| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1993: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
Viral infection, in particular, by reactivation of latent herpes virus has been considered to be a possible explanation for the pathogenesis of idiopathic peripheral facial nerve palsy (Bell's palsy), sudden sensorineural hearing loss, vestibular neuronitis and Ramsey-Hunt syndrome. As of yet, however, latent HSV-1 and VZV in the sensory neurons of the geniculate, spiral or vestibular ganglia and the way for reactivation has been sitll unknown.
Up to now, although we could obviously detect latency-associated transcript (LAT) in trigeminal and geniculte ganglia, only one vestibular ganglia showed positive for LAT and negative in spiral ganglia. We postulated that the difference of infected copy number between these ganglia might influence these results. To elucidate this problem, in this project, we further examined these ganglia using molecular biological technique. A relative amount of LAT between each ganglia were calculated. HSV-1 DNA or copy number of LAT in trigeminal and geniculate ganglia were 10-100 times as many as taht of vbestibular ganglia. The percentage of positive hybridization number for LAT out of total ganglia calculated was 1.2% in trigeminal ganglion and 6.2% in geniculate ganglion. On the other hand, the positive rate in vestibular ganglion was under 0.1% and spiral ganglia showed no positive findings. Our results suggest the neurotropism of HSV-1 may different in each sensory ganglia, but the difference of positive infectid number for LAT between each sensory ganglia remains still nuclear.
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