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J Neuroimmunol. 2003 Aug;141(1-2):40-6.

Interferon-beta suppresses herpes simplex virus type 1 replication in trigeminal ganglion cells through an RNase L-dependent pathway.

Author information

1
Department of Ophthalmology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA. dan-carr@ouhsc.edu

Abstract

The induction of an antiviral state by type I interferons (IFN) was evaluated in primary trigeminal ganglion cell cultures using herpes simplex virus type 1 (HSV-1). Cells treated with mouse IFN-beta consistently showed the greatest resistance to HSV-1 infection in comparison to cells treated with IFN-alpha1, IFN-alpha4, IFN-alpha5, IFN-alpha6, or IFN-alpha9. The antiviral efficacy was dose-dependent and correlated with the induction of the IFN-inducible, antiviral genes, 2'-5' oligoadenylate synthetase (OAS) and double-stranded RNA-dependent protein kinase. In trigeminal ganglion cells deficient in the downstream effector molecule of the OAS pathway, RNase L, the antiviral state induced by IFN-beta was lost.

PMID:
12965252
PMCID:
PMC4060623
DOI:
10.1016/s0165-5728(03)00216-9
[Indexed for MEDLINE]
Free PMC Article

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