Evidence map›Paper›PMID 28003488›Full record

ArticleJournal of virology2017

Ribosome Profiling Reveals Translational Upregulation of Cellular Oxidative Phosphorylation mRNAs during Vaccinia Virus-Induced Host Shutoff.

Aimei Dai, Shuai Cao, Pragyesh Dhungel, Yizhao Luan, Yizhi Liu, Zhi Xie, Zhilong Yang

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Perturbation of RNA homeostasis impairs mitochondrial respiration during poxvirus infection through excess RNA accumulation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  18. Preinitiation Complex Loading onto mRNAs with Long versus Short 5' TLs.International journal of molecular sciences · 2022
    Article
  19. Ribosomes in poxvirus infection.Current opinion in virology · 2022
    Review
  20. Review
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 2 institutions in 2 countries.

Aimei DaiState Key Lab of Ophthalmology, Guangdong Provincial Key Lab of Ophthalmology and Visual Science, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Shuai CaoDivision of Biology, Kansas State University, Manhattan, Kansas, USA.
Pragyesh DhungelDivision of Biology, Kansas State University, Manhattan, Kansas, USA.
Yizhao LuanState Key Lab of Ophthalmology, Guangdong Provincial Key Lab of Ophthalmology and Visual Science, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Yizhi LiuState Key Lab of Ophthalmology, Guangdong Provincial Key Lab of Ophthalmology and Visual Science, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Zhi XieState Key Lab of Ophthalmology, Guangdong Provincial Key Lab of Ophthalmology and Visual Science, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China xiezhi@gmail.com zyang@ksu.edu.
Zhilong YangDivision of Biology, Kansas State University, Manhattan, Kansas, USA xiezhi@gmail.com zyang@ksu.edu.
Sun Yat-sen University · CNKansas State University · US

Funding

Synthetic Chemical Biology CoreP20GM113117 · NIGMS · UNIVERSITY OF KANSAS LAWRENCE · PI OROZCO, ROBIN C. · 2016 to 2025
$23.9M
Host innate immune response induction and shutoff during poxvirus infectionR00AI100919 · NIAID · KANSAS STATE UNIVERSITY · PI YANG, ZHILONG · 2014 to 2015
$494k
NIAID NIH HHS R00 AI100919NIGMS NIH HHS P20 GM113117
6 · The paper itself

Abstract

Vaccinia virus infection causes a host shutoff that is marked by global inhibition of host protein synthesis. Though the host shutoff may facilitate reallocation of cellular resources for viral replication and evasion of host antiviral immune responses, it poses a challenge for continuous synthesis of cellular proteins that are important for viral replication. It is, however, unclear whether and how certain cellular proteins may be selectively synthesized during the vaccinia virus-induced host shutoff. Using simultaneous RNA sequencing and ribosome profiling, two techniques quantifying genome-wide levels of mRNA and active protein translation, respectively, we analyzed the responses of host cells to vaccinia virus infection at both the transcriptional and translational levels. The analyses showed that cellular mRNA depletion played a dominant role in the shutoff of host protein synthesis. Though the cellular mRNAs were significantly reduced, the relative translation efficiency of a subset of cellular mRNAs increased, particularly those involved in oxidative phosphorylation that are responsible for cellular energy production. Further experiments demonstrated that the protein levels and activities of oxidative phosphorylation increased during vaccinia virus infection, while inhibition of the cellular oxidative phosphorylation function significantly suppressed vaccinia virus replication. Moreover, the short 5' untranslated region of the oxidative phosphorylation mRNAs contributed to the translational upregulation. These results provide evidence of a mechanism that couples translational control and energy metabolism, two processes that all viruses depend on host cells to provide, to support vaccinia virus replication during a host shutoff.

Indexed as

Oxidative Phosphorylation5' Untranslated RegionsGene Expression RegulationHeLa CellsHost-Pathogen InteractionsHumansProtein BiosynthesisRibosomesRNA, MessengerSequence Analysis, RNATranscriptomeUp-RegulationVaccinia virus5' Untranslated RegionsRNA, Messengerhost shutoffoxidative phosphorylationpoxvirusribosome profilingRNA-seqtranslational regulationvaccinia virus

Identifiers

PMID28003488
PMCPMC5309933
OpenAlexW2562396165

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.