Oligodendrocytes are a major target of the toxicity of spongiogenic murine retroviruses.

The neurovirulent retroviruses FrCasE and Moloney MLV-ts1 cause noninflammatory spongiform neurodegeneration in mice, manifested clinically by progressive spasticity and paralysis. Neurons have been thought to be the primary target of toxicity of these viruses. However the neurons themselves appear not to be infected, and the possible indirect mechanisms driving the neuronal toxicity have remained enigmatic.

The pseudorabies virus Us2 protein, a virion tegument component, is prenylated in infected cells.

The Us2 gene is conserved among alphaherpesviruses, but its function is not known. We demonstrate here that the pseudorabies virus (PRV) Us2 protein is synthesized early after infection and localizes to cytoplasmic vesicles and to the plasma membrane, despite the lack of a recognizable signal sequence or membrane-spanning domain. Us2 protein is also packaged as part of the tegument of mature virions.

Corticosteroids are unable to protect against pseudorabies virus-induced tissue damage in the developing brain.

After intraocular injection of the virulent pseudorabies virus (PRV) strain Becker into late-stage chicken embryos, the virus spreads and replicates in the brain, where severe edema and hemorrhaging follow. By contrast, the attenuated Bartha strain does not cause severe brain pathology despite viral replication and spread throughout the brain (B. W.