作者: Hai-Fei Jiang , Wei Wang , Xuan Jiang , Wen-Bo Zeng , Zhang-Zhou Shen
DOI: 10.1128/JVI.00127-17
关键词:
摘要: Although a varicella-zoster virus (VZV) vaccine has been used for many years, the neuropathy caused by VZV infection is still major health concern. Open reading frame 7 (ORF7) of recognized as neurotropic gene in vivo, but its neurovirulent role remains unclear. In present study, we investigated effect ORF7 deletion on replication cycle at entry, genome replication, expression, capsid assembly and cytoplasmic envelopment, transcellular transmission differentiated neural progenitor cells (dNPCs) neuroblastoma SH-SY5Y (dSY5Y) cells. Our results demonstrate that protein component tegument layer virions. Deleting did not affect viral or expression typical genes clearly impacted envelopment capsids, resulting dramatic increase envelope-defective particles decrease intact The defect was more severe neuronal dNPCs dSY5Y. also impaired ORF7-deficient among These indicate required cells, probably induced infection.IMPORTANCE neurological damage reactivation commonly manifested clinical problems. Thus, identifying characterizing their functions are important relieving related complications. previously identified potential gene, involvement this found deficiency poor dissemination findings imply plays neuropathy, highlighting strategy to develop neurovirulence-attenuated against chickenpox herpes zoster providing new target intervention VZV.