Affinity for Retinal Pigment Epithelium by Certain Viruses

Fischer, Craig A.

doi:10.1016/0002-9394(73)90673-9

Cited by 7 publications

(2 citation statements)

References 4 publications

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“…In other viral diseases of the eye, the pigment epithelium is often a primary site for entry of virus into the eye as well as for initial replication [Fischer, 1973]. Lympho cytic choriomeningitis (LCM) virus is found initially in the pigment epithelium and later appears in other ocular structures [Monjan and Hogan, 1979] due probably to hemato genous spread.…”

Section: Discussionmentioning

confidence: 99%

Replication of Scrapie Prions in Hamster Eyes Precedes Retinal Degeneration

et al. 1986

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Progressive degeneration of outer retinal structures occurs in hamsters with scrapie. In order to determine the relationship between histopathologic changes and replication of the scrapie agent, hamsters were inoculated intracerebrally with – 107 ID50 units. Animals sacrificed at 50 days after inoculation showed no signs of neurologic dysfunction, but had high titers of the scrapie agent or prions in both neural and nonneural portions of the eye. Prion titers in retina were > 107 ID5o units/ml of 10% (w/v) homogenate and equal to those found in optic nerve and brain. No histopathologic changes were seen by light microscopy in any ocular structure. At 70 days after inoculation, neurologic dysfunction was profound. The titers of the scrapie agent in brain, lens, retinal pigment epithelium, cornea, retina, and optic nerve were not significantly changed compared to those found at 50 days; however, retinal degeneration was severe. No morphologic changes were observed in cornea, pigment epithelium or optic nerve. These findings show that scrapie prion replication to maximal levels precedes the onset of degenerative changes in retina. Furthermore, the retina is preferentially susceptible to the degeneration induced by the scrapie agent while the other ocular structures containing significant levels of prions seem to escape injury.

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Section: Discussionmentioning

confidence: 99%

Replication of Scrapie Prions in Hamster Eyes Precedes Retinal Degeneration

et al. 1986

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“…Such a spread may explain the early and marked in fection of the RPE. Infection of the RPE seems to be a common phenomenon during virus infections both in experimental animals and in man [Fischer, 1973]. In spite of the rather frequent involvement of the nervous system in mumps virus infections [Johnson, 1982] only an occasional case with visual changes has been reported [Marmor, 1979], The regular involvement of the retina in the present study, even with the less neurovirulent m utant strain, raises the question whether minor retinal changes of unknown aetiology in man may be caused by this com mon virus.…”

Section: Discussionmentioning

confidence: 99%

Developmental Disturbances in the Hamster Retina Caused by a Mutant of Mumps Virus

Löve¹,

Malm²,

Rydbeck³

et al. 1985

Dev Neurosci

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Newborn hamsters were inoculated intracerebrally with either the neurovirulent Kilham strain of mumps virus or a mutant (M13) strain of this virus. The M13 strain has an alteration in the haemagglutinin-neuraminidase protein of its envelope and causes a low-grade infection of the brain. Both strains spread consistently to the retina where the Kilham strain caused an extensive necrotizing infection. In contrast, the M13 strain predominantly caused an infection of the retinal pigment epithelium (RPE) with the involvement of scattered neurons in the retina. Only minimal degenerative or inflammatory changes were seen, but at 12 days of age developmental alterations were seen in all eyes. These included stretches with failure of photoreceptor segment development and the formation of folds in the outer nuclear layer. The former changes occurred in areas with loss of RPE cells and the latter generally in connection with displaced pigment-loaded cells from the RPE layer. It is suggested that these retinal alterations are mainly secondary to the RPE infection with the M13 strain.

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