Evidence map›Paper›PMID 30684519›Full record

ArticleVirus research2019

A key anti-viral protein, RSAD2/VIPERIN, restricts the release of measles virus from infected cells.

Cheyne Kurokawa, Ianko D Iankov, Evanthia Galanis

Abstract read
In one paragraph

Article in Virus research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 80 citations in OpenAlex.

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  13. Personalizing Oncolytic Immunovirotherapy Approaches.Molecular diagnosis & therapy · 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.

Cheyne KurokawaDepartment of Molecular Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA. Electronic address: kurokawa.cheyne@mayo.edu.
Ianko D IankovDepartment of Molecular Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA. Electronic address: Iankov.Ianko@mayo.edu.
Evanthia GalanisDepartment of Molecular Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA; Division of Medical Oncology, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA. Electronic address: Galanis.Evanthia@mayo.edu.
Mayo Clinic · US

Funding

The Role of CHFR in Tumorigenesis and Paclitaxel-Sensitivity in Breast CancerP50CA116201 · NCI · MAYO CLINIC ROCHESTER · PI PETER C LUCAS · 2005 to 2026
$49.9M
Use of microfluidic tumor cultures to enable clinical trials of therapies for ovarian cancerP50CA136393 · NCI · MAYO CLINIC ROCHESTER · PI Zhenkun Lou · 2009 to 2026
$37.0M
Targeted MV-CEA as a Potent Antitumor Agent against GBMP50CA108961 · NCI · MAYO CLINIC ROCHESTER · PI O'NEILL, BRIAN PATRICK · 2004 to 2015
$22.5M
Optimizing Delivery of Oncolytic Measles Virus Strains with Cell CarriersR01CA200507 · NCI · MAYO CLINIC ROCHESTER · PI GALANIS, EVANTHIA · 2017 to 2020
$2.3M
NCI NIH HHS P50 CA108961NCI NIH HHS P50 CA116201NCI NIH HHS P50 CA136393NCI NIH HHS R01 CA200507
6 · The paper itself

Abstract

Measles virus (MV), a paramyxovirus, is one of the most contagious human pathogens and is responsible for thousands of deaths annually. Wild-type MV evolved to counter the innate immune system by avoiding both type I interferon (IFN) induction and inhibiting IFN signaling through the JAK/STAT pathway. However, virus replication is significantly inhibited in IFN-pretreated cells. Similarly, MV vaccine derived strains are inhibited by IFN pretreatment, but vaccine strains also induce IFN. Despite the significant progress in understanding the interactions between MV and the IFN pathway, the IFN stimulated genes (ISGs) that inhibit MV replication remain largely unknown. The aim of this study is to identify specific ISGs that mediate restriction of MV. In this study, we report that Radical S-adenosyl methionine domain containing 2 (RSAD2) restricts MV infection at the stage of virus release in infected 293T cells. Furthermore, attenuated MV strains are currently being developed as a novel treatment for solid and hematological malignancies. Therefore, we tested the impact of RSAD2 expression in an oncolytic virotherapy context using a MV permissive ovarian cancer line (SR-B2). As measured in 293T cells, MV release was also impaired in SR-B2 cells transduced to express RSAD2 in vitro. Additionally, oncolytic MV therapeutic efficacy was impaired in SR-B2 cells transduced to express RSAD2 in vivo. Overall, we identify RSAD2 as a novel restriction factor for MV by inhibiting the release of virus. These results provide important information regarding the interaction between MV and the innate immune system, as well as implications for the design of oncolytic MV platforms.

Indexed as

Host-Pathogen InteractionsImmunity, InnateVirus ReleaseCell LineEpithelial CellsHumansMeasles virusOxidoreductases Acting on CH-CH Group DonorsProteinsViperin ProteinOxidoreductases Acting on CH-CH Group DonorsProteinsRSAD2 protein, humanViperin ProteinAntiviralInterferonInterferon stimulated genesMeaslesRSAD2VIPERIN

Identifiers

PMID30684519
PMCPMC6615567
OpenAlexW2913674192

What OpenQuestion holds

Textmetadata
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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.