Depending on their differentiation state, vertebrate neurones can commit suicide after neurotropic virus infection. Such suicide might be an evolved strategy in multicellular organisms for limiting virus expansion. Regulation of suicide in this context operates by a programme similar to that activated during embryogenesis or in response to nervous-system injury and disease. In contrast to immature neurones that can readily initiate apoptosis following infection, mature neurones are generally highly resistant and can survive for long periods if they remain functional. Mature, infected neurones might gain competence to die owing to the attuned activation of pathways that sensitize the cell to subsequent stress. The consequence of either perturbation of function as a result of viral persistence or a chronic but progressive loss of infected neurones might be a failure of key neural functions.
- Cell Death
- Proto-Oncogene Proteins c-bcl-2
- RNA Viruses
- Signal Transduction
- Transcription Factors