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Herpesviral encephalitis
Classification and external resources
ICD-10 B00.4
ICD-9 054.3

Herpesviral encephalitis is encephalitis associated with herpes simplex virus.

Herpes simplex encephalitis (HSE) is a severe viral infection of the human central nervous system. It is estimated to affect at least 1 in 500,000 individuals per year.[1] About 1 in 3 cases of HSE result from primary HSV-1 infection, predominantly occurring in individuals under the age of 18; 2 in 3 cases occur in seropositive persons, few of whom have history of recurrent orofacial herpes. Approximately 50% of individuals that develop HSE are over 50 years of age.[2]

HSE is thought to be caused by the retrograde transmission of virus from a peripheral site on the face following HSV-1 reactivation, along a nerve axon, to the brain.[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. The olfactory nerve may also be involved in HSE,[3] which may explain its prediliction for the temporal lobes of the brain, as the olfactory nerve sends branches there. In horses, a single-nucleotide polymorphism is sufficient to allow the virus to cause neurological disease;[4] but no similar mechanism has been found in humans.

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. Patients typically have a fever.[1] and may have seizures. The electrical activity of the brain changes as the disease progresses, first showing abnormalities in one temporal lobe of the brain, which spread to the other temporal lobe 7–10 days later.[1]

Without treatment, HSE results in rapid death in approximately 70% of cases.[1] HSE is fatal in around 20% of cases treated, and causes serious long-term neurological damage in over half of survivors. Only a small population of survivors (2.5%) regain completely normal brain function.[2]

References

  1. ^ a b c d e Whitley RJ (2006). "Herpes simplex encephalitis: adolescents and adults". Antiviral Res. 71 (2-3): 141–8. doi:10.1016/j.antiviral.2006.04.002. PMID 16675036.  
  2. ^ a b Whitley RJ, Gnann JW (2002). "Viral encephalitis: familiar infections and emerging pathogens". Lancet 359 (9305): 507–13. doi:10.1016/S0140-6736(02)07681-X. PMID 11853816.  
  3. ^ Dinn J (1980). "Transolfactory spread of virus in herpes simplex encephalitis.". Br Med J 281 (6252): 1392. PMID 7437807.  
  4. ^ van de Walle GR, Goupil R, Wishon C, et al. (2009). "A single‐nucleotide polymorphism in a herpesvirus DNA polymerase is sufficient to cause lethal neurological disease". J Infect Dis 200 (1): 20–25. doi:10.1086/599316.  
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