Interferon-β suppresses herpes simplex virus type 1 replication in trigeminal ganglion cells through an RNase L-dependent pathway
Carr, D.J.J., Al-khatib, K., James, C.M. and Silverman, R. (2003) Interferon-β suppresses herpes simplex virus type 1 replication in trigeminal ganglion cells through an RNase L-dependent pathway. Journal of Neuroimmunology, 141 (1-2). pp. 40-46.
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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.
|Publication Type:||Journal Article|
|Murdoch Affiliation:||School of Veterinary and Biomedical Sciences|
|Copyright:||2003 Elsevier B.V|
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