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J Gen Virol 84 (2003), 1403-1410; DOI 10.1099/vir.0.18881-0

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© 2003 Society for General Microbiology

Characterization of a neurovirulent aciclovir-resistant variant of herpes simplex virus

Finn Grey1,{dagger}, Mike Sowa2, Peter Collins2, Rob J. Fenton2, Wendy Harris2, Wendy Snowden2, Stacey Efstathiou1 and Graham Darby2

1 Division of Virology, Department of Pathology, Cambridge University, Tennis Court Road, Cambridge CB2 1QP, UK
2 GlaxoSmithKline, UK Virology Medicines Research Centre, Gunnels Wood Road, Stevenage, Hertfordshire SG1 2NY, UK

Correspondence
Rob Fenton
rob.j.fenton{at}gsk.com
Finn Grey
greyf{at}ohsu.edu

A clinical isolate of herpes simplex virus type 1 that is aciclovir resistant but neurovirulent in mice was described previously. The mutation in this virus is a double G insertion in a run of seven G residues that has been shown previously to be a mutational hotspot. Using a sensitive assay, it has been demonstrated that preparations of this virus are able to induce low but consistent levels of thymidine kinase (TK) activity. However, this activity results from a high frequency mutational event that inserts a further G into the ‘G-string’ motif and thus restores the TK open reading frame. Passage of this virus through the nervous system of mice results in the rapid selection of the TK-positive variant. Thus, this variant is the major component in virus reactivated from latently infected ganglia. Mutation frequency appears to be influenced by the genetic background of the virus.

{dagger}Present address: Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, L220, Portland, Oregon 97239, USA.




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