Evidence map›Paper›PMID 12163586›Full record

ArticleJournal of virology2002

Cytomegalovirus assemblin (pUL80a): cleavage at internal site not essential for virus growth; proteinase absent from virions.

Chee-Kai Chan, Edward J Brignole, Wade Gibson

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. The N- and C-terminal autolytic fragments of CAPN3/p94/calpain-3 restore proteolytic activity by intermolecular complementation.Proceedings of the National Academy of Sciences of the United States of America · 2014
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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

3 authors at 2 institutions in 1 country.

Chee-Kai ChanVirology Laboratories, Department of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Edward J Brignole
Wade Gibson
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

HERPESVIRUS PROTEIN SYNTHESIS &VIRION ASSEMBLYR01AI013718 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GIBSON, D. WADE · 1985 to 2005
$2.1M
HERPESVIRUS PROTEINASE--TARGET FOR ANTIVIRAL THERAPYR01AI032957 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GIBSON, D. WADE · 1992 to 2007
$1.7M
Herpesvirus Protein Synthesis And Virion AssemblyR56AI013718 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GIBSON, D WADE · 2008 to 2008
$410k
NIAID NIH HHS AI13718NIAID NIH HHS AI32957NIAID NIH HHS R01 AI013718NIAID NIH HHS R01 AI032957NIAID NIH HHS R56 AI013718
6 · The paper itself

Abstract

The human cytomegalovirus (HCMV) maturational proteinase is synthesized as an enzymatically active 74-kDa precursor that cleaves itself at four sites. Two of these, called the maturational (M) and release (R) sites, are conserved in the homologs of all herpesviruses. The other two, called the internal (I) and cryptic (C) sites, have recognized consensus sequences only among cytomegalovirus (CMV) homologs and are located in the 28-kDa proteolytic portion of the precursor, called assemblin. I-site cleavage cuts assemblin in half without detected effect on its enzymatic behavior in vitro. To investigate the requirement for this cleavage during virus infection, we used the CMV-bacterial artificial chromosome system (E. M. Borst, G. Hahn, U. H. Koszinowski, and M. Messerle, J. Virol. 73:8320-8329, 1999) to construct a virus encoding a mutant I site (Ala143 to Val) intended to be blocked for cleavage. Characterizations of the resulting mutant (i) confirmed the presence of the mutation in the viral genome and the inability of the mutant virus to effect I-site cleavage in infected cells; (ii) determined that the mutation has no gross effect on the rate of virus production or on the amounts of extracellular virions, noninfectious enveloped particles (NIEPs), and dense bodies; (iii) established that assemblin and its cleavage products are present in NIEPs but are absent from CMV virions, an apparent difference from what is found for virions of herpes simplex virus; and (iv) showed that the 23-kDa protein product of C-site cleavage is more abundant in mutant virus-than in wild-type virus-infected cells and NIEPs. We conclude that the production of infectious CMV requires neither I-site cleavage of assemblin nor the presence of assemblin in the mature virion.

Indexed as

Cell LineChromosomes, Artificial, BacterialCytomegalovirusCytopathogenic Effect, ViralEndopeptidasesHumansMutationSerine EndopeptidasesTransfectionVirionVirus AssemblyassemblinEndopeptidasesSerine Endopeptidases

Identifiers

PMID12163586
PMCPMC136994
OpenAlexW2137395690

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.