Evidence map›Paper›PMID 31740931›Full record

ArticleThe Journal of infectious diseases2020

Single Hepatocyte Hepatitis B Virus Transcriptional Landscape in HIV Coinfection.

Ashwin Balagopal, Hyon S Hwang, Tanner Grudda, Jeffrey Quinn, Richard K Sterling, Mark S Sulkowski, Chloe L Thio

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2020. 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
2.6field-weighted citation impact, top 10% 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.

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  12. [A conceptual framework for dynamics of cccDNA in hepatitis B virus].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023
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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 2 institutions in 1 country.

Ashwin BalagopalJohns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Hyon S HwangJohns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Tanner GruddaJohns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Jeffrey QuinnJohns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Richard K SterlingVirginia Commonwealth University Health System, Richmond, Virginia, USA.
Mark S SulkowskiJohns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Chloe L ThioJohns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Johns Hopkins University · USVirginia Commonwealth University · US

Funding

Spatial Models of Intrahepatic Hepatitis C Virus Propagation in HumansR01AI116868 · NIAID · TRIAD NATIONAL SECURITY, LLC · PI ASHWIN BALAGOPAL, Ruy M Ribeiro · 2016 to 2026
$8.5M
HBV HIV Coinfection Research NetworkR01DK094818 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI STERLING, RICHARD K. · 2013 to 2017
$3.5M
Immune correlates of acute HBV recovery with and without HIVR01AI116269 · NIAID · JOHNS HOPKINS UNIVERSITY · PI COX, ANDREA L, THIO, CHLOE L · 2015 to 2019
$3.2M
Characterization of silently HBV-infected hepatocytes in HIV co-infectionR01AI138810 · NIAID · JOHNS HOPKINS UNIVERSITY · PI BALAGOPAL, ASHWIN, THIO, CHLOE L · 2018 to 2021
$3.2M
NIAID NIH HHS R01 AI116269NIAID NIH HHS R01 AI116868NIAID NIH HHS R01 AI138810NIDDK NIH HHS R01 DK094818
6 · The paper itself

Abstract

backgroundHepatitis B virus (HBV) is a leading cause of liver failure and hepatocellular carcinoma. Approximately 10% of people with HIV also have HBV and are at higher risk of liver disease progression than in HBV monoinfection. Antivirals, common to HIV and HBV, suppress HBV DNA levels but do not eradicate virus because the transcriptional template, covalently closed circular DNA (cccDNA), is long lived in infected hepatocytes.

methodsUsing single-cell laser capture microdissection, we isolated >1100 hepatocytes from 5 HIV/HBV coinfected persons with increasing exposure to HBV antivirals (HB1-HB5; no exposure to >7 years exposure), quantifying cccDNA and pregenomic RNA (pgRNA) in each cell using droplet digital polymerase chain reaction.

resultsThe proportion of infected hepatocytes decreased with antiviral exposure from 96.4% (HB1) to 29.8% (HB5). Upper cccDNA range and median pgRNA decreased from HB1 to HB5 (P < .05 for both). The amount of pgRNA transcribed per cccDNA also decreased from HB1 to HB5 (P < .05). Cells with inactive pgRNA transcription were enriched from 0% (HB1) to 14.3% (HB5) of infected hepatocytes.

conclusionscccDNA transcription is reduced in HIV/HBV coinfected people with longer antiviral duration. Understanding HBV transcriptional regulation may be critical to develop a functional cure.

Indexed as

AdultDNA, CircularDNA, ViralHepatitis B, ChronicHepatitis B e AntigensHepatitis B virusHepatocytesHIV InfectionsHumansMaleMiddle AgedVirus ReplicationDNA, CircularDNA, ViralHepatitis B e AntigensHBV transcriptionHIV/HBV coinfectionintrahepatic hepatitis Bsingle-cell laser capture microdissectionviral landscapeviroscape

Identifiers

PMID31740931
PMCPMC7137881
OpenAlexW2991265526

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.