ArticleViruses2018
Viral Proteins U41 and U70 of Human Herpesvirus 6A Are Dispensable for Telomere Integration.
Article in Viruses, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Human herpesvirus 7 integrates into host telomeres via its telomeric repeat arrays.PLoS pathogens · 2026Article
- The immediate-early protein 1 of human herpesvirus 6B interacts with NBS1 and inhibits ATM signaling.EMBO reports · 2024Article
- Impact of Host Telomere Length on HHV-6 Integration.Viruses · 2022Article
- A Cell Culture System to Investigate Marek's Disease Virus Integration into Host Chromosomes.Microorganisms · 2021Article
- Article
- Evasion of the Host Immune Response by Betaherpesviruses.International journal of molecular sciences · 2021Review
- Unbiased optical mapping of telomere-integrated endogenous human herpesvirus 6.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The U94 Gene of Human Herpesvirus 6: A Narrative Review of Its Role and Potential Functions.Cells · 2020Review
- Endogenization and excision of human herpesvirus 6 in human genomes.PLoS genetics · 2020Article
- Review
- The Role of Marek's Disease Virus UL12 and UL29 in DNA Recombination and the Virus Lifecycle.Viruses · 2019Article
- Chromatin Profiles of Chromosomally Integrated Human Herpesvirus-6A.Frontiers in microbiology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Human herpesvirus-6A and -6B (HHV-6A and -6B) are two closely related betaherpesviruses that infect humans. Upon primary infection they establish a life-long infection termed latency, where the virus genome is integrated into the telomeres of latently infected cells. Intriguingly, HHV-6A/B can integrate into germ cells, leading to individuals with inherited chromosomally-integrated HHV-6 (iciHHV-6), who have the HHV-6 genome in every cell. It is known that telomeric repeats flanking the virus genome are essential for integration; however, the protein factors mediating integration remain enigmatic. We have previously shown that the putative viral integrase U94 is not essential for telomere integration; thus, we set out to assess the contribution of potential viral recombination proteins U41 and U70 towards integration. We could show that U70 enhances dsDNA break repair via a homology-directed mechanism using a reporter cell line. We then engineered cells to produce shRNAs targeting both U41 and U70 to inhibit their expression during infection. Using these cells in our HHV-6A in vitro integration assay, we could show that U41/U70 were dispensable for telomere integration. Furthermore, additional inhibition of the cellular recombinase Rad51 suggested that it was also not essential, indicating that other cellular and/or viral factors must mediate telomere integration.
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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.