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1 is and directing treatment in cases of acute retinal necrosis.
2 ral eye becomes infected and undergoes acute retinal necrosis.
3 e that T cells play a role in development of retinal necrosis.
4 e retina, despite initial lack of observable retinal necrosis.
5 Six of 7 specimens had foci of retinal necrosis.
6 gmentation and thinning, iris recession with retinal necrosis and hypotony, a filtering conjunctival
8 arrive in the sensory retina at the onset of retinal necrosis and not during acute retinitis and the
9 al injury, with central sclopetaria retinae, retinal necrosis, and surrounding commotio retinae with
10 etinal whitening without clinically apparent retinal necrosis] and necrotizing retinochoroiditis) at
12 fy determinants of adverse outcomes in acute retinal necrosis (ARN), presenting characteristics and i
13 simplex virus-type 2 (HSV-2) can cause acute retinal necrosis (ARN), which can lead to exudative and
16 c necrotizing MCMV retinitis (full-thickness retinal necrosis associated with virus inclusions and cy
18 sensory retina coincident with the onset of retinal necrosis (day 11 p.i.), and CD4+ and CD8+ T cell
19 /6 mice and exhibited absolute resistance to retinal necrosis following subretinal MCMV inoculation,
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