Alterations of the Central Nervous System (CNS) in rats surviving acute infection with a virulent strain of Venezuelan Equine Encephalitis (VEE) virus were studied by light and electron microscopy. Cavitary necrosis of the cerebral cortex, macrophage activity and degenerative axonal changes were considered to be sequelae of the lesions induced during the acute phase of the infection. Mononuclear cell infiltrates of the neuropil, 3 mth after inoculation, were related to the immune response of the host. Focal lesions and mononuclear cell activity in the brain are thought to be the equivalent of the lesions induced in the CNS of humans during VEE virus infection. The findings are discussed in the light of recent reports of cerebral dysfunction occurring as a sequel of VEE virus infection in children.

Infection of cultured Aedes aegypti mosquito cells with Venezuelan equine encephalitis virus (Mucambo subtype) results in the establishment of a chronic non-cytopathic infection. Infected cells could be ‘cured’ when they were grown in the presence of immune serum for 3–4 passages. ‘Cured’ cells could then be subcultured repeatedly, in the absence of immune serum, without showing any indication of infectious virus production. When ‘cured’ cells were exposed to 50 µg/ml of 5-iodo-2-deoxyuridine for 24 h, efficient induction of virus was observed. The enhancement of virus replication could not be related with increased susceptibility of the uninfected cell population. The phenotype (plaque size and virulence) of the induced virus resembles more closely that of the standard virus than the phenotype of the virus produced in chronically infected mosquito cells. These findings indicate that virus information can be maintained in chronically infected mosquito cells in a latent inducíble form, and constitute indirect evidence suggesting the existence of a DNA provirus in this system.