[5] Most individuals with HSE show a decrease in their level of consciousness and an altered mental state presenting as confusion, and changes in personality.

Increased numbers of white blood cells can be found in patient's cerebrospinal fluid, without the presence of pathogenic bacteria and fungi.

[6] Definite diagnosis requires testing of the cerebrospinal fluid (CSF) by a lumbar puncture (spinal tap) for presence of the virus.

[1] The virus lies dormant in the ganglion of the trigeminal cranial nerve, but the reason for reactivation, and its pathway to gain access to the brain, remains unclear, though changes in the immune system caused by stress clearly play a role in animal models of the disease.

In horses, a single-nucleotide polymorphism is sufficient to allow the virus to cause neurological disease;[13] but no similar mechanism has been found in humans.

Complete prior to lumbar puncture to exclude significantly increased ICP, obstructive hydrocephalus, mass effect[14] Brain MRI—Increased T2 signal intensity in frontotemporal region → viral (HSV) encephalitis[15] Herpesviral encephalitis can be treated with high-dose intravenous acyclovir, which should be infused 10 mg/kg(adult) over 1 hour to avoid kidney failure.

Without treatment, HSE results in rapid death in approximately 70% of cases; survivors suffer severe neurological damage.