Evidence map›Paper›PMID 20142477›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

The early autophagic pathway is activated by hepatitis B virus and required for viral DNA replication.

Donna Sir, Yongjun Tian, Wen-ling Chen, David K Ann, Tien-Sze Benedict Yen, Jing-Hsiung James Ou

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 178 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
178citing papers in PubMed, 1 pooled it
11.4field-weighted citation impact, top 1% 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

178 citing papers in PubMed, 1 synthesis or guideline pooled it, 338 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Mechanism and regulation of mitophagy in liver diseases: a review.Frontiers in cell and developmental biology · 2025
    Review
  16. Hepatitis B virus entry, assembly, and egress.Microbiology and molecular biology reviews : MMBR · 2024
    Review
  17. Article
  18. Article
  19. Viruses and autophagy: bend, but don't break.Nature reviews. Microbiology · 2024
    Review
  20. Review

118 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Donna SirDepartment of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, CA 90033, USA.
Yongjun Tian
Wen-ling Chen
David K Ann
Tien-Sze Benedict Yen
Jing-Hsiung James Ou
University of Southern California · USCity Of Hope National Medical Center · USUniversity of California, San Francisco · US

Funding

Virus-host interactions in hepatocarcinogenesisP01CA123328 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LAI, MICHAEL M.C. · 2007 to 2011
$5.3M
Role of PreS2 Mutants in Pathogenesis of Chronic Hepatitis BR01CA055578 · NCI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI PULLIAM, LYNN · 1992 to 2011
$3.3M
NCI NIH HHS CA055578NCI NIH HHS CA123328NCI NIH HHS P01 CA123328NCI NIH HHS R01 CA055578
6 · The paper itself

Abstract

Autophagy is a catabolic process by which cells remove long-lived proteins and damaged organelles for recycling. Viral infections may also induce autophagic response. Here we show that hepatitis B virus (HBV), a pathogen that chronically infects approximately 350 million people globally, can enhance autophagic response in cell cultures, mouse liver, and during natural infection. This enhancement of the autophagic response is not coupled by an increase of autophagic protein degradation and is dependent on the viral X protein, which binds to and enhances the enzymatic activity of phosphatidylinositol 3-kinase class III, an enzyme critical for the initiation of autophagy. Further analysis indicates that autophagy enhances HBV DNA replication, with minimal involvement of late autophagic vacuoles in this process. Our studies thus demonstrate that a DNA virus can use autophagy to enhance its own replication and indicate the possibility of targeting the autophagic pathway for the treatment of HBV patients.

Indexed as

AutophagyVirus ReplicationAnimalsBase SequenceBlotting, NorthernBlotting, SouthernCells, CulturedDNA, ViralEnzyme ActivationHepatitis B virusMicePhosphatidylinositol 3-KinasesRNA, Small InterferingDNA, ViralPhosphatidylinositol 3-KinasesRNA, Small Interfering

Identifiers

PMID20142477
PMCPMC2840127
OpenAlexW2081358375

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.