Evidence map›Paper›PMID 33120225›Full record

ArticleVirology2021

Evolution of resistance to fluoroquinolones by dengue virus serotype 4 provides insight into mechanism of action and consequences for viral fitness.

Stacey L P Scroggs, Jordan T Gass, Ramesh Chinnasamy, Steven G Widen, Sasha R Azar, Shannan L Rossi, Jeffrey B Arterburn, Nikos Vasilakis, Kathryn A Hanley

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Stacey L P ScroggsDepartment of Biology, New Mexico State University, Las Cruces, NM, USA. Electronic address: stacey.scroggs@nih.gov.
Jordan T GassDepartment of Biology, New Mexico State University, Las Cruces, NM, USA.
Ramesh ChinnasamyDepartment of Chemistry and Biochemistry, New Mexico State University, Las Cruces, NM, USA.
Steven G WidenDepartment of Biochemistry & Molecular Biology, The University of Texas Medical Branch, Galveston, TX, USA.
Sasha R AzarDepartment of Pathology, The University of University of Texas Medical Branch, Galveston, TX, USA.
Shannan L RossiDepartment of Pathology, The University of University of Texas Medical Branch, Galveston, TX, USA; Institute for Human Infection and Immunity, The University of University of Texas Medical Branch, Galveston, TX, USA.
Jeffrey B ArterburnDepartment of Chemistry and Biochemistry, New Mexico State University, Las Cruces, NM, USA.
Nikos VasilakisDepartment of Pathology, The University of University of Texas Medical Branch, Galveston, TX, USA; Center for Biodefense and Emerging Infectious Diseases, The University of University of Texas Medical Branch, Galveston, TX, USA; Center for Tropical Diseases, The University of University of Texas Medical Branch, Galveston, TX, USA; Institute for Human Infection and Immunity, The University of University of Texas Medical Branch, Galveston, TX, USA.
Kathryn A HanleyDepartment of Biology, New Mexico State University, Las Cruces, NM, USA.
New Mexico State University · USThe University of Texas Medical Branch at Galveston · US

Funding

Mechanisms and Public Health Impact of Sylvatic Dengue Virus Emergence in BorneoU01AI115577 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI VASILAKIS, NIKOS · 2016 to 2019
$2.4M
A new synergy for flavivirus therapy: RNAi enhancement and viral mutagensR21AI092041 · NIAID · NEW MEXICO STATE UNIVERSITY LAS CRUCES · PI ARTERBURN, JEFFREY B, HANLEY, KATHRYN ALYCE · 2011 to 2012
$391k
NIAID NIH HHS R21 AI092041NIAID NIH HHS U01 AI115577
6 · The paper itself

Abstract

Drugs against flaviviruses such as dengue (DENV) and Zika (ZIKV) virus are urgently needed. We previously demonstrated that three fluoroquinolones, ciprofloxacin, enoxacin, and difloxacin, suppress replication of six flaviviruses. To investigate the barrier to resistance and mechanism(s) of action of these drugs, DENV-4 was passaged in triplicate in HEK-293 cells in the presence or absence of each drug. Resistance to ciprofloxacin was detected by the seventh passage and to difloxacin by the tenth, whereas resistance to enoxacin did not occur within ten passages. Two putative resistance-conferring mutations were detected in the envelope gene of ciprofloxacin and difloxacin-resistant DENV-4. In the absence of ciprofloxacin, ciprofloxacin-resistant viruses sustained a significantly higher viral titer than control viruses in HEK-293 and HuH-7 cells and resistant viruses were more stable than control viruses at 37 °C. These results suggest that the mechanism of action of ciprofloxacin and difloxacin involves interference with virus binding or entry.

Indexed as

Biological EvolutionAdaptation, BiologicalAnimalsAntiviral AgentsCell LineChlorocebus aethiopsCiprofloxacinDengueDengue VirusDrug Resistance, ViralEnoxacinFluoroquinolonesGenetic FitnessHEK293 CellsHost Microbial InteractionsHumansAntiviral AgentsCiprofloxacindifloxacinEnoxacinFluoroquinolonesAntiviralCiprofloxacinDengue virusDifloxacinEnoxacinEvolutionFitnessFluoroquinoloneMechanism-of-actionResistance

Identifiers

PMID33120225
PMCPMC7528753
OpenAlexW3091304356

What Socratic 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 Socratic graph.