ArticleJournal of virology2012
Construction and manipulation of a new Kaposi's sarcoma-associated herpesvirus bacterial artificial chromosome clone.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 298 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.
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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
298 citing papers in PubMed, 374 citations in OpenAlex.
- KSHV vIRF3-PKM2 interaction induces SMAD5 acetylation, promoting Kaposi's sarcoma progression.Experimental & molecular medicine · 2026Article
- Oncogenic viral infection triggers LAMP2A SUMOylation and chaperone-mediated autophagy to promote tumorigenesis.Nature microbiology · 2026Article
- Article
- Metabolomic Analysis of Lytic KSHV Infection: Induced Host Nucleotide Metabolism Is Required for Infectious Virus Production.Viruses · 2026Article
- Global Lipidomic Analysis of Lytic KSHV Infection: The Lipid Chaperone FABP4 Supports Maximal Infectious Virion Production.Viruses · 2026Article
- A newly developed eGFP-traceable recombinant rhesus lymphocryptovirus, a tool to study viral infection and replicationJournal of virology · 2026Article
- KSHV-infected endothelial cells expand and up-regulate angiogenic pathways and CXCR4 in patient-derived Kaposi sarcoma models.Science translational medicine · 2026Article
- Kaposi's Sarcoma-associated herpesvirus uses a novel protein fold to hijack RNA Polymerase II for viral late gene transcription.bioRxiv : the preprint server for biology · 2026Article
- Stage-specific regulation of KSHV infection by HIF-1α.Journal of virology · 2026Article
- Global Lipidomic Analysis of Lytic KSHV Infection: The lipid chaperone FABP4 is required for maximal infectious virion production.bioRxiv : the preprint server for biology · 2026Article
- Non-canonical histone H3.3 and its chaperones HIRA and DAXX participate in the regulation of KSHV latency.bioRxiv : the preprint server for biology · 2026Article
- The Kaposi's sarcoma-associated herpesvirus viral genome packaging accessory factor ORF68 forms cytoplasmic puncta dependent on the viral tyrosine kinase.bioRxiv : the preprint server for biology · 2026Article
- Interferon-β induction heterogeneity during KSHV infection is correlated to levels and activation of the transcription factors ATF2 and RelA, and not IRF3.PLoS pathogens · 2026Article
- Monoclonal neutralizing antibodies elicited by infection with Kaposi sarcoma-associated herpesvirus reveal critical sites of vulnerability on gH/gL.PLoS pathogens · 2026Article
- KSHV TR deletion episomes uncover enhancer-promoter dynamics in gene regulation.PLoS pathogens · 2025Article
- Review
- Primary envelopment of Kaposi's sarcoma-associated herpesvirus at the nucleoplasmic reticulum.Journal of virology · 2025Article
- The Kaposi's sarcoma-associated herpesvirus TBP mimic uses a noncanonical DNA-binding mode to promote viral late gene transcription.Nucleic acids research · 2025Article
- Characterization of the Kaposi's sarcoma-associated herpesvirus terminase complex component ORF29.Microbiology spectrum · 2025Article
- Interferon-β induction heterogeneity during KSHV infection is correlated to levels and activation of the transcription factors ATF2 and RelA, and not IRF3.bioRxiv : the preprint server for biology · 2025Article
238 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Efficient genetic modification of herpesviruses such as Kaposi's sarcoma-associated herpesvirus (KSHV) has come to rely on bacterial artificial chromosome (BAC) technology. In order to facilitate this approach, we generated a new KSHV BAC clone, called BAC16, derived from the rKSHV.219 virus, which stems from KSHV and Epstein-Barr virus-coinfected JSC1 primary effusion lymphoma (PEL) cells. Restriction enzyme and complete sequencing data demonstrate that the KSHV of JSC1 PEL cells showed a minimal level of sequence variation across the entire viral genome compared to the complete genomic sequence of other KSHV strains. BAC16 not only stably propagated in both Escherichia coli and mammalian cells without apparent genetic rearrangements, but also was capable of robustly producing infectious virions (∼5 × 10(7)/ml). We also demonstrated the utility of BAC16 by generating deletion mutants of either the K3 or K5 genes, whose products are E3 ligases of the membrane-associated RING-CH (MARCH) family. While previous studies have shown that individual expression of either K3 or K5 results in efficient downregulation of the surface expression of major histocompatibility complex class I (MHC-I) molecules, we found that K5, but not K3, was the primary factor critical for the downregulation of MHC-I surface expression during KSHV lytic reactivation or following de novo infection. The data presented here demonstrate the utility of BAC16 for the generation and characterization of KSHV knockout and mutant recombinants and further emphasize the importance of functional analysis of viral genes in the context of the KSHV genome besides the study of individual gene expression.
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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.