Evidence map›Paper›PMID 15163753›Full record

ArticleJournal of virology2004

Short duration of elevated vIRF-1 expression during lytic replication of human herpesvirus 8 limits its ability to block antiviral responses induced by alpha interferon in BCBL-1 cells.

Veronika P Pozharskaya, Laura L Weakland, James C Zimring, Laurie T Krug, Elizabeth R Unger, Andrew Neisch, Harish Joshi, Naoki Inoue, Margaret K Offermann

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Human Gammaherpesvirus 8 Oncogenes Associated with Kaposi's Sarcoma.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Molecular biology of human herpesvirus 8: novel functions and virus-host interactions implicated in viral pathogenesis and replication.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2014
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

9 authors at 4 institutions in 1 country.

Veronika P PozharskayaWinship Cancer Institute, Emory University, 1365-B Clifton Road N.E., Atlanta, GA 30322, USA.
Laura L Weakland
James C Zimring
Laurie T Krug
Elizabeth R Unger
Andrew Neisch
Harish Joshi
Naoki Inoue
Margaret K Offermann
Winship Cancer InstituteCenters for Disease Control and Prevention · USPiedmont Cancer Institute · USEmory University · US

Funding

SUBVERSION OF HOST ANTIVIRAL DEFENSES BY HHV8 VIRFR01CA079402 · NCI · EMORY UNIVERSITY · PI OFFERMANN, MARGARET K · 1998 to 2002
$832k
NCI NIH HHS R01 CA 79402
6 · The paper itself

Abstract

Human herpesvirus 8 (HHV-8) encodes multiple proteins that disrupt the host antiviral response, including viral interferon (IFN) regulatory factor 1 (vIRF-1). The product of the vIRF-1 gene blocks responses to IFN when overexpressed by transfection, but the functional consequence of vIRF-1 that is expressed during infection with HHV-8 is not known. These studies demonstrate that BCBL-1 cells that were latently infected with HHV-8 expressed low levels of vIRF-1 that were associated with PML bodies, whereas much higher levels of vIRF-1 were transiently expressed during the lytic phase of HHV-8 replication. The low levels of vIRF-1 that were associated with PML bodies were insufficient to block alpha IFN (IFN-alpha)-induced alterations in gene expression, whereas cells that expressed high levels of vIRF-1 were resistant to some changes induced by IFN-alpha, including the expression of the double-stranded-RNA-activated protein kinase. High levels of vIRF-1 were expressed for only a short period during the lytic cascade, so many cells with HHV-8 in the lytic phase responded to IFN-alpha with increased expression of antiviral genes and enhanced apoptosis. Furthermore, the production of infectious virus was severely compromised when IFN-alpha was present early during the lytic cascade. These studies indicate that the transient expression of high levels of vIRF-1 is inadequate to subvert many of the antiviral effects of IFN-alpha so that IFN-alpha can effectively induce apoptosis and block production of infectious virus when present early in the lytic cascade of HHV-8.

Indexed as

Up-RegulationVirus ReplicationB-LymphocytesCell LineDNA-Binding ProteinsHerpesvirus 8, HumanHumansInterferon-alphaInterferon Regulatory FactorsTime FactorsTranscription FactorsViral ProteinsVirus LatencyDNA-Binding ProteinsInterferon-alphaInterferon Regulatory FactorsTranscription Factorsviral interferon regulatory factorsViral Proteins

Identifiers

PMID15163753
PMCPMC416518
OpenAlexW2071140725

What OpenQuestion holds

Textmetadata
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.