ArticleScientific reports2017
Kaposi's sarcoma-associated herpesvirus ORF34 is essential for late gene expression and virus production.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 57 citations in OpenAlex.
- The Kaposi's sarcoma-associated herpesvirus TBP mimic uses a noncanonical DNA-binding mode to promote viral late gene transcription.Nucleic acids research · 2025Article
- AlphaFold models of host-pathogen interactions elucidate the prevalence and structural modes of molecular mimicry.bioRxiv : the preprint server for biology · 2025Article
- Genome evolution of Kaposi sarcoma-associated herpesvirus (KSHV).Journal of virology · 2025Article
- Viral cis-regulatory elements as sensors of cellular states and environmental cues.Trends in genetics : TIG · 2024Review
- The cellular Notch1 protein promotes KSHV reactivation in an Rta-dependent manner.Journal of virology · 2024Article
- Conserved cysteine residues in Kaposi's sarcoma herpesvirus ORF34 are necessary for viral production and viral pre-initiation complex formation.Journal of virology · 2024Article
- Conserved cysteine residues in Kaposi's sarcoma herpesvirus ORF34 are necessary for viral production and viral pre-initiation complex formation.bioRxiv : the preprint server for biology · 2024Article
- Better late than never: A unique strategy for late gene transcription in the beta- and gammaherpesviruses.Seminars in cell & developmental biology · 2023Review
- The viral packaging motor potentiates Kaposi's sarcoma-associated herpesvirus gene expression late in infection.PLoS pathogens · 2023Article
- Kaposi's sarcoma-associated herpesvirus induces specialised ribosomes to efficiently translate viral lytic mRNAs.Nature communications · 2023Article
- Kaposi's Sarcoma-Associated Herpesvirus ORF21 Enhances the Phosphorylation of MEK and the Infectivity of Progeny Virus.International journal of molecular sciences · 2023Article
- Article
- Biomolecular Fluorescence Complementation Profiling and Artificial Intelligence Structure Prediction of the Kaposi's Sarcoma-Associated Herpesvirus ORF18 and ORF30 Interaction.International journal of molecular sciences · 2022Article
- A Two-tiered functional screen identifies herpesviral transcriptional modifiers and their essential domains.PLoS pathogens · 2022Article
- Kaposi's Sarcoma-Associated Herpesvirus ORF7 Is Essential for Virus Production.Microorganisms · 2021Article
- The FAT10 post-translational modification is involved in the lytic replication of Kaposi's sarcoma-associated herpesvirus.Journal of virology · 2021Article
- UBE1a Suppresses Herpes Simplex Virus-1 Replication.Viruses · 2020Article
- Article
- Review
- Quantitative Proteomics Analysis of Lytic KSHV Infection in Human Endothelial Cells Reveals Targets of Viral Immune Modulation.Cell reports · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's disease. KSHV establishes a life-long infection in its host and alternates between a latent and lytic infection state. During lytic infection, lytic-related genes are expressed in a temporal manner and categorized as immediate early, early, and late gene transcripts. ORF34 is an early-late gene that interacts with several viral transcription-associated factors, however its physiological importance remains poorly understood. Here, we investigated the role of ORF34 during KSHV infection by generating ORF34-deficient KSHV, using a bacterial artificial chromosome system. Our results reveal that ORF34-deficient KSHV exhibited significantly attenuated late gene expression and viral production but did not affect viral DNA replication. ORF34 interacted with transcription factors ORF18, ORF24, ORF31, and ORF66, and a novel ORF34-interaction partner, ORF23. The C-terminal region of ORF34 was important for interaction with ORF24 and viral production. Our data support a model, in which ORF34 serves as a hub for recruiting a viral transcription complex to ORF24 to promote late viral gene expression.
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