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Viral Encephalomyelitis

Figure 1

Schematic diagram of the potential outcomes after virus infection of neurons.

Virus infection itself may induce death of the infected neuron, especially in young individuals. Neuronal death can also result from the local release of excitotoxic neurotransmitters (e.g., glutamate) and inflammatory mediators. Neurons can also survive infection and virus replication can be controlled through noncytolytic mechanisms such as local production of antiviral antibody and interferon (IFN)-γ. In the latter case, viral nucleic acid persists intracellularly and long-term immune control is necessary to prevent virus reactivation.

Figure 1

doi: https://doi.org/10.1371/journal.ppat.1002004.g001