Evidence map›Paper›PMID 8627697›Full record

ArticleJournal of virology1996

Characterization of nuclear structures in cells infected with herpes simplex virus type 1 in the absence of viral DNA replication.

C J Lukonis, S K Weller

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 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Review
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  4. 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
  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
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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

2 authors at 1 institution in 1 country.

C J LukonisDepartment of Microbiology, University of Connecticut Health Center, Farmington 06030, USA.
S K Weller
UConn Health · US

Funding

GENETICS OF HSV DNA REPLICATIONR01AI021747 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI WELLER, SANDRA K, WRIGHT, DENNIS L. · 1985 to 2024
$9.9M
GENETICS OF HSV DNA REPLICATIONR37AI021747 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI WELLER, SANDRA K · 1998 to 2007
$3.3M
NIAID NIH HHS AI21747
6 · The paper itself

Abstract

Herpes simplex virus type 1 DNA replication occurs in nuclear domains termed replication compartments, which are areas of viral single-stranded DNA-binding protein (UL29) localization (M.P. Quinlan, L. B. Chen, and D. M. Knipe, Cell 36:857-868). In the presence of herpesvirus-specific polymerase inhibitors, UL29 localizes to punctate nuclear foci called prereplicative sites. Using versions of the helicase-primase complex proteins containing short peptide epitopes which can be detected in an immunofluorescence assay, we have found that the helicase-primase complex localizes to prereplicative sites and replication compartments. To determine if prereplicative site formation is dependent upon these and other essential viral replication proteins, we have studied UL29 localization in cells infected with replication-defective viruses. Cells infected with viruses that fail to express one of the three helicase-primase subunits or the origin-binding protein show a diffuse nuclear staining for UL29. However, in the presence of polymerase inhibitors, mutant-infected cells contain UL29 in prereplicative sites. Replication-defective viruses containing subtle mutations in the helicase or origin-binding proteins behaved identically to their null mutant counterparts. In contrast, cells infected with viral mutants which fail to express the polymerase protein contain prereplicative sites in the absence and presence of polymerase inhibitors. We propose that active viral polymerase prevents the formation of prereplicative sites. Models of the requirement of essential viral replication proteins in the assembly of prereplicative sites are presented.

Indexed as

Virus ReplicationAnimalsBase SequenceCell NucleusChlorocebus aethiopsDefective VirusesDNA-Binding ProteinsDNA-Directed DNA PolymeraseDNA HelicasesDNA PrimaseDNA ReplicationDNA, ViralEpitopesHerpesvirus 1, HumanHumansMolecular Sequence DataDNA-Binding ProteinsDNA-Directed DNA PolymeraseDNA HelicasesDNA PrimaseDNA, ViralEpitopeshelicase-primase, Human herpesvirus 1ICP8 protein, SimplexvirusPhosphonoacetic AcidUL9 protein, Human herpesvirus 1Viral Proteins

Identifiers

PMID8627697
PMCPMC190000
OpenAlexW2166482322

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.