title: Superior Versus Inferior Vestibular Neuritis: Are There Intrinsic Differences in Infection, Reactivation, or Production of Infectious Particles Between the Vestibular Ganglia?
abstract: OBJECTIVE
  Intrinsic differences in neurons of the vestibular ganglia result in the increased likelihood of superior vestibular ganglion involvement in vestibular neuritis.
  
  
  BACKGROUND
  Vestibular neuritis is hypothesized to result from herpes simplex type I (HSV1) infection or reactivation in vestibular ganglia. Involvement of the inferior vestibular ganglion is extremely rare in patients with vestibular neuritis.
  
  
  METHODS
  Primary cultures of rat superior and inferior vestibular ganglion neurons (VGNs) were cultivated separately. Neurons were lytically and latently infected with HSV1 with a US11-green fluorescent protein (GFP) chimera. Percentage lytic infection and baseline reactivation was assessed by microscopy for GFP fluorescence. Trichostatin-A (TSA) was used to stimulate HSV1 reactivation. Virion production was assessed by viral titers. Relative numbers of latency-associated (LAT) transcripts were determined by real-time reverse-transcription polymerase chain reaction (real-time RT-PCR).
  
  
  RESULTS
  Lytic infection rates were equivalent between the two ganglia (p > 0.05). Lytic infections yielded similar amounts of plaque-forming units (p > 0.05). Relative amounts of LAT transcripts did not differ between latently infected superior and inferior VGNs. Latently infected cultures showed no differences in rates of baseline and TSA-induced HSV1 reactivation (p > 0.05). Production of virions was not significantly different between reactivated, latently infected superior versus inferior VGNs (p = 0.45).
  
  
  CONCLUSIONS
  Differences in prevalence of superior and inferior vestibular neuritis do not result from intrinsic differences in HSV1 infection or virion production of these neurons. Other factors, such as the length and width of the bony canal containing the ganglia and nerves, account for the greater involvement of the superior vestibular ganglion in vestibular neuritis.
authors.affiliation: *Department of Otolaryngology, New York University School of Medicine, New York, New York; †Department of Otolaryngology-Head and Neck Surgery, Temple University School of Medicine, Philadelphia; and ‡Department of Neuroscience, Temple University School of Medicine, Philadelphia, Pennsylvania, U.S.A.
authors.forename: Shruti
authors.initials: S
authors.lastname: Nayak
authors.forename: Lifan
authors.initials: L
authors.lastname: He
authors.forename: Pamela Carol
authors.initials: PC
authors.lastname: Roehm
mesh_terms: D000818:Animals; D002678:Chimera; D005260:Female; D005724:Ganglia / Q000473:pathology* / Q000821:virology; D049452:Green Fluorescent Proteins / Q000235:genetics; D006561:Herpes Simplex / Q000473:pathology / Q000821:virology; D018259:Herpesvirus 1, Human; D006877:Hydroxamic Acids / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000473:pathology / Q000821:virology; D016133:Polymerase Chain Reaction; D051381:Rats; D017207:Rats, Sprague-Dawley; D014725:Vestibular Nerve / Q000473:pathology* / Q000821:virology; D020338:Vestibular Neuronitis / Q000209:etiology / Q000473:pathology* / Q000821:virology; D014722:Vestibule, Labyrinth / Q000473:pathology / Q000821:virology; D014775:Virus Activation / Q000187:drug effects; D017735:Virus Latency
chemical_list: D006877:Hydroxamic Acids; D049452:Green Fluorescent Proteins; C012589:trichostatin A