Neurological involvement in mice after infection with a cold-adapted herpes simplex type 2 virus.
Experimental intracerebral infection of 4-week-old mice with the MS strain of herpes simplex virus type 2 or its derivative cold variant was compared. The infectious process was followed in both the brain tissue and the trigeminal ganglia, using hematoxylin and eosin and antigenic tracing with indirect peroxidase-antiperoxidase staining. The wild-type virus elicited a severe meningitis and necrotic lesions by 7 days post-inoculation in the brain. The cold variant produced a mild meningitis and no necrotic lesions. In both viral infections, the neuron seemed to be the target cell at the early stages. Infection with the wild-type strain was able to spread through host tissues and produce confluent lesions, whereas infection with the cold mutant seemed to be confined to individual neurons. Data suggest that the cold variant is restricted in its ability to lyse the cells and spread in the host nervous tissue.
D000818:Animals; D001921:Brain / Q000382:microbiology* / Q000473:pathology; D003080:Cold Temperature; D006561:Herpes Simplex / Q000382:microbiology* / Q000473:pathology; D008214:Lymphocytes / Q000473:pathology; D008587:Meningitis, Viral / Q000209:etiology* / Q000473:pathology; D051379:Mice; D008815:Mice, Inbred Strains; D009336:Necrosis; D009474:Neurons / Q000382:microbiology; D018139:Simplexvirus / Q000254:growth & development*; D012668:Trigeminal Ganglion / Q000382:microbiology*; D014276:Trigeminal Nerve / Q000382:microbiology*