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Interferon-β suppresses herpes simplex virus type 1 replication in trigeminal ganglion cells through an RNase L-dependent pathway
Journal article   Peer reviewed

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

D.J.J. Carr, K. Al-khatib, C.M. James and R. Silverman
Journal of Neuroimmunology, Vol.141(1-2), pp.40-46
2003
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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-β consistently showed the greatest resistance to HSV-1 infection in comparison to cells treated with IFN-α1, IFN-α4, IFN-α5, IFN-α6, or IFN-α9. 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-β was lost.

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Collaboration types
Domestic collaboration
International collaboration
Citation topics
1 Clinical & Life Sciences
1.161 Virology - Identification & Sequencing
1.161.315 Herpesvirus Dynamics
Web Of Science research areas
Immunology
Neurosciences
ESI research areas
Neuroscience & Behavior
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