Evidence map›Paper›PMID 16912297›Full record

ArticleJournal of virology2006

Differences and similarities in viral life cycle progression and host cell physiology after infection of human dendritic cells with modified vaccinia virus Ankara and vaccinia virus.

Ann Chahroudi, David A Garber, Patrick Reeves, Luzheng Liu, Daniel Kalman, Mark B Feinberg

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

41 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  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

6 authors at 2 institutions in 1 country.

Ann ChahroudiEmory Vaccine Center, Atlanta, Georgia 30329, USA.
David A Garber
Patrick Reeves
Luzheng Liu
Daniel Kalman
Mark B Feinberg
Emory and Henry College · USEmory University · US

Funding

Project Coordination and Product DevelopmentU19AI061728 · NIAID · EMORY UNIVERSITY · PI PRIDDY, FRANCES H · 2004 to 2008
$14.3M
RECOMBINANT YELLOW FEVER VIRUS AS A CANDIDATE AIDS VACCINEP01AI046007 · NIAID · UNIVERSITY OF ZURICH · PI FEINBERG, MARK B. · 1999 to 2003
$6.7M
NIAID NIH HHS P01 AI046007NIAID NIH HHS P01-AI46007NIAID NIH HHS U19 AI061728NIAID NIH HHS U19-AI061728
6 · The paper itself

Abstract

Modified vaccinia virus Ankara (MVA) is an attenuated strain of vaccinia virus (VV) that has attracted significant attention as a candidate viral vector vaccine for immunization against infectious diseases and treatment of malignancies. Although MVA is unable to replicate in most nonavian cells, vaccination with MVA elicits immune responses that approximate those seen after the administration of replication-competent strains of VV. However, the mechanisms by which these viruses elicit immune responses and the determinants of their relative immunogenicity are incompletely understood. Studying the interactions of VV and MVA with cells of the human immune system may elucidate these mechanisms, as well as provide a rational basis for the further enhancement of the immunogenicity of recombinant MVA vectors. Toward this end, we investigated the consequences of MVA or VV infection of human dendritic cells (DCs), key professional antigen-presenting cells essential for the generation of immune responses. We determined that a block to the formation of intracellular viral replication centers results in abortive infection of DCs with both VV and MVA. MVA inhibited cellular protein synthesis more rapidly than VV and displayed a distinct pattern of viral protein expression in infected DCs. MVA also induced apoptosis in DCs more rapidly than VV, and DC apoptosis after MVA infection was associated with an accelerated decline in the levels of intracellular Bcl-2 and Bcl-X(L). These findings suggest that antigen presentation pathways may contribute differentially to the immunogenicity of VV and MVA and that targeted modifications of virus-induced DC apoptosis may further increase the immunogenicity of MVA-vectored vaccines.

Indexed as

Genetic VectorsVirus ReplicationApoptosisDendritic CellsDNA, ViralHumansProteinsProteomeProto-Oncogene Proteins c-bcl-2Vaccinia virusViral ProteinsViral VaccinesDNA, ViralProteinsProteomeProto-Oncogene Proteins c-bcl-2Viral ProteinsViral Vaccines

Identifiers

PMID16912297
PMCPMC1563888
OpenAlexW1983599364

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.