ArticleJournal of virology2024
Identification of stimuli that enhance human herpesvirus 6A (HHV-6A) replication and reconstitution.
Article in Journal of virology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- A Patient-Derived iPSC-Based Model Reveals Neural Lineage-Specific Transcription of Endogenous HHV-6B.The Journal of infectious diseases · 2026Article
- Human herpesvirus 7 integrates into host telomeres via its telomeric repeat arrays.PLoS pathogens · 2026Article
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Despite the availability of bacterial artificial chromosome (BAC) systems for human herpesvirus 6A (HHV-6A), reconstitution of infectious viruses is very challenging and time consuming. In this study, we developed approaches to improve the reconstitution process and enhance virus replication to overcome these technical challenges. Using dimethyl sulfoxide and exonuclease V, we significantly increased the efficiency of BAC transfections into JJHan T cells. We tested several stimulation strategies to enhance lytic replication and identified mitogens and glucocorticoids that, in combination, improve virus replication. In addition, we demonstrated that the interferon-mediated response impairs virus reconstitution and that the JAK1/JAK2 inhibitor ruxolitinib resulted in an immense improvement. Furthermore, hypoxia-inducible factor 1 alpha stabilization by IOX2 drastically accelerated virus reconstitution, indicating that the hypoxic response is a crucial regulator of HHV-6A replication. Our study sheds light on strategic approaches that improve replication and reconstitution of this ubiquitous human herpesvirus. IMPORTANCE: HHV-6A is a betaherpesvirus that infects a wide range of human tissues and establishes lifelong latency in the host. Its reactivation has been implicated in several diseases, including multiple sclerosis, encephalitis, myocarditis, and chronic fatigue syndrome, although its pathogenetic role remains elusive. The efficacy of common antiviral drugs is limited, and no specific drugs target HHV-6A infection. The data of this study shed light on stimuli and potential pathways that influence HHV-6A replication and reconstitution. Our strategies not only simplify virus propagation and reconstitution to study HHV-6A biology but also provide the basis for the development of therapeutic strategies.
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