Herpes simplex virus type 2 infection induced apoptosis in peritoneal macrophages independent of Fas and tumor necrosis factor-receptor signaling

Fleck, Martin and Mountz, John D. and Hsu, Hui-Chen and Wu, Jiango and Edwards, Carl K. and Kern, Earl R. (1999) Herpes simplex virus type 2 infection induced apoptosis in peritoneal macrophages independent of Fas and tumor necrosis factor-receptor signaling. VIRAL IMMUNOLOGY, 12 (3). pp. 263-275. ISSN 0882-8245,

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Abstract

Freshly isolated macrophages from mature mice are poorly or nonpermissive for infections with HSV. However, despite lack of significant viral replication, HSV infection has been demonstrated to induce substantial cell death among macrophages, To determine if HSV-induced cytotoxicity of macrophages is due to apoptosis, peritoneal macrophages were obtained from C57BL/6 (B6) mice, and apoptosis was analyzed following HSV-2 infection irt vitro. Macrophages underwent apoptosis upon HSV-2 infection indicated by annexin V staining, labeling of DNA strand breaks and electronmicroscopy, Apoptosis was associated with macrophage activation demonstrated by upregulation of MHC class II and Mac-1 surface expression. Though there was also an upregulation of Fas (Apo-1/CD95) and tumor necrosis factor (TNF)-receptor 1 (TNF-R1) pathways, inhibition of Fas by soluble Fas and blocking of TNF-alpha using a TNF-binding protein did not prevent HSV-induced apoptosis, Moreover, apoptosis was not impaired in HSV-2 infected macrophages from Fas-deficient B6-lpr/lpr mice suggesting involvement of other apoptosis pathways, or activation of Fas or TNF-R pathways downstream of the receptor level. The present results demonstrate that HSV-2 infection leads to activation and subsequent apoptosis in peritoneal macrophages independent of Fas or TNF-R1 signaling.

Item Type: Article
Uncontrolled Keywords: PROGRAMMED CELL-DEATH; T-LYMPHOCYTES; FACTOR-ALPHA; INTERFERON-ALPHA/BETA; INTRINSIC RESISTANCE; MOUSE MACROPHAGES; BLOCKS APOPTOSIS; GAMMA-INTERFERON; NEURONAL DEATH; NEONATAL MICE;
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Innere Medizin I
Depositing User: Dr. Gernot Deinzer
Date Deposited: 06 Dec 2022 07:46
Last Modified: 06 Dec 2022 07:46
URI: https://pred.uni-regensburg.de/id/eprint/48747

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