Evidence map›Paper›PMID 27852858›Full record

ArticleJournal of virology2017

Mapping of Functional Subdomains in the Terminal Protein Domain of Hepatitis B Virus Polymerase.

Daniel N Clark, John M Flanagan, Jianming Hu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Phylogenetic evidence supporting the nonenveloped nature of hepadnavirus ancestors.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

3 authors at 1 institution in 1 country.

Daniel N ClarkDepartment of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA dnc142@psu.edu.
John M FlanaganDepartment of Biochemistry and Molecular Biology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA.
Jianming HuDepartment of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA.
Pennsylvania State University · US

Funding

MECHANISMS OF HEPADNAVIRUS ASSEMBLY AND REPLICATIONR01AI043453 · NIAID · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI HU, JIANMING · 1999 to 2017
$5.9M
Mechanisms of Hepadnavirus Assembly and ReplicationR37AI043453 · NIAID · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI Jianming Hu · 2018 to 2026
$3.8M
NIAID NIH HHS R37 AI043453
6 · The paper itself

Abstract

Hepatitis B virus (HBV) encodes a multifunction reverse transcriptase or polymerase (P), which is composed of several domains. The terminal protein (TP) domain is unique to HBV and related hepadnaviruses and is required for specifically binding to the viral pregenomic RNA (pgRNA). Subsequently, the TP domain is necessary for pgRNA packaging into viral nucleocapsids and the initiation of viral reverse transcription for conversion of the pgRNA to viral DNA. Uniquely, the HBV P protein initiates reverse transcription via a protein priming mechanism using the TP domain as a primer. No structural homologs or high-resolution structure exists for the TP domain. Secondary structure prediction identified three disordered loops in TP with highly conserved sequences. A meta-analysis of mutagenesis studies indicated these predicted loops are almost exclusively where functionally important residues are located. Newly constructed TP mutations revealed a priming loop in TP which plays a specific role in protein-primed DNA synthesis beyond simply harboring the site of priming. Substitutions of potential sites of phosphorylation surrounding the priming site demonstrated that these residues are involved in interactions critical for priming but are unlikely to be phosphorylated during viral replication. Furthermore, the first 13 and 66 TP residues were shown to be dispensable for protein priming and pgRNA binding, respectively. Combining current and previous mutagenesis work with sequence analysis has increased our understanding of TP structure and functions by mapping specific functions to distinct predicted secondary structures and will facilitate antiviral targeting of this unique domain. IMPORTANCE: HBV is a major cause of viral hepatitis, liver cirrhosis, and hepatocellular carcinoma. One important feature of this virus is its polymerase, the enzyme used to create the DNA genome from a specific viral RNA by reverse transcription. One region of this polymerase, the TP domain, is required for association with the viral RNA and production of the DNA genome. Targeting the TP domain for antiviral development is difficult due to the lack of homology to other proteins and high-resolution structure. This study mapped the TP functions according to predicted secondary structure, where it folds into alpha helices or unstructured loops. Three predicted loops were found to be the most important regions functionally and the most conserved evolutionarily. Identification of these functional subdomains in TP will facilitate its targeting for antiviral development.

Indexed as

Protein Interaction Domains and MotifsAmino Acid SequenceConserved SequenceGene Products, polHepatitis B virusHumansModels, MolecularMutationPhenotypeProtein Conformation, alpha-HelicalRNA-Binding ProteinsRNA, MessengerRNA, ViralGene Products, polP protein, Hepatitis B virusRNA-Binding ProteinsRNA, MessengerRNA, ViralDNA polymerasehepadnavirushepatitis B virusprotein primingreverse transcriptaseRNA bindingterminal protein

Identifiers

PMID27852858
PMCPMC5244320
OpenAlexW2552763363

What OpenQuestion holds

Textmetadata
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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.