HSV and the CNS

Abstract

Herpes simplex virus encephalitis (HSVE) is an encephalitis with a predelection for the temporal lobes and related structures that is caused by HSV-1 or HSV-2. Because HSV has many properties that would be ideal for a gene transfer vector targeting the nervous system, an understanding of HSVE is of experimental, as well as clinical, importance to neuroscientists. Herpesviruses have a characteristic architecture of the virion. The molecular aspects of HSVE include the consequences of latency and neurovirulence. Studies on neurovirulence have focused on peripheral multiplication of HSV, the invasion of the CNS, and growth in the CNS. The virus appears to gain access to the CNS via the olfactory and trigeminal nerves and, transneuronally, the limbic system. The definition of latency has still to be clarified; in general, latency includes three separable phases: establishment, maintenance, and reactivation. In humans, there exists a large overlap of clinical presentations of patients with HSVE and those of patients with encephalitis of other origin. However, the presence of memory loss, personality changes, and olfactory hallucinations correlate with the limbic and temporal lobe pathology in HSVE and are characteristic. Several factors correlate with poor outcome in patients: age, time of establishment of therapy, and level of consciousness on admission of patients.