Evidence map›Paper›PMID 8627698›Full record

ArticleJournal of virology1996

Functional order of assembly of herpes simplex virus DNA replication proteins into prereplicative site structures.

L M Liptak, S L Uprichard, D M Knipe

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 118 citations in OpenAlex.

  1. Review
  2. Article
  3. Coalescing replication compartments provide the opportunity for recombination between coinfecting herpesviruses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  4. Article
  5. Herpes simplex virus 1 ICP8 mutant lacking annealing activity is deficient for viral DNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  6. Article
  7. Article
  8. Antiviral Activity of Hatay Propolis Against Replication of Herpes Simplex Virus Type 1 and Type 2.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

L M LiptakDepartment of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA.
S L Uprichard
D M Knipe
Harvard University · US

Funding

GENETICS OF HERPESVIRUS TRANSFORMATIONR01CA026345 · NCI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI KNIPE, DAVID M · 1985 to 2000
$346k
GENETICS OF HERPESVIRUS TRANSFORMATIONR37CA026345 · NCI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI KNIPE, DAVID M · 1988 to 1995
–
NCI NIH HHS CA26345NIAID NIH HHS AI07245
6 · The paper itself

Abstract

Herpes simplex virus replicates its DNA within nuclear structures called replication compartments. In contrast, in cells in which viral DNA replication is inhibited, viral replication proteins localize to punctate structures called prereplicative sites. We have utilized viruses individually mutated in each of the seven essential replication genes to assess the function of each replication protein in the assembly of these proteins into prereplicative sites. We observed that four replication proteins, UL5, UL8 UL52, and UL9, are necessary for the localization of ICP8 (UL29) to prereplicative sites natural infection conditions. Likewise, four of the seven viral DNA replication proteins, UL5, UL52, UL9, and ICP8, are necessary for the localization of the viral DNA polymerase to prereplicative sites. On the basis of these results, we present a model for prereplicative site formation in infected cells in which the helicase-primase components (UL5, UL8, and UL52), the origin-binding protein (UL9), and the viral single-stranded DNA-binding protein (ICP8) assemble together to initiate the process. This is followed by the recruitment of the viral polymerase into the structures, a step facilitated by the polymerase accessory protein, UL42. Host cell factors can apparently substitute for some of these viral proteins under certain conditions, because the viral protein requirements for prereplicative site formation are reduced in transfected cells and in infected cells treated with drugs that inhibit DNA synthesis.

Indexed as

DNA ReplicationVirus ReplicationAnimalsCell NucleusChlorocebus aethiopsDNA-Binding ProteinsDNA-Directed DNA PolymeraseDNA HelicasesDNA PrimaseDNA, ViralGene DeletionHerpesvirus 1, HumanHumansPhosphonoacetic AcidTransfectionVero CellsDNA-Binding ProteinsDNA-Directed DNA PolymeraseDNA HelicasesDNA PrimaseDNA, Viralhelicase-primase, Human herpesvirus 1ICP8 protein, SimplexvirusPhosphonoacetic AcidUL9 protein, Human herpesvirus 1Viral Proteins

Identifiers

PMID8627698
PMCPMC190001
OpenAlexW2161315598

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.