CYTOKINE-MEDIATED SURVIVAL FROM LETHAL HERPES-SIMPLEX VIRUS-INFECTION - ROLE OF PROGRAMMED NEURONAL DEATH

被引：44

作者：

GEIGER, KD

GURUSHANTHAIAH, D

HOWES, EL

LEWANDOWSKI, GA

REED, JC

BLOOM, FE

SARVETNICK, NE

机构：

[1] Scripps Res Inst, DEPT NEUROPHARMACOL, LA JOLLA, CA 92037 USA

[2] UNIV CALIF SAN FRANCISCO, DEPT PATHOL ANAT, SAN FRANCISCO, CA 94110 USA

[3] LA JOLLA CANC RES FDN, LA JOLLA, CA 92037 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1995年 / 92卷 / 08期

关键词：

INTERFERON GAMMA; TRANSGENIC MICE; APOPTOSIS; BCL2;

D O I：

10.1073/pnas.92.8.3411

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

The mechanisms responsible for cytokine-mediated antiviral effects are not fully understood. We approached this problem by studying the outcome of intraocular herpes simplex (HSV) infection in transgenic mice that express interferon gamma in the photoreceptor cells of the retina. These transgenic mice showed selective survival from lethal HSV-2 infection manifested in both eyes, the optic nerve, and the brain. Although transgenic mice developed greater inflammatory responses to the virus in the eyes, inflammation and viral titers in their brains were equivalent to nontransgenic mice. However, survival of transgenic mice correlated with markedly lower numbers of central neurons undergoing apoptosis. The protooncogene Bcl2 was found to be induced in the HSV-2-infected brains of transgenic mice, allowing us to speculate on its role in fostering neuronal survival in this model. These observations imply a complex interaction between cytokine, virus, and host cellular factors. Our results suggest a cytokine-regulated salvage pathway that allows for survival of infected neurons.

引用

页码：3411 / 3415

页数：5

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