Apoptosis induction after herpes simplex virus infection differs according to cell type in vivo

Apoptosis induction after herpes simplex virus infection differs according to cell type in vivo We compared apoptosis induction in mice following three routes of infection. After intravenous infection, wild-type herpes simplex virus (HSV) types 1 and 2 and US3Δ mutants infected the adrenal gland and caused apoptosis. Corneal infection with wild-type virus resulted in apoptosis in a fraction of infected epithelium cells. Interestingly, many uninfected cells were apoptotic in the retina. Although neurons in the trigeminal ganglion were heavily infected, no apoptotic neurons were observed. Intracranial infection with wild-type virus resulted in HSV-infected cells inside the brain; however, most of the infected neurons escaped apoptosis. In contrast, infection with US3Δ and γ 1 34.5Δ mutants caused apoptosis in infected neurons. Cleaved caspase-8 and p53 were detected in apoptotic cells in the adrenal gland and the brain; however, phospho-JNK was detected only in apoptotic cells of the brain. These results suggest that the activation of apoptotic signaling proteins differs depending on the host cell type and modulates the induction of apoptosis in HSV-infected cells. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Apoptosis induction after herpes simplex virus infection differs according to cell type in vivo

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Publisher
Springer Journals
Copyright
Copyright © 2010 by Springer-Verlag
Subject
Biomedicine; Infectious Diseases; Medical Microbiology ; Virology
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-010-0712-2
Publisher site
See Article on Publisher Site

Abstract

We compared apoptosis induction in mice following three routes of infection. After intravenous infection, wild-type herpes simplex virus (HSV) types 1 and 2 and US3Δ mutants infected the adrenal gland and caused apoptosis. Corneal infection with wild-type virus resulted in apoptosis in a fraction of infected epithelium cells. Interestingly, many uninfected cells were apoptotic in the retina. Although neurons in the trigeminal ganglion were heavily infected, no apoptotic neurons were observed. Intracranial infection with wild-type virus resulted in HSV-infected cells inside the brain; however, most of the infected neurons escaped apoptosis. In contrast, infection with US3Δ and γ 1 34.5Δ mutants caused apoptosis in infected neurons. Cleaved caspase-8 and p53 were detected in apoptotic cells in the adrenal gland and the brain; however, phospho-JNK was detected only in apoptotic cells of the brain. These results suggest that the activation of apoptotic signaling proteins differs depending on the host cell type and modulates the induction of apoptosis in HSV-infected cells.

Journal

Archives of VirologySpringer Journals

Published: Aug 1, 2010

References

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