Dueland A N
Department of Neurology, Ulleval Hospital, Oslo, Norway.
Scand J Infect Dis Suppl. 1996;100:46-50.
Varicella zoster virus (VZV) is the causative agent of chickenpox (varicella) and shingles (zoster). The study of latency and reactivation has been hampered by the fact that the virus is strictly human and grows to low titres in tissue culture. Molecular biology techniques have opened a new era of VZV research. The site of VZV latency was determined to be sensory ganglia by Southern blotting and later by PCR technology. It was also demonstrated that the entire virus genome is present in the latently infected ganglia and that VZV is latent in multiple ganglia along the entire human neuraxis. Since the amount of latent VZV per cell is very low, the question of which cell type is involved in VZV latency could not be conclusively settled by the use of traditional in situ hybridization studies. However, we have now demonstrated the presence of latent VZV DNA in neurons only, by using a more sensitive method which employs a combination of in situ PCR and in situ hybridization. The transcriptional activity of VZV during latency is still not completely clear. Ganglia are small and the total amount of latent VZV is low, therefore conventional methods to detect latent VZV have proved limited. Nevertheless, the detection of a latent transcript from the SalI C region of the virus was demonstrated by Southern hybridization of cDNA synthesized from RNA isolated from latently-infected ganglia. Further studies have localized this transcript to the open reading frame of VZV gene 21. The study of VZV latency and reactivation has, until now, been dependent on the investigation of post mortem human tissue. However, simian varicella virus seems to be the simian counterpart to human VZV. The 2 viruses exhibit DNA homology as well as similarities in clinical, virological, and immunological features. Further studies of VZV infections may open new and possibly unpredictable opportunities in varicella virus research.
水痘带状疱疹病毒（VZV）是水痘（鸡痘）和带状疱疹的病原体。由于该病毒严格感染人类且在组织培养中生长至低滴度，潜伏期和再激活的研究受到了阻碍。分子生物学技术开启了VZV研究的新纪元。通过Southern印迹法，随后又通过PCR技术确定VZV的潜伏部位为感觉神经节。还证明了潜伏感染的神经节中存在完整的病毒基因组，并且VZV潜伏在整个人类神经轴的多个神经节中。由于每个细胞中潜伏性VZV的量非常低，使用传统的原位杂交研究无法最终确定哪种细胞类型参与VZV潜伏。然而，我们现在通过使用一种更敏感的方法，即结合原位PCR和原位杂交，证明仅在神经元中存在潜伏性VZV DNA。VZV在潜伏期的转录活性仍不完全清楚。神经节很小，潜伏性VZV的总量很低，因此传统的检测潜伏性VZV的方法已被证明是有限的。尽管如此，通过对从潜伏感染的神经节中分离的RNA合成的cDNA进行Southern杂交，证明了从病毒的SalI C区域检测到潜伏转录本。进一步的研究已将该转录本定位到VZV基因21的开放阅读框。到目前为止，VZV潜伏期和再激活的研究一直依赖于对人类尸检组织的调查。然而，猴水痘病毒似乎是人类VZV的猴对应物。这两种病毒表现出DNA同源性以及临床、病毒学和免疫学特征的相似性。对VZV感染的进一步研究可能会在水痘病毒研究中开辟新的、可能不可预测的机会。
