April 1996
Volume 37, Issue 5
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Articles  |   April 1996
Spread of murine cytomegalovirus to inner ocular structures following disruption of the blood-retina barrier in immunosuppressed BALB/c mice.
Author Affiliations
  • Y Duan
    Department of Cellular and Structural Biology, The University of Texas Health Science Center at San Antonio, TX 78284, USA.
  • R Hernandez
    Department of Cellular and Structural Biology, The University of Texas Health Science Center at San Antonio, TX 78284, USA.
  • L Pang
    Department of Cellular and Structural Biology, The University of Texas Health Science Center at San Antonio, TX 78284, USA.
  • S S Atherton
    Department of Cellular and Structural Biology, The University of Texas Health Science Center at San Antonio, TX 78284, USA.
Investigative Ophthalmology & Visual Science April 1996, Vol.37, 935-940. doi:
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    • Get Citation

      Y Duan, R Hernandez, L Pang, S S Atherton; Spread of murine cytomegalovirus to inner ocular structures following disruption of the blood-retina barrier in immunosuppressed BALB/c mice.. Invest. Ophthalmol. Vis. Sci. 1996;37(5):935-940.

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Abstract

PURPOSE: The aims of this study were to determine whether disruption of the blood-retina barrier (BRB) increases spread of murine cytomegalovirus (MCMV) to the eye after intraperitoneal inoculation and whether systemic immunosuppression influences the location of MCMV in the ocular compartment. METHODS: The BRB of the left eye of normal and immunosuppressed mice was disrupted by supraciliary inoculation of tissue culture medium followed 2 hours later by intraperitoneal injection of MCMV. Plaque assay of homogenized ocular tissue was used to determine the frequency of virus-positive eyes and the titer of virus in the eyes. Beta-galactosidase staining of frozen sections was used to locate virus in the eyes. RESULTS: In nonimmunosuppressed mice, the frequency of virus isolation, as well as the titer of virus, were significantly higher in eyes in which the BRB had been disrupted. Although the frequency of virus isolation was the same in both eyes of immunosuppressed mice, the titer of virus was significantly higher in the eye in which the BRB had been disrupted. The most striking result was that the location of virus was different in the nondisrupted eyes of immunosuppressed mice than it was in the disrupted eyes of immunosuppressed mice. In the former, virus was seen only in the outer ocular structures (conjunctiva, sclera, lacrimal gland), whereas in the latter, virus was observed in the retina and anterior segment (iris, ciliary body) as well as the outer ocular structures. CONCLUSIONS: The results of these studies suggest that ocular damage followed by increased spread of virus to and within the eye during systemic infection with CMV may be one mechanism by which development of CMV retinitis is facilitated in patients with acquired immune deficiency syndrome.

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