Open AccessPrevalence of HSV‐1 LAT in Human Trigeminal, Geniculate, and Vestibular Ganglia and Its Implication for Cranial Nerve Syndromes
Author(s) -
Theil Diethilde,
Arbusow Viktor,
Derfuss Tobias,
Strupp Michael,
Pfeiffer Matthias,
Mascolo Andrea,
Brandt Thomas
Publication year - 2001
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/j.1750-3639.2001.tb00408.x
Subject(s) - geniculate ganglion , scarpa's ganglion , vestibular system , anatomy , vestibular nerve , herpes simplex virus , trigeminal ganglion , geniculate , pathology , vestibular nuclei , ganglion , biology , trigeminal nerve , cranial nerves , sensory system , medicine , neuroscience , virus , virology , palsy , alternative medicine , nucleus
Herpes simplex virus type 1 (HSV‐1) enters sensory neurons and can remain latent there until reactivation. During latency restricted HSV‐1 gene expression takes place in the form of latency‐associated transcripts (LAT). LAT has been demonstrated to be important not only for latency but also for reactivation, which may cause cranial nerve disorders. Tissue sections of the trigeminal ganglia (TG), geniculate ganglia (GG), and the vestibular ganglia (VG) from seven subjects were examined for the presence of LAT using the in situ hybridization technique. LAT was found on both sides in all TG (100%), on both sides of five subjects (70%) in the GG, and in none of the VG. Using a second more sensitive detection method (RT‐PCR), we found LAT in the VG of seven of ten other persons (70%). This is the first study to demonstrate viral latency in the VG, a finding that supports the hypothesis that vestibular neuritis is caused by HSV‐1 reactivation. The distribution of LAT in the cranial nerve ganglia indicates that primary infection occurs in the TG and GG and subsequently spreads along the faciovestibular anastomosis to the VG.