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Alphaherpesvirus Saimiri in Rabbits: A Model For Human Encephalitis?

D. A. Leib

Department of Medical Microbiology, University of Liverpool, P.O. Box 147, Liverpool L69 3BX, U.K.

One (KM91) of a series of isolates of alphaherpesvirus saimiri (HVS) produced rapidly fatal encephalitis in rabbits following intradermal infection, whereas the others (KM180, KM322 and KM338) were non-lethal and produced ganglionitis and prolonged latency. Alphaherpesvirus saimiri KM91 initially produced ganglionitis but quickly ascended the spinal cord to the brain causing death 10 days post-infection. Prior infection with any of the three benign isolates or inoculation with -propiolactone (PL)-inactivated HVS KM91 protected rabbits from lethal encephalitis when they were subsequently challenged with a lethal dose of HVS KM91. Each of 20 rabbits co-inoculated in the same site with a lethal dose of HVS KM91 and either HVS KM322 (1.5 x 10³ to 1.5 x 10⁵ p.f.u.) or PL-inactivated HVS KM322 (1 x 10⁷ p.f.u. equivalents) survived. In contrast only half of those co-inoculated with HVS KM91 and PL-inactivated HVS KM91 (1 x 10⁷ p.f.u. equivalents) survived. Co-inoculation of lethal HVS KM91 (75 p.f.u.) and benign HVS KM322 (1.5 x 10³ p.f.u.) into opposite flanks resulted in protection from encephalitis in one of four rabbits. Alphaherpesvirus saimiri KM91 was shown to have the capacity to become latent in dorsal root ganglia if the rabbit did not die.

Keywords: neurovirulence, encephalitis, alphaherpesvirus saimiri

Present address: Laboratory of Tumor Virus Genetics, Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, U.S.A.

Received 30 October 1987; accepted 24 February 1988.