Evidence map›Paper›PMID 37632027›Full record

ArticleViruses2023

Host Derivation of Sindbis Virus Influences Mammalian Type I Interferon Response to Infection.

John M Crawford, Aaron M Buechlein, Davis A Moline, Douglas B Rusch, Richard W Hardy

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

5 authors at 1 institution in 1 country.

John M CrawfordDepartment of Biology, Indiana University, Bloomington, IN 47405, USA.
Aaron M BuechleinCenter for Genomics and Bioinformatics, Indiana University, Bloomington, IN 47405, USA.
Davis A MolineDepartment of Biology, Indiana University, Bloomington, IN 47405, USA.
Douglas B RuschCenter for Genomics and Bioinformatics, Indiana University, Bloomington, IN 47405, USA.
Richard W HardyDepartment of Biology, Indiana University, Bloomington, IN 47405, USA.
Indiana University Bloomington · US

Funding

Epitranscriptomic Regulation of Alphavirus Replication and TransmissionR21AI153785 · NIAID · TRUSTEES OF INDIANA UNIVERSITY · PI HARDY, RICHARD W · 2020 to 2021
$422k
NIAID NIH HHS R21 AI153785
6 · The paper itself

Abstract

Arboviruses are defined by their ability to replicate in both mosquito vectors and mammalian hosts. There is good evidence that arboviruses "prime" their progeny for infection of the next host, such as via differential glycosylation of their outer glycoproteins or packaging of host ribosomal subunits. We and others have previously shown that mosquito-derived viruses more efficiently infect mammalian cells than mammalian-derived viruses. These observations are consistent with arboviruses acquiring host-specific adaptations, and we hypothesized that a virus derived from either the mammalian host or mosquito vector elicits different responses when infecting the mammalian host. Here, we perform an RNA-sequencing analysis of the transcriptional response of Human Embryonic Kidney 293 (HEK-293) cells to infection with either mosquito (Aedes albopictus, C7/10)- or mammalian (Baby Hamster Kidney, BHK-21)-derived Sindbis virus (SINV). We show that the C7/10-derived virus infection leads to a more robust transcriptional response in HEK-293s compared to infection with the BHK-derived virus. Surprisingly, despite more efficient infection, we found an increase in interferon-β (IFN-β) and interferon-stimulated gene (ISG) transcripts in response to the C7/10-derived virus infection versus the BHK-derived virus infection. However, translation of interferon-stimulated genes was lower in HEK-293s infected with the C7/10-derived virus, starkly contrasting with the transcriptional response. This inhibition of ISG translation is reflective of a more rapid overall shut-off of host cell translation following infection with the C7/10-derived virus. Finally, we show that the C7/10-derived virus infection of HEK-293 cells leads to elevated levels of phosphorylated eukaryotic translation elongation factor-2 (eEF2), identifying a potential mechanism leading to the more rapid shut-off of host translation. We postulate that the rapid shut-off of host translation in mammalian cells infected with the mosquito-derived virus acts to counter the IFN-β-stimulated transcriptional response.

Indexed as

AedesInterferon Type IAnimalsCricetinaeHEK293 CellsHumansInfantInterferon-betaMammalsSindbis VirusInterferon-betaInterferon Type Ialphavirusarbovirustranslational shut-offtype I IFN

Identifiers

PMID37632027
PMCPMC10458878
OpenAlexW4385555369

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.