Evidence map›Paper›PMID 33053346›Full record

ArticleCell reports2020

Quantitative Proteomics Analysis of Lytic KSHV Infection in Human Endothelial Cells Reveals Targets of Viral Immune Modulation.

Ildar Gabaev, James C Williamson, Thomas W M Crozier, Thomas F Schulz, Paul J Lehner

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Review
  6. Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025
    Review
  7. DR5 is a restriction factor for human herpesviruses.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Comparative Review of the Conserved UL24 Protein Family in Herpesviruses.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
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  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Ildar GabaevDepartment of Medicine, University of Cambridge, Hills Road, Cambridge CB2 0QQ, UK; Cambridge Institute for Therapeutic Immunology and Infectious Disease (CITIID), University of Cambridge, Puddicombe Way, Cambridge CB2 0AW, UK. Electronic address: ig329@cam.ac.uk.
James C WilliamsonDepartment of Medicine, University of Cambridge, Hills Road, Cambridge CB2 0QQ, UK; Cambridge Institute for Therapeutic Immunology and Infectious Disease (CITIID), University of Cambridge, Puddicombe Way, Cambridge CB2 0AW, UK.
Thomas W M CrozierDepartment of Medicine, University of Cambridge, Hills Road, Cambridge CB2 0QQ, UK; Cambridge Institute for Therapeutic Immunology and Infectious Disease (CITIID), University of Cambridge, Puddicombe Way, Cambridge CB2 0AW, UK.
Thomas F SchulzInstitute of Virology, Hannover Medical School, Carl-Neuberg-Straße 1, Hannover 30625, Germany; German Center for Infection Research, Hannover-Braunschweig, Germany.
Paul J LehnerDepartment of Medicine, University of Cambridge, Hills Road, Cambridge CB2 0QQ, UK; Cambridge Institute for Therapeutic Immunology and Infectious Disease (CITIID), University of Cambridge, Puddicombe Way, Cambridge CB2 0AW, UK. Electronic address: pjl30@cam.ac.uk.
University of Cambridge · GBMedizinische Hochschule Hannover · DE

Funding

Medical Research Council MR/R001405/1Wellcome Trust 210688/Z/18/Z
6 · The paper itself

Abstract

Kaposi's sarcoma herpesvirus (KSHV) is an oncogenic human virus and the leading cause of mortality in HIV infection. KSHV reactivation from latent- to lytic-stage infection initiates a cascade of viral gene expression. Here we show how these changes remodel the host cell proteome to enable viral replication. By undertaking a systematic and unbiased analysis of changes to the endothelial cell proteome following KSHV reactivation, we quantify >7,000 cellular proteins and 71 viral proteins and provide a temporal profile of protein changes during the course of lytic KSHV infection. Lytic KSHV induces >2-fold downregulation of 291 cellular proteins, including PKR, the key cellular sensor of double-stranded RNA. Despite the multiple episomes per cell, CRISPR-Cas9 efficiently targets KSHV genomes. A complementary KSHV genome-wide CRISPR genetic screen identifies K5 as the viral gene responsible for the downregulation of two KSHV targets, Nectin-2 and CD155, ligands of the NK cell DNAM-1 receptor.

Indexed as

ImmunomodulationProteomicsAntigens, Differentiation, T-LymphocyteCell LineDNA-Directed DNA PolymeraseDown-RegulationeIF-2 KinaseEndothelial CellsGene LibraryGene OntologyGenes, ViralGenetic TestingHerpesvirus 8, HumanHumansKineticsLigandsAntigens, Differentiation, T-LymphocyteDNA-Directed DNA PolymeraseeIF-2 KinaseLigandsProteomeT Lineage-Specific Activation Antigen 1Viral ProteinsherpesvirusHHV-8host cell restriction factorsKSHVlytic reactivationNK cell receptor ligandsproteomicsviral immune evasion

Identifiers

PMID33053346
PMCPMC7567700
OpenAlexW3093251266

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.