The JH2604 deletion variant of herpes simplex virus type 2 (HG52) fails to produce necrotizing encephalitis following intracranial inoculation of mice.
The pathological changes and distribution of virus antigen in mouse brains were studied following intracranial inoculation of 3 week old BALB/c mice with the herpes simplex virus (HSV) type 2 strain HG52 and its deletion variant JH2604. The variant JH2604 failed to produce necrotizing encephalitis compared to the parental HG52. The morphological changes induced in JH2604-infected brains consisted of localized perivascular cuffing by lymphocytes and infiltration by immune cells. Immunohistochemical studies using polyclonal anti-HSV serum showed that JH2604 antigens were localized at the site of inoculation with no evidence of neuronal involvement. Wild-type HSV-infected brains demonstrated a wide distribution of antigens both in neuronal and supporting cells. These data provide evidence that the non-neurovirulent phenotype of JH2604 is due to inability to replicate within neuronal cells of the central nervous system and pinpoints a precise role for the HG52 sequences contained within the 1488 bp subfragment of TRL/IRL deleted in JH2604.
Taha
M Y
MY
MRC Virology Unit, Institute of Virology, Glasgow, U.K.
Brown
S M
SM
Clements
G B
GB
Graham
D I
DI
D000818:Animals; D001921:Brain / Q000382:microbiology* / Q000473:pathology; D002872:Chromosome Deletion; D004660:Encephalitis / Q000382:microbiology* / Q000473:pathology; D014644:Genetic Variation; D006561:Herpes Simplex / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D012016:Reference Values; D018139:Simplexvirus / Q000235:genetics* / Q000472:pathogenicity; D014774:Virulence / Q000235:genetics