Evidence map›Paper›PMID 18971270›Full record

ArticleJournal of virology2009

Activation of pattern recognition receptor-mediated innate immunity inhibits the replication of hepatitis B virus in human hepatocyte-derived cells.

Haitao Guo, Dong Jiang, Dongling Ma, Jinhong Chang, Anne Marie Dougherty, Andrea Cuconati, Timothy M Block, Ju-Tao Guo

Abstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

64 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
  2. Article
  3. Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  4. Article
  5. TRIF-dependent signaling and its role in liver diseases.Frontiers in cell and developmental biology · 2024
    Review
  6. Hepatitis B virus-induced hepatocellular carcinoma: a persistent global problem.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2023
    Review
  7. Review
  8. [Mechanism and clinical significance of HBV reactivation after anti-HCV therapy].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Pattern Recognition Receptors: Significance of Expression in the Liver.Archivum immunologiae et therapiae experimentalis · 2020
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

4 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

8 authors at 2 institutions in 1 country.

Haitao GuoDepartment of Microbiology and Immunology, Drexel Institute for Biotechnology and Virology Research, Drexel University College of Medicine, Doylestown, Pennsylvania 18901, USA.
Dong Jiang
Dongling Ma
Jinhong Chang
Anne Marie Dougherty
Andrea Cuconati
Timothy M Block
Ju-Tao Guo
Drexel University · USBaruch S. Blumberg Institute · US

Funding

Imino sugars for flavivirus infections of bioterrorU01AI061441 · NIAID · DREXEL UNIVERSITY · PI BLOCK, TIMOTHY M · 2005 to 2010
$7.8M
NIAID NIH HHS AI061441NIAID NIH HHS U01 AI061441
6 · The paper itself

Abstract

Recognition of virus infections by pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), retinoic acid-inducible gene I (RIG-I), and melanoma differentiation associated gene 5 (MDA5), activates signaling pathways, leading to the induction of inflammatory cytokines that limit viral replication. To determine the effects of PRR-mediated innate immune response on hepatitis B virus (HBV) replication, a 1.3mer HBV genome was cotransfected into HepG2 or Huh7 cells with plasmid expressing TLR adaptors, myeloid differentiation primary response gene 88 (MyD88), and TIR-domain-containing adaptor-inducing beta interferon (TRIF), or RIG-I/MDA5 adaptor, interferon promoter stimulator 1 (IPS-1). The results showed that expressing each of the three adaptors dramatically reduced the levels of HBV mRNA and DNA in both HepG2 and Huh7 cells. However, HBV replication was not significantly affected by treatment of HBV genome-transfected cells with culture media harvested from cells transfected with each of the three adaptors, indicating that the adaptor-induced antiviral response was predominantly mediated by intracellular factors rather than by secreted cytokines. Analyses of involved signaling pathways revealed that activation of NF-kappaB is required for all three adaptors to elicit antiviral response in both HepG2 and Huh7 cells. However, activation of interferon regulatory factor 3 is only essential for induction of antiviral response by IPS-1 in Huh7 cells, but not in HepG2 cells. Furthermore, our results suggest that besides NF-kappaB, additional signaling pathway(s) are required for TRIF to induce a maximum antiviral response against HBV. Knowing the molecular mechanisms by which PRR-mediated innate defense responses control HBV infections could potentially lead to the development of novel therapeutics that evoke the host cellular innate antiviral response to control HBV infections.

Indexed as

Cell LineDNA, ViralHepatitis B virusHepatocytesHumansNF-kappa BReceptors, Pattern RecognitionRNA, MessengerRNA, ViralVirus ReplicationDNA, ViralNF-kappa BReceptors, Pattern RecognitionRNA, MessengerRNA, Viral

Identifiers

PMID18971270
PMCPMC2612386
OpenAlexW2135457568

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.