Evidence map›Paper›PMID 32102874›Full record

ArticleJournal of virology2020

BPIFB3 Regulates Endoplasmic Reticulum Morphology To Facilitate Flavivirus Replication.

Azia S Evans, Nicholas J Lennemann, Carolyn B Coyne

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. The role of autophagy in viral infections.Journal of biomedical science · 2023
    Review
  6. Article
  7. Review
  8. Article
  9. Dual-fluorescent reporter for live-cell imaging of the ER during DENV infection.Frontiers in cellular and infection microbiology · 2022
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. ER-Phagy and Microbial Infection.Frontiers in cell and developmental biology · 2021
    Review
  17. Review
  18. Article
  19. Review
  20. Article
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.

Azia S EvansDepartment of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.ORCID 0000-0002-8309-5222
Nicholas J LennemannDepartment of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.ORCID 0000-0002-6379-0965
Carolyn B CoyneDepartment of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA coynec2@pitt.edu.ORCID 0000-0002-1884-6309
University of Pittsburgh · US

Funding

Viral Persistence and PathogenesisT32AI049820 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DELUCA, NEAL A. · 2001 to 2024
$5.5M
Enterovirus Infection of Polarized Intestinal CellsR01AI081759 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI COYNE, CAROLYN B · 2009 to 2024
$5.0M
NIAID NIH HHS R01 AI081759NIAID NIH HHS T32 AI049820
6 · The paper itself

Abstract

Flaviviruses, including dengue virus (DENV) and Zika virus (ZIKV), rely heavily on the availability of endoplasmic reticulum (ER) membranes throughout their life cycle, and degradation of ER membranes restricts flavivirus replication. Accordingly, DENV and ZIKV restrict ER turnover by protease-mediated cleavage of reticulophagy regulator 1 (RETREG1), also known as FAM134B, an autophagy receptor responsible for targeted ER sheet degradation. Given that the induction of autophagy may play an important role in flavivirus replication, the antiviral role of RETREG1 suggests that specialized autophagic pathways may have differential effects on the flavivirus life cycle. We previously identified BPI fold-containing family B member 3 (BPIFB3) as a regulator of autophagy that negatively controls enterovirus replication. Here, we show that in contrast to enteroviruses, BPIFB3 functions as a positive regulator of DENV and ZIKV infection and that its RNA interference-mediated silencing inhibits the formation of viral replication organelles. Mechanistically, we show that depletion of BPIFB3 enhances RETREG1-dependent reticulophagy, leading to enhanced ER turnover and the suppression of viral replication. Consistent with this, the antiviral effects of BPIFB3 depletion can be reversed by RETREG1 silencing, suggesting a specific role for BPIFB3 in regulating ER turnover. These studies define BPIFB3 as a required host factor for both DENV and ZIKV replication and further contribute to our understanding of the requirements for autophagy during flavivirus infection.

Indexed as

AutophagyCarrier ProteinsCell LineDengue VirusEndoplasmic ReticulumFlavivirusFlavivirus InfectionsHost-Pathogen InteractionsHumansRNA InterferenceVirus ReplicationZika VirusZika Virus InfectionBPIFB3 protein, humanCarrier ProteinsautophagyBPIFB3flavivirusreticulophagyviral membrane manipulationviral replication

Identifiers

PMID32102874
PMCPMC7163128
OpenAlexW3007948305

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.