Evidence map›Paper›PMID 31043530›Full record

ArticleJournal of virology2019

Host-Specific NS5 Ubiquitination Determines Yellow Fever Virus Tropism.

Lisa Miorin, Maudry Laurent-Rolle, Giuseppe Pisanelli, Pierre Hendrick Co, Randy A Albrecht, Adolfo García-Sastre, Juliet Morrison

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 35 citations in OpenAlex.

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  11. Functional Roles and Host Interactions ofPathogens (Basel, Switzerland) · 2025
    Review
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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 5 institutions in 2 countries.

Lisa Miorin *Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Maudry Laurent-Rolle *Section of Infectious Diseases, Yale University, New Haven, Connecticut, USA.
Giuseppe PisanelliDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Pierre Hendrick CoDepartment of Biology, Queens College, City University of New York, New York, New York, USA.
Randy A AlbrechtDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.ORCID 0000-0003-4008-503X
Adolfo García-SastreDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA adolfo.garcia-sastre@mssm.edu juliet.morrison@ucr.edu.
Juliet MorrisonDepartment of Microbiology and Plant Pathology, University of California, Riverside, California, USA adolfo.garcia-sastre@mssm.edu juliet.morrison@ucr.edu.ORCID 0000-0001-7387-6351
Icahn School of Medicine at Mount Sinai · USQueens College, CUNY · USUniversity of California, Riverside · USUniversity of Naples Federico II · ITYale University · US

Funding

Project 3 - Ex vivo immune profiling of dengue viruses and vaccinesU19AI118610 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MERAD, MIRIAM · 2015 to 2021
$46.6M
Interferon signaling inhibition by the Zika virus NS5 proteinR21AI129486 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GARCIA-SASTRE, ADOLFO · 2017 to 2018
$466k
NIAID NIH HHS R21 AI129486NIAID NIH HHS U19 AI118610
6 · The paper itself

Abstract

The recent yellow fever virus (YFV) epidemic in Brazil in 2017 and Zika virus (ZIKV) epidemic in 2015 serve to remind us of the importance of flaviviruses as emerging human pathogens. With the current global flavivirus threat, there is an urgent need for antivirals and vaccines to curb the spread of these viruses. However, the lack of suitable animal models limits the research questions that can be answered. A common trait of all flaviviruses studied thus far is their ability to antagonize interferon (IFN) signaling so as to enhance viral replication and dissemination. Previously, we reported that YFV NS5 requires the presence of type I IFN (IFN-α/β) for its engagement with human signal transducer and activator of transcription 2 (hSTAT2). In this manuscript, we report that like the NS5 proteins of ZIKV and dengue virus (DENV), YFV NS5 protein is able to bind hSTAT2 but not murine STAT2 (mSTAT2). Contrary to what has been demonstrated with ZIKV NS5 and DENV NS5, replacing mSTAT2 with hSTAT2 cannot rescue the YFV NS5-STAT2 interaction, as YFV NS5 is also unable to interact with hSTAT2 in murine cells. We show that the IFN-α/β-dependent ubiquitination of YFV NS5 that is required for STAT2 binding in human cells is absent in murine cells. In addition, we demonstrate that mSTAT2 restricts YFV replication

Indexed as

UbiquitinationViral TropismAnimalsHEK293 CellsHumansInterferon-alphaInterferon-betaMiceMice, KnockoutSTAT2 Transcription FactorViral Nonstructural ProteinsYellow fever virusZika VirusInterferon-alphaInterferon-betaNS5 protein, flavivirusSTAT2 protein, humanStat2 protein, mouseSTAT2 Transcription FactorViral Nonstructural Proteinsflavivirushost tropisminterferoninterferon antagonismNS5STAT2yellow fever virus

Identifiers

PMID31043530
PMCPMC6600188
OpenAlexW2943702971

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.