Evidence map›Paper›PMID 40871369›Full record

ArticleMicroorganisms2025

BST-2 Promotes N Protein Degradation and Inhibits Viral Replication Through the MARCHF8/NDP52 Autophagy Pathway.

Chenchen Zhao, Yan Qin, Haixin Huang, Yuying Li, Xinyu Zhang, Lin Zhou, Lulu Xie, Yimin Zhou, Yanqing Hu, Wei Chen and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Microorganisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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.

Chenchen ZhaoWenzhou Key Laboratory for Virology and Immunology, Institute of Virology, Wenzhou University, Wenzhou 325035, China.ORCID 0009-0000-6723-5195
Yan QinWenzhou Key Laboratory for Virology and Immunology, Institute of Virology, Wenzhou University, Wenzhou 325035, China.
Haixin HuangWenzhou Key Laboratory for Virology and Immunology, Institute of Virology, Wenzhou University, Wenzhou 325035, China.
Yuying LiWenzhou Key Laboratory for Virology and Immunology, Institute of Virology, Wenzhou University, Wenzhou 325035, China.
Xinyu ZhangWenzhou Key Laboratory for Virology and Immunology, Institute of Virology, Wenzhou University, Wenzhou 325035, China.
Lin ZhouWenzhou Key Laboratory for Virology and Immunology, Institute of Virology, Wenzhou University, Wenzhou 325035, China.
Lulu XieWenzhou Key Laboratory for Virology and Immunology, Institute of Virology, Wenzhou University, Wenzhou 325035, China.
Yimin ZhouWenzhou Key Laboratory for Virology and Immunology, Institute of Virology, Wenzhou University, Wenzhou 325035, China.
Yanqing HuWenzhou Key Laboratory for Virology and Immunology, Institute of Virology, Wenzhou University, Wenzhou 325035, China.
Wei ChenWenzhou Key Laboratory for Virology and Immunology, Institute of Virology, Wenzhou University, Wenzhou 325035, China.ORCID 0009-0004-1976-4462
Tian LanWenzhou Key Laboratory for Virology and Immunology, Institute of Virology, Wenzhou University, Wenzhou 325035, China.
Wen-Chao SunWenzhou Key Laboratory for Virology and Immunology, Institute of Virology, Wenzhou University, Wenzhou 325035, China.ORCID 0000-0002-8845-6242

Funding

Wenzhou Basic Agricultural Science and Technology Project N2023002 and Y20220136
6 · The paper itself

Abstract

Swine acute diarrhea syndrome coronavirus (SADS-CoV) is a recently discovered enteric coronavirus that has caused considerable economic losses in the pig industry. SADS-CoV was first reported in 2017 in Guangdong Province, China, and subsequently in Fujian, Guangxi, Henan and Jiangxi Provinces. Bone marrow stromal cell antigen 2 (BST-2), also known as tetherin, acts as an antiviral protein to limit the release of a wide range of enveloped viruses. However, the relationship between BST-2 and SADS-CoV has rarely been studied. Here, we showed that endogenous BST-2 expression is downregulated by SADS-CoV infection in Vero-E6 and ST cells by 2- to 3-fold. The overexpression of BST-2 inhibited SADS-CoV replication, whereas the knockdown of the BST-2 gene in Vero cells restored SADS-CoV replication. Further study revealed that BST-2 targets the SADS-CoV nucleocapsid protein (N) and decreases N protein expression, and that the BST-2 transmembrane (TM) domain is essential for this activity. Moreover, the degradation of the SADS-CoV N protein promoted by BST-2 is mediated by the membrane-associated ring-CH-type finger 8 (MARCHF8)/calcium binding and coiled-coil domain 2 (NDP52) autophagosome pathway. Overall, we found that BST-2 suppresses viral proliferation by inducing the breakdown of the SADS-CoV N protein via the MARCHF8/NDP52 pathway.

Indexed as

BST2/tetherinMARCHF8NDP52SADS-CoV

Identifiers

PMID40871369
PMCPMC12388171

What OpenQuestion holds

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Registered trials

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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.