Evidence map›Paper›PMID 30649299›Full record

ReviewFEMS microbiology reviews2019

Immunodeficiencies that predispose to pathologies by human oncogenic γ-herpesviruses.

Blossom Damania, Christian Münz

Open access · bronzeAbstract readReview
In one paragraph

Review in FEMS microbiology reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.8field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
  2. Article
  3. LANA-specific CD4Nature communications · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
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  10. Review
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  12. Article
  13. Review
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  15. Review
  16. Article
  17. Review
  18. Review
  19. Resurrecting Epstein-Barr Virus.Pathogens (Basel, Switzerland) · 2022
    Article
  20. Human herpesvirus diversity is altered in HLA class I binding peptides.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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

2 authors at 2 institutions in 2 countries.

Blossom DamaniaLineberger Cancer Research Center and Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27514, USA.
Christian MünzViral Immunobiology, Institute of Experimental Immunology, University of Zürich, 8057 Zürich, Switzerland.
University of North Carolina at Chapel Hill · USUniversity of Zurich · CH

Funding

Vironomics and Biostatistics CoreP01CA019014 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOSSOM A DAMANIA, NANCY JOAN RAAB-TRAUB · 1985 to 2026
$43.8M
Role of KSHV Viral Proteins in Signaling and PathogenesisR01CA096500 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAMANIA, BLOSSOM A · 2002 to 2022
$6.0M
Modulation of Innate Immunity by KSHVR01DE028211 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAMANIA, BLOSSOM A · 2018 to 2022
$2.1M
Impact of HIV on the Tumor MicroenvironmentR01CA228172 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAMANIA, BLOSSOM A, DITTMER, DIRK P · 2018 to 2022
$2.0M
NCI NIH HHS P01 CA019014NCI NIH HHS R01 CA096500NCI NIH HHS R01 CA228172NIDCR NIH HHS R01 DE028211
6 · The paper itself

Abstract

Human γ-herpesviruses include the closely related tumor viruses Epstein Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV). EBV is the most growth-transforming pathogen known and is linked to at least seven human malignancies. KSHV is also associated with three human cancers. Most EBV- and KSHV-infected individuals fortunately remain disease-free despite persistent infection and this is likely due to the robustness of the immune control that they mount against these tumor viruses. However, upon immune suppression EBV- and KSHV-associated malignancies emerge at increased frequencies. Moreover, primary immunodeficiencies with individual mutations that predispose to EBV or KSHV disease allow us to gain insights into a catalog of molecules that are required for the immune control of these tumor viruses. Curiously, there is little overlap between the mutation targets that predispose individuals to EBV versus KSHV disease, even so both viruses can infect the same host cell, human B cells. These differences will be discussed in this review. A better understanding of the crucial components in the near-perfect life-long immune control of EBV and KSHV should allow us to target malignancies that are associated with these viruses, but also induce similar immune responses against other tumors.

Indexed as

Genetic Predisposition to DiseaseHerpesviridaeHerpesvirus 4, HumanHerpesvirus 8, HumanHost-Pathogen InteractionsHumansImmunocompetenceImmunologic Deficiency SyndromesNeoplasmsOncogenic VirusesBurkitt's lymphomaEpstein Barr virushemophagocytic lymphohistiocytosisHodgkin's lymphomaKaposi sarcomaKaposi sarcoma-associated herpesvirusprimary effusion lymphoma

Identifiers

PMID30649299
PMCPMC6435449
OpenAlexW2909909804

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.