Evidence map›Paper›PMID 34858407›Full record

ArticleFrontiers in immunology2021

SARS-CoV-2 Nsp5 Activates NF-κB Pathway by Upregulating SUMOylation of MAVS.

Weiling Li, Jialu Qiao, Qiang You, Shan Zong, Qian Peng, Yuchen Liu, Song Hu, Wei Liu, Shufen Li, Xiji Shu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 2 pooled it
4.1field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Mucosal immune response in biology, disease prevention and treatment.Signal transduction and targeted therapy · 2025
    Pooled it
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  17. Classification and regulatory interactions of key transcription factors in COVID-19.Frontiers in cellular and infection microbiology · 2025
    Review
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  19. Article
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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

11 authors at 2 institutions in 1 country.

Weiling LiWuhan Institute of Biomedical Sciences, School of Medicine, Jianghan University, Wuhan, China.
Jialu QiaoWuhan Institute of Biomedical Sciences, School of Medicine, Jianghan University, Wuhan, China.
Qiang YouWuhan Institute of Biomedical Sciences, School of Medicine, Jianghan University, Wuhan, China.
Shan ZongWuhan Institute of Biomedical Sciences, School of Medicine, Jianghan University, Wuhan, China.
Qian PengWuhan Institute of Biomedical Sciences, School of Medicine, Jianghan University, Wuhan, China.
Yuchen LiuWuhan Institute of Biomedical Sciences, School of Medicine, Jianghan University, Wuhan, China.
Song HuWuhan Institute of Biomedical Sciences, School of Medicine, Jianghan University, Wuhan, China.
Wei LiuWuhan Institute of Biomedical Sciences, School of Medicine, Jianghan University, Wuhan, China.
Shufen LiState Key Laboratory of Virology, Wuhan Institute of Virology, Center for Biosafety Mega-Science, Chinese Academy of Sciences, Wuhan, China.
Xiji ShuWuhan Institute of Biomedical Sciences, School of Medicine, Jianghan University, Wuhan, China.
Binlian SunWuhan Institute of Biomedical Sciences, School of Medicine, Jianghan University, Wuhan, China.
Jianghan University · CNWuhan Institute of Virology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The COVID-19 is an infectious disease caused by SARS-CoV-2 infection. A large number of clinical studies found high-level expression of pro-inflammatory cytokines in patients infected with SARS-CoV-2, which fuels the rapid development of the disease. However, the specific molecular mechanism is still unclear. In this study, we found that SARS-CoV-2 Nsp5 can induce the expression of cytokines IL-1β, IL-6, TNF-α, and IL-2 in Calu-3 and THP1 cells. Further research found that Nsp5 enhances cytokine expression through activating the NF-κB signaling pathway. Subsequently, we investigated the upstream effectors of the NF-κB signal pathway on Nsp5 overexpression and discovered that Nsp5 increases the protein level of MAVS. Moreover, Nsp5 can promote the SUMOylation of MAVS to increase its stability and lead to increasing levels of MAVS protein, finally triggering activation of NF-κB signaling. The knockdown of MAVS and the inhibitor of SUMOylation treatment can attenuate Nsp5-mediated NF-κB activation and cytokine induction. We identified a novel role of SARS-CoV-2 Nsp5 to enhance cytokine production by activating the NF-κB signaling pathway.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell LineChlorocebus aethiopsCoronavirus 3C ProteasesCOVID-19CytokinesEnzyme ActivationHEK293 CellsHumansImmunity, InnateInterleukin-1betaInterleukin-2Interleukin-6NF-kappa BSARS-CoV-23C-like proteinase, SARS-CoV-2Adaptor Proteins, Signal TransducingCoronavirus 3C ProteasesCytokinesIL1B protein, humanIL2 protein, humanIL6 protein, humanInterleukin-1betaInterleukin-2Interleukin-6MAVS protein, humanNF-kappa BTNF protein, humanTumor Necrosis Factor-alphacytokineMAVSNF-κBNsp5SARS-CoV-2SUMOylation

Identifiers

PMID34858407
PMCPMC8631293
OpenAlexW3213008578

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.