Production of encephalitis restricted to the temporal lobes by experimental reactivation of herpes simplex virus.
A model was developed in which reactivation of latent infections with herpes simplex virus type 1 was induced in trigeminal ganglia and central nervous system olfactory centers of rabbits by administration of cyclophosphamide and dexamethasone. Latent infections were reactivated at a significantly higher frequency in rabbits infected with a highly virulent strain of virus than in those infected with a strain of lower neurovirulence. Electroencephalographic abnormalities that were largely confined to the posterior lateral cerebral hemispheres and corresponding inflammatory lesions were seen in rabbits acutely infected with the highly virulent strain, whereas no brain electrical abnormalities and only mild inflammatory lesions were seen in rabbits acutely infected with the strain of low neurovirulence. Reactivation of the highly neurovirulent strain produced focal brain necrosis restricted to the temporal lobes, which was similar to the disease produced in humans and which correlated with progressive worsening of brain electrical abnormalities.
D000818:Animals; D003520:Cyclophosphamide; D003907:Dexamethasone; D004569:Electroencephalography; D004660:Encephalitis / Q000382:microbiology* / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006561:Herpes Simplex / Q000382:microbiology* / Q000473:pathology / Q000503:physiopathology; D009336:Necrosis; D011817:Rabbits; D018139:Simplexvirus / Q000302:isolation & purification / Q000472:pathogenicity*; D013702:Temporal Lobe / Q000382:microbiology / Q000473:pathology; D013997:Time Factors; D012668:Trigeminal Ganglion / Q000382:microbiology / Q000473:pathology; D014774:Virulence
D003907:Dexamethasone; D003520:Cyclophosphamide