Evidence map›Paper›PMID 29317664›Full record

ArticleNature communications2018

Human cytomegalovirus-encoded US9 targets MAVS and STING signaling to evade type I interferon immune responses.

Hyun Jin Choi, Areum Park, Sujin Kang, Eunhye Lee, Taeyun A Lee, Eun A Ra, Jiseon Lee, Sungwook Lee, Boyoun Park

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

87 citing papers in PubMed, 113 citations in OpenAlex.

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  19. [Mechanism and significance of cell senescence induced by viral infection].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
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27 more citing papers are in PubMed but not listed here.

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.

Hyun Jin ChoiDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, South Korea.
Areum ParkDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, South Korea.
Sujin KangDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, South Korea.
Eunhye LeeDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, South Korea.
Taeyun A LeeDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, South Korea.
Eun A RaDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, South Korea.
Jiseon LeeImmunotherapeutics Branch, Research Institute, National Cancer Center, Goyang, 10408, South Korea.
Sungwook LeeImmunotherapeutics Branch, Research Institute, National Cancer Center, Goyang, 10408, South Korea. swlee1905@ncc.re.kr.
Boyoun ParkDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, South Korea. bypark@yonsei.ac.kr.
Yonsei University · KRNational Cancer Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human cytomegalovirus (HCMV) has evolved sophisticated immune evasion mechanisms that target both the innate and adaptive immune responses. However, how HCMV encoded proteins are involved in this immune escape is not clear. Here, we show that HCMV glycoprotein US9 inhibits the IFN-β response by targeting the mitochondrial antiviral-signaling protein (MAVS) and stimulator of interferon genes (STING)-mediated signaling pathways. US9 accumulation in mitochondria attenuates the mitochondrial membrane potential, leading to promotion of MAVS leakage from the mitochondria. Furthermore, US9 disrupts STING oligomerization and STING-TBK1 association through competitive interaction. Intriguingly, US9 blocks interferon regulatory factor 3 (IRF3) nuclear translocation and its cytoplasmic domain is essential for inhibiting IRF3 activation. Mutant HCMV lacking US7-16 is impaired in antagonism of MAVS/STING-mediated IFN-β expression, an effect that is reversible by the introduction of US9. Our findings indicate that HCMV US9 is an antagonist of IFN signaling to persistently evade host innate antiviral responses.

Indexed as

Adaptor Proteins, Signal TransducingCells, CulturedHEK293 CellsHeLa CellsHost-Pathogen InteractionsHumansImmune EvasionInterferon Regulatory Factor-3Interferon Type IMembrane GlycoproteinsMembrane ProteinsMitochondriaSignal TransductionSTING ProteinU937 CellsViral ProteinsAdaptor Proteins, Signal TransducingInterferon Regulatory Factor-3Interferon Type IIRF3 protein, humanMAVS protein, humanMembrane GlycoproteinsMembrane ProteinsSTING1 protein, humanSTING ProteinUS9 protein, Human herpesvirus 5Viral Proteins

Identifiers

PMID29317664
PMCPMC5760629
OpenAlexW2781731842

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.