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1 Department of Neurology, University of Glasgow, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF
and2 MRC Virology Unit, Church Street, Glasgow G11 5JR, U.K.
The herpes simplex virus type 1 (HSV-1) mutant in1814 lacks the ability to trans-activate immediate early gene transcription and enter lytic replication but it can establish and reactivate from latency. We therefore investigated the number of neurons that expressed latency-associated transcripts (LATs) in animals latently infected with in1814, the rescued revertant (1814R), or wild-type (wt) HSV-1. The percentage of LAT+ neurons increased with increasing doses of each of the viruses. After inoculation of equal amounts of infectious virus many more LAT+ neurons were observed in animals infected with in1814 than with 1814R or wt HSV-1. Whereas the LAT+ neurons in animals infected with 1814R or wt HSV-1 were largely confined to lumbar dorsal root ganglia (DRG) L4/L5/L6 (those which innervate the lower leg), in animals infected with in1814 they were also present in DRG not directly involved with such innervation (thoracic 12 and 13, L1, L2 and L3). We concluded that the large number of LAT+ neurons observed with in1814 was related to the high particle numbers in the inoculum and that spread of virus was related to limited replication as well as to the low neurovirulence of in1814. This spread was not unique to in1814 but when it occurred with more virulent viruses such as 1814R or wt HSV-1, it resulted in the death of the host.
Received 11 September 1992;
accepted 25 January 1993.
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