Evidence map›Paper›PMID 25907557›Full record

ArticleThe Journal of biological chemistry2015

The Us3 Protein of Herpes Simplex Virus 1 Inhibits T Cell Signaling by Confining Linker for Activation of T Cells (LAT) Activation via TRAF6 Protein.

Yin Yang, Songfang Wu, Yu Wang, Shuang Pan, Bei Lan, Yaohui Liu, Liming Zhang, Qianli Leng, Da Chen, Cuizhu Zhang and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  14. Frontiers in immunology · 2017
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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

12 authors at 2 institutions in 2 countries.

Yin YangKey laboratory of Microbial Functional Genomics of the Ministry of Education, College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China.
Songfang WuKey laboratory of Microbial Functional Genomics of the Ministry of Education, College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China.
Yu WangKey laboratory of Microbial Functional Genomics of the Ministry of Education, College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China.
Shuang PanKey laboratory of Microbial Functional Genomics of the Ministry of Education, College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China.
Bei LanKey laboratory of Microbial Functional Genomics of the Ministry of Education, College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China.
Yaohui LiuKey laboratory of Microbial Functional Genomics of the Ministry of Education, College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China.
Liming ZhangKey laboratory of Microbial Functional Genomics of the Ministry of Education, College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China.
Qianli LengKey laboratory of Microbial Functional Genomics of the Ministry of Education, College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China.
Da ChenKey laboratory of Microbial Functional Genomics of the Ministry of Education, College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China.
Cuizhu ZhangKey laboratory of Microbial Functional Genomics of the Ministry of Education, College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China. Electronic address: czz912@aliyun.com.
Bin HeDepartment of Microbiology and Immunology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612. Electronic address: tshuo@uic.edu.
Youjia CaoKey laboratory of Microbial Functional Genomics of the Ministry of Education, College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China. Electronic address: caoyj@nankai.edu.cn.
Nankai University · CNUniversity of Illinois Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Herpes simplex virus 1 (HSV-1) is the most prevalent human virus and causes global morbidity because the virus is able to infect multiple cell types. Remarkably, HSV infection switches between lytic and latent cycles, where T cells play a critical role. However, the precise way of virus-host interactions is incompletely understood. Here we report that HSV-1 productively infected Jurkat T-cells and inhibited antigen-induced T cell receptor activation. We discovered that HSV-1-encoded Us3 protein interrupted TCR signaling and interleukin-2 production by inactivation of the linker for activation of T cells. This study unveils a mechanism by which HSV-1 intrudes into early events of TCR-mediated cell signaling and may provide novel insights into HSV infection, during which the virus escapes from host immune surveillance.

Indexed as

Adaptor Proteins, Signal TransducingHerpes SimplexHerpesvirus 1, HumanHumansImmune EvasionInterleukin-2Jurkat CellsMembrane ProteinsProtein Serine-Threonine KinasesReceptors, Antigen, T-CellSignal TransductionT-LymphocytesTNF Receptor-Associated Factor 6Viral ProteinsAdaptor Proteins, Signal TransducingIL2 protein, humanInterleukin-2LAT protein, humanMembrane ProteinsProtein Serine-Threonine KinasesReceptors, Antigen, T-CellTNF Receptor-Associated Factor 6US3 protein, Human herpesvirus 1Viral ProteinsHSV-1interleukinLATsignalingTCRTRAF6ubiquitinationUs3

Identifiers

PMID25907557
PMCPMC4505477
OpenAlexW649948575

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.