ArticlePLoS pathogens2026
Human herpesvirus 7 integrates into host telomeres via its telomeric repeat arrays.
Article in PLoS pathogens, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human herpesvirus 7 (HHV-7) is a ubiquitous betaherpesvirus and a causative agent of roseola infantum. HHV-7 harbors telomeric repeat arrays (TMR) identical to human telomeres at the ends of its genome. While similar repeats contribute to human herpesvirus 6 (HHV-6) integration into host telomeres, HHV-7 integration and the role of the TMR remained elusive. Using fluorescence in situ hybridization and nanopore sequencing, we demonstrate that HHV-7 efficiently integrates into host telomeres in persistently infected cells. To determine the role of the TMR in the virus life cycle, we generated the first HHV-7 reverse genetic system and mutants lacking the TMR. These mutants revealed that the TMR are dispensable for HHV-7 replication, but play a crucial role in the integration process and genome maintenance in persistently infected cells. This study provides a reverse genetic system for HHV-7, and offers important insights into the biology of this ubiquitous human pathogen.
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