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superior versus inferior vestibular neuritis: are there intrinsic differences in infection, reactivation, or production of infectious particles between the vestibular ganglia? 上半规管与下半规管前庭神经炎:前庭神经节之间在感染、再激活或感染性颗粒产生方面是否存在内在差异?

Superior Versus Inferior Vestibular Neuritis: Are There Intrinsic Differences in Infection, Reactivation, or Production of Infectious Particles Between the Vestibular Ganglia?

作者信息

Nayak Shruti, He Lifan, Roehm Pamela Carol

机构信息

*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.

出版信息

Otol Neurotol. 2015 Aug;36(7):1266-74. doi: 10.1097/MAO.0000000000000758.

Abstract

HYPOTHESIS

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).

CONCLUSION

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.

摘要

假设

前庭神经节神经元的内在差异导致前庭上神经节更易受累于前庭神经炎。

背景

据推测,前庭神经炎是由I型单纯疱疹病毒(HSV1)在前庭神经节感染或再激活所致。在前庭神经炎患者中,前庭下神经节受累极为罕见。

方法

分别培养大鼠前庭上神经节和下神经节神经元(VGNs)的原代培养物。用携带US11-绿色荧光蛋白(GFP)嵌合体的HSV1对神经元进行裂解性和潜伏性感染。通过显微镜观察GFP荧光评估裂解性感染百分比和基线再激活情况。使用曲古抑菌素A(TSA)刺激HSV1再激活。通过病毒滴度评估病毒粒子产生情况。通过实时逆转录聚合酶链反应(实时RT-PCR)测定潜伏相关(LAT)转录本的相对数量。

结果

两个神经节的裂解性感染率相当(p>0.05)。裂解性感染产生的空斑形成单位数量相似(p>0.05)。潜伏感染的前庭上神经节和下神经节神经元之间LAT转录本的相对数量没有差异。潜伏感染的培养物在基线和TSA诱导的HSV1再激活率方面没有差异(p>0.05)。再激活的、潜伏感染的前庭上神经节与下神经节神经元之间病毒粒子产生没有显著差异(p = 0.45)。

结论

前庭上神经炎和下神经炎患病率的差异并非源于这些神经元HSV1感染或病毒粒子产生的内在差异。其他因素,如包含神经节和神经的骨管的长度和宽度,导致前庭上神经节在前庭神经炎中更易受累。

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