Evidence map›Paper›PMID 22553339›Full record

ArticleJournal of virology2012

Autophagic clearance of Sin Nombre hantavirus glycoprotein Gn promotes virus replication in cells.

Islam T M Hussein, Erdong Cheng, Safder S Ganaie, Michael J Werle, Sheema Sheema, Absarul Haque, Muhammad A Mir

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  15. Autophagy in Negative-Strand RNA Virus Infection.Frontiers in microbiology · 2018
    Review
  16. Article
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  19. Article
  20. The role of autophagy in intracellular pathogen nutrient acquisition.Frontiers in cellular and infection microbiology · 2015
    Review
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

7 authors at 1 institution in 1 country.

Islam T M HusseinDepartment of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, KS, USA.
Erdong Cheng
Safder S Ganaie
Michael J Werle
Sheema Sheema
Absarul Haque
Muhammad A Mir
University of Kansas Medical Center · US

Funding

Identification and characterization of inhibitors for hantavirus replicationR01AI095236 · NIAID · UNIVERSITY OF KANSAS MEDICAL CENTER · PI MIR, MOHAMMAD A · 2011 to 2013
$1.1M
Role of Cellular P-bodies and Hantavirus Nucleocapsid Protein in Viral mRNA "capR21AI083672 · NIAID · UNIVERSITY OF KANSAS MEDICAL CENTER · PI MIR, MOHAMMAD A · 2009 to 2010
$413k
NIAID NIH HHS 5R01AI095236-02NIAID NIH HHS 5R21AI083672-02NIAID NIH HHS R01 AI095236NIAID NIH HHS R21 AI083672
6 · The paper itself

Abstract

Hantavirus glycoprotein precursor (GPC) is posttranslationally cleaved into two glycoproteins, Gn and Gc. Cells transfected with plasmids expressing either GPC or both Gn and Gc revealed that Gn is posttranslationally degraded. Treatment of cells with the autophagy inhibitors 3-methyladenine, LY-294002, or Wortmanin rescued Gn degradation, suggesting that Gn is degraded by the host autophagy machinery. Confocal microscopic imaging showed that Gn is targeted to autophagosomes for degradation by an unknown mechanism. Examination of autophagy markers LC3-I and LC3-II demonstrated that both Gn expression and Sin Nombre hantavirus (SNV) infection induce autophagy in cells. To delineate whether induction of autophagy and clearance of Gn play a role in the virus replication cycle, we downregulated autophagy genes BCLN-1 and ATG7 using small interfering RNA (siRNA) and monitored virus replication over time. These studies revealed that inhibition of host autophagy machinery inhibits Sin Nombre virus replication in cells, suggesting that autophagic clearance of Gn is required for efficient virus replication. Our studies provide mechanistic insights into viral pathogenesis and reveal that SNV exploits the host autophagy machinery to decrease the intrinsic steady-state levels of an important viral component for efficient replication in host cells.

Indexed as

AutophagyVirus ReplicationAdenineAndrostadienesAnimalsAutophagy-Related Protein 7Cell LineChlorocebus aethiopsChromonesGlycoproteinsHeLa CellsHumansMorpholinesProteolysisRNA InterferenceRNA, Small Interfering2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one3-methyladenineAdenineAndrostadienesATG7 protein, humanAutophagy-Related Protein 7ChromonesGlycoproteinsMorpholinesRNA, Small InterferingUbiquitin-Activating EnzymesViral Envelope ProteinsWortmannin

Identifiers

PMID22553339
PMCPMC3416297
OpenAlexW2087317149

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.