weeks post–infection = 4.4 +/– 1.2 disc areas, p<0.0001 versus UV inactivated virus). The frequency of large lesions > 2 disc areas was greater among infected mice (UV = 10%, 6 days = 57%, 6 weeks = 91% and 12 weeks = 100%, p<0.001). PCR demonstrated abundant latent/persistent virus in lung. Conclusion: These studies indicate that chronic cytomegalovirus infection may promote increased CNV size and severity. Although the mechanism remains unclear, persistent infection of circulating macrophages is a likely possibility.

Keywords: age–related macular degeneration • choroid: neovascularization • cytomegalovirus 
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