Evidence map›Paper›PMID 9420287›Full record

ArticleJournal of virology1998

Mechanism of Borna disease virus entry into cells.

D Gonzalez-Dunia, B Cubitt, J C de la Torre

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Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
–field-weighted citation impact
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

51 citing papers in PubMed.

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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.

D Gonzalez-DuniaDepartment of Neuropharmacology, The Scripps Research Institute, La Jolla, California 92037, USA.
B Cubitt
J C de la Torre

Funding

MOLECULAR BIOLOGY OF BORNA DISEASE VIRUS (BDV)R01NS032355 · NINDS · SCRIPPS RESEARCH INSTITUTE · PI DE LA TORRE, JUAN C. · 1996 to 2004
$1.2M
NINDS NIH HHS NS 32355-02NINDS NIH HHS R01 NS032355
6 · The paper itself

Abstract

We have investigated the entry pathway of Borna disease virus (BDV). Virus entry was assessed by detecting early viral replication and transcription. Lysosomotropic agents (ammonium chloride, chloroquine, and amantadine), as well as energy depletion, prevented BDV infection, indicating that BDV enters host cells by endocytosis and requires an acidic intracellular compartment to allow membrane fusion and initiate infection. Consistent with this hypothesis, we observed that BDV-infected cells form extensive syncytia upon low-pH treatment. Entry of enveloped viruses into animal cells usually requires the membrane-fusing activity of viral surface glycoproteins (GPs). BDV GP is expressed as two products of 84 and 43 kDa (GP-84 and GP-43, respectively). We show here that only GP-43 is present at the surface of BDV-infected cells and therefore is likely the viral polypeptide responsible for triggering fusion events. We also present evidence that GP-43, which corresponds to the C terminus of GP-84, is generated by cleavage of GP-84 by the cellular protease furin. Hence, we propose that BDV GP-84 is involved in attachment to the cell surface receptor whereas its furin-cleaved product, GP-43, is involved in pH-dependent fusion after internalization of the virion by endocytosis.

Indexed as

AmantadineAmmonium ChlorideAnimalsBorna disease virusCell LineChloroquineCytopathogenic Effect, ViralEndocytosisGiant CellsHydrogen-Ion ConcentrationLysosomesMembrane FusionRatsTranscription, GeneticViral ProteinsVirus ReplicationAmantadineAmmonium ChlorideChloroquineViral Proteins

Identifiers

PMID9420287
PMCPMC109436

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.