Infected T98G glioblastoma cells support human cytomegalovirus reactivation from latency

Shuang Cheng, Xuan Jiang, Bo Yang, Le Wen, Fei Zhao, Wen Bo Zeng, Xi Juan Liu, Xiao Dong, Jin Yan Sun, Ying Zi Ming, Hua Zhu, Simon Rayner, Qiyi Tang, Elizabeth Fortunato, Min Hua Luo

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


T98G cells have been shown to support long-term human cytomegalovirus (HCMV) genome maintenance without infectious virus release. However, it remains unclear whether these viral genomes could be reactivated. To address this question, a recombinant HCMV (rHCMV) containing a GFP gene was used to infect T98G cells, and the infected cells absent of infectious virus production were designated T98G-LrV. Upon dibutyryl cAMP plus IBMX (cAMP/IBMX) treatment, a serial of phenomena were observed, including GFP signal increase, viral genome replication, lytic genes expression and infectious viruses release, indicating the reactivation of HCMV in T98G-LrV cells from a latent status. Mechanistically, HCMV reactivation in the T98G-LrV cells induced by cAMP/IBMX was associated with the PKA-CREB signaling pathway. These results demonstrate that HCMV was latent in T98G-LrV cells and could be reactivated. The T98G-LrV cells represent an effective model for investigating the mechanisms of HCMV reactivation from latency in the context of neural cells.

Original languageAmerican English
Pages (from-to)205-215
Number of pages11
StatePublished - Oct 2017

ASJC Scopus subject areas

  • Virology


  • Human cytomegalovirus
  • Latent cell model of brain origin
  • Latent infection
  • Reactivation
  • T98G cells


Dive into the research topics of 'Infected T98G glioblastoma cells support human cytomegalovirus reactivation from latency'. Together they form a unique fingerprint.

Cite this