Evidence map›Paper›PMID 28592529›Full record

ArticleJournal of virology2017

Guanylate-Binding Protein 1 Inhibits Nuclear Delivery of Kaposi's Sarcoma-Associated Herpesvirus Virions by Disrupting Formation of Actin Filament.

Zhe Zou, Zhihua Meng, Chao Ma, Deguang Liang, Rui Sun, Ke Lan

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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

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  18. Journal of virology · 2021
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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

6 authors at 5 institutions in 1 country.

Zhe ZouSchool of Life Science, Shanghai University, Shanghai, China.
Zhihua MengSchool of Life Science, Shanghai University, Shanghai, China.
Chao MaSchool of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Deguang LiangKey Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai Chinese Academy of Sciences, Shanghai, China.
Rui SunKey Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai Chinese Academy of Sciences, Shanghai, China.
Ke LanState Key Laboratory of Virology, College of Life Science, Wuhan University, Wuhan, China klan@whu.edu.cn.
Shanghai University · CNChinese Academy of Sciences · CNInstitut Pasteur of Shanghai · CNShanghaiTech University · CNWuhan University · CN

Funding

Versatile functions of LANA in KSHV pathogenesisR01AI116442 · NIAID · WUHAN UNIVERSITY · PI LAN, KE · 2015 to 2019
$517k
NIAID NIH HHS R01 AI116442
6 · The paper itself

Abstract

Kaposi's sarcoma-associated herpesvirus (KSHV) is a typical gammaherpesvirus that establishes persistent lifelong infection in host cells. In order to establish successful infection, KSHV has evolved numerous immune evasion strategies to bypass or hijack the host immune system. However, host cells still produce immune cytokines abundantly during primary KSHV infection. Whether the immune effectors produced are able to inhibit viral infection and how KSHV successfully conquers these immune effectors remain largely unknown. The guanylate-binding protein 1 (GBP1) gene is an interferon-stimulated gene and exerts antiviral functions on several RNA viruses; however, its function in DNA virus infection is less well understood. In this study, we found that KSHV infection increases both the transcriptional and protein levels of GBP1 at the early stage of primary infection by activating the NF-κB pathway. The overexpression of GBP1 significantly inhibited KSHV infection, while the knockdown of GBP1 promoted KSHV infection. The GTPase activity and dimerization of GBP1 were demonstrated to be responsible for its anti-KSHV activity. Furthermore, we found that GBP1 inhibited the nuclear delivery of KSHV virions by disrupting the formation of actin filaments. Finally, we demonstrated that replication and transcription activator (RTA) promotes the degradation of GBP1 through a proteasome pathway. Taken together, these results provide a new understanding of the antiviral mechanism of GBP1, which possesses potent anti-KSHV activity, and suggest the critical role of RTA in the evasion of the innate immune response during primary infection by KSHV.

Indexed as

Host-Pathogen InteractionsImmune EvasionActin CytoskeletonBiological TransportCell LineGTP-Binding ProteinsHerpesvirus 8, HumanHumansImmediate-Early ProteinsProtein MultimerizationTrans-ActivatorsVirionGBP1 protein, humanGTP-Binding ProteinsImmediate-Early ProteinsRta protein, Human herpesvirus 8Trans-Activatorsactin filamentsGBP1GTPase activityKaposi's sarcoma-associated herpesvirusKSHVRTA

Identifiers

PMID28592529
PMCPMC5533911
OpenAlexW2622243504

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.