Evidence map›Paper›PMID 30126685›Full record

ReviewCytokine2019

Interferon signaling during Hepatitis B Virus (HBV) infection and HBV-associated hepatocellular carcinoma.

Saravana Kumar Kailasam Mani, Ourania Andrisani

Open access · greenAbstract readReview
In one paragraph

Review in Cytokine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Observational
  3. Generating mRNA Encoding Anti-HBV Designer Epigenome Modifiers.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  4. Conserved Functions ofInternational journal of molecular sciences · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Role of STAT1 in the resistance of HBV to IFN-α.Experimental and therapeutic medicine · 2021
    Article
  11. 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

2 authors at 2 institutions in 1 country.

Saravana Kumar Kailasam ManiDepartment of Basic Medical Sciences and Purdue Center for Cancer Research, Purdue University, West Lafayette, IN 47907, USA. Electronic address: skailasa@purdue.edu.
Ourania AndrisaniDepartment of Basic Medical Sciences and Purdue Center for Cancer Research, Purdue University, West Lafayette, IN 47907, USA. Electronic address: andrisao@purdue.edu.
Center for Cancer Research · USPurdue University West Lafayette · US

Funding

Transgenic Mouse Core Facility Shared Resource (TMCF-SR)P30CA023168 · NCI · PURDUE UNIVERSITY WEST LAFAYETTE · PI John Tesmer · 1985 to 2026
$43.4M
Role of CREB/ATF Proteins in Hepatocyte Growth ControlR01DK044533 · NIDDK · PURDUE UNIVERSITY WEST LAFAYETTE · PI ANDRISANI, OURANIA M. · 1999 to 2021
$5.1M
NCI NIH HHS P30 CA023168NIDDK NIH HHS R01 DK044533
6 · The paper itself

Abstract

Chronic Hepatitis B Virus (HBV) infection is linked to hepatocellular carcinoma (HCC) pathogenesis. The World Health Organization estimates that globally 257 million people are chronic HBV carriers at risk of developing liver cancer. Current therapies for prevention and treatment of HCC are inadequate. Although interferon-based treatment strategies hold great promise for combating chronic infection and HCC, many patients do not respond to the IFN-based drugs for reasons not completely understood. Interferon signaling plays key roles in activation of innate and adaptive immunity. However, HBV has evolved various mechanisms to suppress IFN signaling. In this review, we present the basics about HBV infection and interferon signaling. Next, we discuss mechanisms through which HBV downregulates the function -activity and transcription- of the transcription factor STAT1 during acute and chronic infection. STAT1 is activated in response to all types (I/II/III) of interferon signaling and is essential in mediating all types (I/II/III) of interferon responses. Lastly, we discuss emerging evidence from different human cancers linking loss of interferon signaling to aggressive cancer and cancer stem cells. Whether the same occurs during HBV-associated hepatocarcinogenesis is discussed and currently under investigation.

Indexed as

Immunity, InnateAnimalsCarcinoma, HepatocellularHepatitis BHepatitis B, ChronicHepatitis B virusHumansInterferonsLiver NeoplasmsNeoplastic Stem CellsSignal TransductionSTAT1 Transcription FactorInterferonsSTAT1 protein, humanSTAT1 Transcription FactorCancer stem cellsHepatitis B Virus (HBV)Hepatocellular carcinomaInnate immunityInterferon (IFN) signaling

Identifiers

PMID30126685
PMCPMC6411443
OpenAlexW2887056465

What OpenQuestion holds

Textmetadata
LicenceTDM
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.