A herpes simplex type 1 ICPO deletion mutant demonstrates diminished pathogenicity during acute ocular infection in different host animals.
We compared a previously characterized herpes simplex type 1 alpha 0 deletion mutant, dlx3.1, which produced no functional ICP0, with its wild-type parental strain, KOS, during acute ocular infection of different host animals. Acute pathogenicity of the viral strains in NZ rabbits, Balb/c and A/J mice was evaluated by keratitis scores, ocular and trigeminal ganglionic viral titers, and host survival. We found that dlx3.1 was significantly less pathogenic than KOS. Host differences proved very important in the evaluation of acute pathogenicity. A species-dependent enhancement of ocular pathogenicity was demonstrated for dlx3.1 following a larger viral inoculum and host immunosuppression. We conclude that alpha 0 gene function appears to play an important role during acute ocular pathogenicity of HSV-1 in animal models. Furthermore, in vivo pathogenicity studies contribute important information in the evaluation of essential viral gene function.
Gordon
Y J
YJ
Eye and Ear Institute of Pittsburgh, Pennsylvania 15213.
Romanowski
E
E
Balouris
C
C
Araullo-Cruz
T
T
D000208:Acute Disease; D000818:Animals; D002872:Chromosome Deletion; D005123:Eye / Q000382:microbiology; D005260:Female; D007635:Keratitis, Dendritic / Q000382:microbiology* / Q000401:mortality; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008815:Mice, Inbred Strains; D009154:Mutation; D011817:Rabbits; D018139:Simplexvirus / Q000235:genetics* / Q000472:pathogenicity; D013534:Survival; D012668:Trigeminal Ganglion / Q000382:microbiology