What is the pathogenesis of herpes simplex encephalitis (HSE)?

Updated: Jul 17, 2018
  • Author: Wayne E Anderson, DO, FAHS, FAAN; Chief Editor: Niranjan N Singh, MBBS, MD, DM, FAHS, FAANEM  more...
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The pathogenesis of HSE in humans is poorly understood. Neurons are quickly overwhelmed by a lytic and hemorrhagic process distributed in an asymmetric fashion throughout the medial temporal and inferior frontal lobes. Wasay et al reported temporal lobe involvement in 60% of patients. [9] Fifty-five percent of patients demonstrated temporal and extratemporal pathology, and 15% of patients demonstrated extratemporal pathology exclusively. Involvement of the basal ganglia, cerebellum, and brainstem is uncommon.

The exact mechanism of cellular damage is unclear, but it may involve both direct virus-mediated and indirect immune-mediated processes. The ability of HSV-1 to induce apoptosis (programmed cell death, or “cellular suicide”) in neuronal cells, a property not shared by HSV-2, might explain why the former causes virtually all cases of herpes simplex encephalitis in immunocompetent older children and adults. [10, 11]

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