Evidence map›Paper›PMID 22531713›Full record

ReviewThe international journal of biochemistry & cell biology2012

Antiviral therapies: focus on hepatitis B reverse transcriptase.

Eleftherios Michailidis, Karen A Kirby, Atsuko Hachiya, Wangdon Yoo, Sun Pyo Hong, Soo-Ok Kim, William R Folk, Stefan G Sarafianos

Abstract readReview
In one paragraph

Review in The international journal of biochemistry & cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. HBV replication inhibitors.Antiviral research · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. [Advances in clinical research on rtA181 mutation in hepatitis B virus].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Structural basis of HIV inhibition by translocation-defective RT inhibitor 4'-ethynyl-2-fluoro-2'-deoxyadenosine (EFdA).Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  17. Article
  18. Review
  19. Article
  20. 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

8 authors.

Eleftherios MichailidisChristopher S. Bond Life Sciences Center, Department of Molecular Microbiology & Immunology, University of Missouri, Columbia, MO 65211, USA.
Karen A Kirby
Atsuko Hachiya
Wangdon Yoo
Sun Pyo Hong
Soo-Ok Kim
William R Folk
Stefan G Sarafianos

Funding

Ultrapotent Inhibitors of Wild-type and Multi-drug Resistant HIVR01AI076119 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI SARAFIANOS, STEFAN G · 2008 to 2018
$4.1M
Ultrapotent Inhibitors of Wild-type and Multi-drug Resistant HIVR37AI076119 · NIAID · EMORY UNIVERSITY · PI Stefan G Sarafianos · 2020 to 2026
$3.6M
Novel antivirals targeting the RNase H activity of HIV reverse transcriptaseR01AI100890 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI SARAFIANOS, STEFAN G, WANG, ZHENGQIANG · 2012 to 2016
$3.6M
Microbicide properties of RT inhibitor combinationsR33AI079801 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PARNIAK, MICHAEL A · 2010 to 2012
$1.4M
Microbicide properties of RT inhibitor combinationsR21AI079801 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PARNIAK, MICHAEL A · 2008 to 2009
$421k
Structure-based expansion of neutralization ability of KD-247, an anti-V3 mAbR21AI094715 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI SARAFIANOS, STEFAN G · 2010 to 2011
$415k
NIAID NIH HHS AI076119NIAID NIH HHS AI079801NIAID NIH HHS AI094715NIAID NIH HHS R01 AI076119NIAID NIH HHS R01 AI100890NIAID NIH HHS R21 AI079801NIAID NIH HHS R21 AI094715NIAID NIH HHS R33 AI079801NIAID NIH HHS R37 AI076119
6 · The paper itself

Abstract

Hepatitis B virus (HBV) is the etiologic agent of mankind's most serious liver disease. While the availability of a vaccine has reduced the number of new HBV infections, the vaccine does not benefit the approximately 350 million people already chronically infected by the virus. Most of the drugs approved by the FDA for the treatment of hepatitis B target the reverse transcriptase (RT or P gene product) and are nucleoside RT inhibitors (NRTIs) that suppress viral replication. However, prolonged monotherapies directed against a single target result in the emergence of viral resistance. HBV genotypic differences affect NRTI resistance, and because the reading frames of the S (surface antigen) and P genes partially overlap, genomic differences that affect the surface of the virus may also alter the viral polymerase sequence, function and drug susceptibility. The scope of this review is to assess the effects of HBV genotypic variation on the development of drug resistance to NRTIs. Some RT residues that vary among different genotypes are in the vicinity of residues that mutate and give rise to NRTI resistance. Interactions between these amino acids can help explain the effect of HBV genotype on the development of NRTI resistance during antiviral therapies, and might help in the design of improved therapeutic strategies.

Indexed as

Amino Acid SequenceAntiviral AgentsBase SequenceDrug Resistance, ViralGenotypeHepatitis B, ChronicHepatitis B virusHumansMolecular Sequence DataReverse Transcriptase InhibitorsRNA-Directed DNA PolymeraseAntiviral AgentsReverse Transcriptase InhibitorsRNA-Directed DNA Polymerase

Identifiers

PMID22531713
PMCPMC3522522

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.