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Virology. 2017 Oct;510:205-215. doi: 10.1016/j.virol.2017.07.023. Epub 2017 Jul 24.

Infected T98G glioblastoma cells support human cytomegalovirus reactivation from latency.

Author information

1
State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China.
2
The 3rd Xiangya Hospital, Central-South University, Changsha 410013, China.
3
Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers New Jersey Medical School, Newark, NJ 07101-1709, USA.
4
Department of Medical Genetics, Oslo University Hospital, University of Oslo, Oslo 0316, Norway.
5
Department of Microbiology, Howard University College of Medicine, Howard University, Washington, DC 20059, USA.
6
Department of Biological Sciences and Center for Reproductive Biology, University of Idaho, Moscow, ID 83844-3051, USA. Electronic address: lfort@uidaho.edu.
7
State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China; University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address: luomh@wh.iov.cn.

Abstract

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.

KEYWORDS:

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

PMID:
28750324
PMCID:
PMC6263025
DOI:
10.1016/j.virol.2017.07.023
[Indexed for MEDLINE]
Free PMC Article

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