Necrotizing retinitis in severe combined immunodeficiency mice following intracameral inoculation of herpes simplex virus type 1

Hiroko Minagawa, Ying Liu, Tatsuro Ishibashi, Hajime Inomata, Rvoichi Mori

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Necrotizing retinitis in severe combined immunodeficiency (SCID) mice following intracameral inoculation of herpes simplex virus type 1 provided an experimental model for acute retinal necrosis in AIDS and other immunocompromised patients. In order to assess the involvement of the immunological response in the pathogenesis, adoptive transfer experiments were conducted. Without transfer, SCID mice developed predominantly unilateral necrotizing retinitis and died within 10 days. Transfer of immune serum lengthened the survival time but resulted in bilateral necrotizing retinitis. Two of 5 mice transferred with CD4+ T cells and none of 7 transferred with CD8+ T cells developed bilateral necrotizing retinitis. Our results indicate that ipsilateral retinal necrosis occurs with or without a specific immunological response, and that antibodies and/or CD4+ T cells accelerate the contralateral retinal necrosis.

Original languageEnglish
Pages (from-to)253-260
Number of pages8
JournalOphthalmic Research
Volume26
Issue number4
DOIs
Publication statusPublished - Jan 1 1994

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Retinitis
Severe Combined Immunodeficiency
Human Herpesvirus 1
T-Lymphocytes
Necrosis
Acute Retinal Necrosis Syndrome
Adoptive Transfer
Immunocompromised Host
Antibody Formation
Immune Sera
Acquired Immunodeficiency Syndrome
Theoretical Models

All Science Journal Classification (ASJC) codes

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

Necrotizing retinitis in severe combined immunodeficiency mice following intracameral inoculation of herpes simplex virus type 1. / Minagawa, Hiroko; Liu, Ying; Ishibashi, Tatsuro; Inomata, Hajime; Mori, Rvoichi.

In: Ophthalmic Research, Vol. 26, No. 4, 01.01.1994, p. 253-260.

Research output: Contribution to journalArticle

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