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著者: Hiroshi Aizawa, Fumio Ohtani, Yasushi Furuta, Hirofumi Sawa, Satoshi Fukuda
雑誌名: J Med Virol. 2004 Oct;74(2):355-60. doi: 10.1002/jmv.20181.
Abstract/Text
The mechanism by which reactivation of varicella-zoster virus (VZV) causes facial paralysis in Ramsay Hunt syndrome remains unclear. The relationship between VZV load and the onset of facial paralysis was analyzed in 42 patients with Ramsay Hunt syndrome. The patients were divided into three groups according to the times of appearance of zoster and of facial paralysis; group I (zoster preceding, n = 13), group II (simultaneous, n = 22), group III (paralysis preceding, n = 7). A real-time quantitative PCR assay was used to measure VZV DNA copy number in saliva, and paired sera were assayed for anti-VZV IgG and IgM antibodies. In group I, the VZV DNA-positive rate was low and virus load decreased gradually after the initial hospital visit around the time of onset of paralysis. The level of anti-VZV antibodies had in most cases already increased at that time. In group III, viral load tended to increase after the onset of paralysis and peaked around the time of appearance of zoster. The level of anti-VZV antibodies was low at the onset of paralysis but showed a significant increase when paired sera were tested. In group II, virus load and changes in level of anti-VZV antibodies either resembled group I or group III behavior. These results indicate that facial paralysis in Ramsay Hunt syndrome can occur at various times between the early and the regression phase of VZV reactivation, suggesting that there are variable patterns of development of facial nerve dysfunction caused by VZV reactivation and the progression of neuritis.
PMID 15332286 J Med Virol. 2004 Oct;74(2):355-60. doi: 10.1002/jmv.20181.
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