Latent and lytic infection of isolated guinea pig enteric ganglia by varicella zoster virus.
Latent and lytic infection of isolated guinea pig enteric ganglia by varicella zoster virus.
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DOI：
10.1002/jmv.10325
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发表时间：
2003-01-01
影响因子：
12.7
通讯作者：
Gershon, Michael D.
中科院分区：
文献类型：
--
作者：
Chen, Jason J.;Gershon, Anne A.;Gershon, Michael D.
水痘带状疱疹病毒（VZV）已被证明可以在体外感染豚鼠肠道神经元。当培养物主要由神经元组成并暴露于无细胞VZV时，建立了分离的肠神经元的潜伏感染。潜伏感染的神经元在体外存活数周，并表达编码orf4、21、29、40、62和63的mRNA，但不表达编码orf14 （gC）或68 （gE）的mRNA（尽管编码糖蛋白的DNA存在）。表达的蛋白与潜伏VZV的人类感觉神经元中表达的蛋白相同。除mRNA外，orf4、21、29、62和63的免疫反应性均可检测。orf62和29蛋白是细胞质蛋白，而不是核内蛋白。VZV不会优先感染和/或潜伏在肠道内初级传入神经元中，这表明病毒潜伏在这些神经元中。当肠壁的神经元和非神经元细胞的混合培养物暴露于无细胞的VZV或当分离的肠道神经元暴露于细胞相关的VZV时，就会发生溶解性感染。溶解性感染发生后，肠内神经元在48小时内死亡。死亡前，神经元表达VZV糖蛋白，包括gE和gB， orf62和29蛋白在核内。这种新的动物模型将有助于研究VZV潜伏期和预防VZV感染、潜伏期和再激活的治疗效果。
Varicella zoster virus (VZV) has been demonstrated to infect guinea pig enteric neurons in vitro. Latent infection of isolated enteric neurons is established when the cultures predominantly consist of neurons and they are exposed to cell-free VZV. Neurons harboring latent infection survive for weeks in vitro and express mRNA encoding ORFs 4, 21, 29, 40, 62, and 63, but not 14 (gC) or 68 (gE) (although DNA encoding the glycoproteins is present). The expressed proteins are the same as those that are also expressed in human sensory neurons harboring latent VZV. In addition to mRNA, the immunoreactivities of ORFs 4, 21, 29, 62, and 63 can be detected. ORF 62 and 29 proteins are cytoplasmic and not intranuclear. VZV does not preferentially infect and/or become latent in intrinsic enteric primary afferent neurons indicating that the virus is latent in these neurons. Lytic infection occurs when mixed cultures of neurons and non-neuronal cells of the bowel wall are exposed to cell-free VZV or when isolated enteric neurons are exposed to cell-associated VZV. When lytic infection occurs, enteric neurons die within 48 hr. Prior to their death, neurons express VZV glycoproteins, including gE and gB, and ORF 62 and 29 proteins are intranuclear. This new animal model should facilitate studies of VZV latency and the efficacy of therapies designed to prevent VZV infection, latency, and reactivation.