Evidence map›Paper›PMID 20032178›Full record

ArticleJournal of virology2010

Vaccinia virus particles mix inefficiently, and in a way that would restrict viral recombination, in coinfected cells.

Y-C James Lin, D H Evans

Abstract read
In one paragraph

Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. The Biology of Nucleus-Forming Jumbo Phages.Annual review of genetics · 2025
    Review
  2. Evolutionarily conserved grammar rules viral factories of amoeba-infecting members of the hyperdiverseProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Monkeypox virus: The changing facets of a zoonotic pathogen.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2022
    Review
  5. Article
  6. Poxvirus Recombination.Pathogens (Basel, Switzerland) · 2022
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Poxvirus DNA replication.Cold Spring Harbor perspectives in biology · 2013
    Review
  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

2 authors at 1 institution in 1 country.

Y-C James LinAlberta Institute for Viral Immunology and Department of Medical Microbiology and Immunology, Faculty of Medicine and Dentistry, The University of Alberta, Alberta, Canada.
D H Evans
University of Alberta · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

It is well established that poxviruses are subjected to genetic recombination, but attempts to map vaccinia virus genes using classical genetic crosses were historically confounded by high levels of experimental noise and a poor correlation between physical and genetic map distances. These virus-by-virus crosses also never produced the 50% recombinant progeny that should be seen in experiments involving distant markers. Poxviruses replicate in membrane-wrapped cytoplasmic structures called virosomes (or factories) and we have developed a method for tracking the development of these structures using live cell imaging and cells expressing phage lambda Cro protein fused to enhanced green fluorescent protein (EGFP). The EGFP-cro protein binds nonspecifically to DNA and permits live cell imaging of developing vaccinia virus factories. Using this method, we see virosomes first appearing about 4 to 5 h postinfection. The early virosomes exhibit a compact appearance and then, after a period of exponential growth lasting several hours, blur and start to dissipate in a process presumably linked to viral packaging. During the growth period, the virosomes migrate toward the nuclear periphery while colliding and fusing at a rate dependent upon the numbers of infecting particles. However, even at high multiplicities of infection (10 PFU/cell), we estimate approximately 20% of the virosomes never fuse. We have also used fluorescence in situ hybridization (FISH) methods to study virosomes formed by the fusion of viruses carrying different gene markers. FISH showed that DNA mixes rather poorly within fused virosomes and the amount of mixing is inversely dependent on the time between virosome appearance and fusion. Our studies suggest that the intracellular movement and mixing of virosomes create constraints that reduce opportunities for forming recombinants and that these phenomena create outcomes reflected in classical poxvirus genetics.

Indexed as

Recombination, GeneticVaccinia virusDNA, ViralGenetic MarkersGenome, ViralIn Situ Hybridization, FluorescenceRecombinant Fusion ProteinsVirionVirus AssemblyVirus ReplicationDNA, ViralGenetic MarkersRecombinant Fusion Proteins

Identifiers

PMID20032178
PMCPMC2820930
OpenAlexW2136247706

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.