Infected T98G glioblastoma cells support human cytomegalovirus reactivation from latency
2017
Cheng, Shuang | Jiang, Xuan | Yang, Bo | Wen, Le | Zhao, Fei | Zeng, Wen-Bo | Liu, Xi-Juan | Dong, Xiao | Sun, Jin-Yan | Ming, Ying-Zi | Zhu, Hua | Rayner, Simon | Tang, Qiyi | Fortunato, Elizabeth | Luo, Min-Hua
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.
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