Evidence map›Paper›PMID 22045987›Full record

ArticlemBio2011

Restricted Kaposi's sarcoma (KS) herpesvirus transcription in KS lesions from patients on successful antiretroviral therapy.

Dirk P Dittmer

Open access · goldAbstract read
In one paragraph

Article in mBio, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 35 citations in OpenAlex.

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  12. AMC-070: Lenalidomide Is Safe and Effective in HIV-Associated Kaposi Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
  13. Article
  14. Article
  15. Pilot Trial AMC-063: Safety and Efficacy of Bortezomib in AIDS-associated Kaposi Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
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  18. Review
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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

1 author at 1 institution in 1 country.

Dirk P DittmerDepartment of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, and Center for AIDS Research, University of North Carolina, Chapel Hill, North Carolina, USA. ddittmer@med.unc.edu
Johns Hopkins University Center for AIDS Research

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
ART Modulation of Viral Pathogenesis in Oral EpitheliaR01DE018304 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DITTMER, DIRK P · 2007 to 2025
$6.9M
Regulation of the KSHV Latent PromoterR01CA109232 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DITTMER, DIRK P · 2004 to 2014
$2.5M
NCI NIH HHS CA019014NCI NIH HHS CA109232NCI NIH HHS P01 CA019014NCI NIH HHS R01 CA109232NIDCR NIH HHS DE018304NIDCR NIH HHS R01 DE018304
6 · The paper itself

Abstract

unlabelledKaposi's sarcoma (KS) is caused by Kaposi's sarcoma-associated herpesvirus (KSHV; human herpesvirus 8). KS is an AIDS-defining cancer, and it is changing in the post-antiretroviral therapy (post-ART) era. In countries with ready access to ART, approximately one-third of KS cases present in patients with undetectable HIV loads and CD4 counts of ≥200 cells/µl. This is in contrast to pre-ART era KS, which was associated with systemic HIV replication and CD4 counts of ≤200 cells/µl. Using primary patient biopsy specimens, we identified a novel molecular signature that characterizes AIDS KS lesions that develop in HIV-suppressed patients on ART: KSHV transcription is limited in HIV-suppressed patients. With one exception, only the canonical viral latency mRNAs were detectable. In contrast, early AIDS KS lesions expressed many more viral mRNAs, including, for instance, the viral G protein-coupled receptor (vGPCR). IMPORTANCE: This is the first genomewide study of Kaposi's sarcoma-associated herpesvirus (KSHV) transcription in KS lesions in the post-antiretroviral (post-ART) era. It shows that the gene expression of KSHV is altered in patients on ART, and it provides clinical evidence for active AIDS (as characterized by high HIV load and low CD4 counts) being a potential modulator of KSHV transcription. This implies a novel mode of pathogenesis (tightly latent KS), which may inform KS cancer treatment options in the post-ART era.

Indexed as

Transcription, GeneticAnti-HIV AgentsHerpesvirus 8, HumanHIVHIV InfectionsHumansRNA, ViralSarcoma, KaposiVirus ReplicationAnti-HIV AgentsRNA, Viral

Identifiers

PMID22045987
PMCPMC3202757
OpenAlexW2133082612

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.