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Apparent stability of herpes simplex virus genomes isolated from primary and recurrent infections and dorsal root ganglia in the mouse

J. M. Blondeau^*, J. A. Embil^, and E. S. Mcfarlane

Departments of Microbiology, Dalhousie University, and the Izaak Walton Killam Hospital for Children, Halifax, Nova Scotia B3J 3G9, Canada

Community Health and Epidemiology and Pediatrics, Dalhousie University, and the Izaak Walton Killam Hospital for Children, Halifax, Nova Scotia B3J 3G9, Canada

Requests for offprints should be sent to Dr J. A. Embil, Infection and Immunology Research Laboratory, Izaak Walton Killam Hospital for Children, 5850 University Avenue, Halifax, Nova Scotia B3J 3G9, Canada.

Received March 28, 1988
Accepted June 27, 1988

Following natural or experimental primary infection, herpes simplex virus (HSV) becomes latent in sensory ganglia. Reactivation of latent virus may lead to recurrent disease. If HSV DNA remains stable during primary, recurrent and latent infections, that stability would enable us to trace the transmission of HSV from one individual to another. We inoculated mice in the ear pinna with HSV and collected virus at various intervals during primary infection. In mice surviving primary infections, recurrent disease was induced from which virus was isolated. Virus was also recovered from explanted dorsal root ganglia. Virus isolates were characterised by restriction endonuclease digestion and compared with the original inoculate(s). The data indicate that in all cases except two, the isolates from primary and recurrent infections remained identical to the original inoculates.