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Herpes encephalitis and Abeta plaques
Author(s) -
Bearer Elaine L,
Woltjer Randy,
Donahue John E,
Kilpatrick Kathleen
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.873.16
Subject(s) - encephalitis , herpes simplex virus , borrelia burgdorferi , virology , disease , immunology , medicine , virus , viral encephalitis , biology , pathology , antibody
Since the early 20 th century it has been known that infectious organisms, such as the treponemal spirochete causing syphilis, induce Abeta plaques in the brain. Recent evidence shows similar Abeta with Borrelia Burgdorferi , causative agent for Lyme disease. We are investigating whether the common viral pathogen, Herpes simplex virus I and II, might also induce plaque formation in the acute stages of encephalitis. As we reported, Herpes simplex virus (HSV) interacts with cellular machinery that is altered in Alzheimer's disease (Cheng et al. 2011). Here we analyzed human brain tissue from three subjects across the lifespan: a 9 day‐old, a 8 yr‐old, and a 76 yr‐old, with documented HSV for the presence of AD pathology. In all three cases, Abeta was present without evidence of phospho‐tau. Neither clinical history nor distribution of Abeta deposits was consistent with pre‐existing Alzheimer's disease in the older subject. In cases of non‐herpetic viral encephalitis, we found no Abeta deposits. We conclude that HSV can induce the formation of Abeta deposits. Since perinatal HSV encephalitis afflicts >;1500 newborns per year in the US, and even when the acute phase is successfully treated infection persists for life, this result demands follow‐up to ascertain if plaques persist and if chronic active HSV in the brain continues, producing more Abeta deposition. Supported by NS046810, NS062184 (ELB).