ArticleJournal of virology2007
Long-term infection and shedding of human cytomegalovirus in T98G glioblastoma cells.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
44 citing papers in PubMed, 54 citations in OpenAlex.
- Article
- Investigation of Epstein-Barr virus or human cytomegalovirus in pediatric gliomas: A retrospective single-center study from Tunisia.Biochemistry and biophysics reports · 2026Article
- Does human cytomegalovirus provide a novel therapeutic target for patients with glioblastoma?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.PLoS pathogens · 2025Article
- Association between brain cancer immunogenetic profile and in silico immunogenicities of 11 viruses.Scientific reports · 2023Article
- Human cytomegalovirus hijacks host stress response fueling replication stress and genome instability.Cell death and differentiation · 2022Article
- iTRAQ-Based Proteomics Analysis of Human Cytomegalovirus Latency and Reactivation in T98G Cells.Journal of virology · 2022Article
- Molecular modelling of the HCMV IL-10 protein isoforms and analysis of their interaction with the human IL-10 receptor.PloS one · 2022Article
- Identification of UL69 Gene and Protein in Cytomegalovirus-Transformed Human Mammary Epithelial Cells.Frontiers in oncology · 2021Article
- Efficient proliferation and mitosis of glioblastoma cells infected with human cytomegalovirus is mediated by RhoA GTPase.Molecular medicine reports · 2020Article
- Article
- Persistent HCMV infection of a glioblastoma cell line contributes to the development of resistance to temozolomide.Virus research · 2020Article
- Human Cytomegalovirus Compromises Development of Cerebral Organoids.Journal of virology · 2019Article
- The Susceptibility of Primary Dermis Fibroblasts from the Chinese Tree Shrew to Human Cytomegalovirus Infection.Virologica Sinica · 2019Article
- Human cytomegalovirus G protein-coupled receptor US28 promotes latency by attenuating c-fos.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Article
- Dendritic cells cross-talk with tumour antigen-specific CD8Clinical and experimental immunology · 2018Article
- Infected T98G glioblastoma cells support human cytomegalovirus reactivation from latency.Virology · 2017Article
- Article
- Human Cytomegalovirus nuclear egress and secondary envelopment are negatively affected in the absence of cellular p53.Virology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Human cytomegalovirus (HCMV) is the leading viral cause of birth defects, affecting primarily the central nervous system (CNS). To further understand this CNS pathology, cells from glioblastoma cell lines T98G and A172, the astrocytic glioblastoma cell line CCF-STTG1 (CCF), and the neuroblastoma cell line SH-SY5Y (SY5Y) were infected with HCMV. CCF and SY5Y cells were fully permissive for infection, while A172 cells were nonpermissive. In T98G cells, the majority of cells showed viral deposition into the nucleus by 6 h postinfection (hpi); however, viral immediate-early gene expression was observed in only approximately 30% of cells in the first 72 h. In viral antigen (Ag)-positive cells, although the development of complete viral replication centers was delayed, fully developed centers formed by 96 hpi. Interestingly, even at very late times postinfection, a mixture of multiple small, bipolar, and large foci was always present. The initial trafficking of input pp65 into the nucleus was also delayed. Titer and infectious-center assays showed a small number of T98G cells shedding virus at very low levels. Surprisingly, both Ag-positive and Ag-negative cells continued to divide; because of this continuous division, we adopted a protocol for passaging the T98G cells every third day to prevent overcrowding. Under this protocol, detectable infectious-virus shedding continued until passage 5 and viral gene expression continued through eight passages. This evidence points to T98G cells as a promising model for long-term infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.