Evidence map›Paper›PMID 42464369›Full record

ArticleVeterinary research2026

In vitro and in vivo studies of GAPLINC identify it as a critical host factor involved in the regulation of influenza A virus infection.

Lulu Wang, Haiyan Xu, Jiajie Li, Qianxi Zhang, Guanghui Chui, Shihong Yan, Song Wang, Shile Huang, Ji-Long Chen

Abstract read
In one paragraph

Article in Veterinary research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Lulu WangKey Laboratory of Animal Pathogen Infection and Immunology of Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Haiyan XuKey Laboratory of Animal Pathogen Infection and Immunology of Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Jiajie LiKey Laboratory of Animal Pathogen Infection and Immunology of Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Qianxi ZhangKey Laboratory of Animal Pathogen Infection and Immunology of Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Guanghui ChuiKey Laboratory of Animal Pathogen Infection and Immunology of Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Shihong YanKey Laboratory of Animal Pathogen Infection and Immunology of Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Song WangKey Laboratory of Animal Pathogen Infection and Immunology of Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Shile HuangDepartment of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA, 71103, USA.
Ji-Long ChenKey Laboratory of Animal Pathogen Infection and Immunology of Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China. chenjilong@fafu.edu.cn.

Funding

Fujian Agriculture and Forestry University Science and Technology Innovation Fund KFB23094the National Natural Science Foundation of China U23A20235
6 · The paper itself

Abstract

Although previous studies have suggested a role for GAPLINC in regulating influenza A virus (IAV) infection, the functional involvement of GAPLINC in IAV infection in vitro and in vivo remains largely unknown. Here, we found that expression of lncRNA GAPLINC is significantly downregulated by infections with several strains of IAV, including PR8, WSN, H3N2, and H9N2. Interestingly, infections with several other viruses, such as pseudorabies virus (PRV), Sendai virus (SeV), and Herpes simplex virus (HSV), also result in a significant reduction in GAPLINC expression. During IAV infection, activation of NF-κB and the downstream IL-6/STAT3 signaling pathway contribute, at least in part, to the downregulation of GAPLINC expression. Knockdown of GAPLINC in host cells impairs the viral replication, whereas overexpression of GAPLINC increases the viral titers. Both heterozygous GAPLINC knockout (KO) mice (GAPLINC

Indexed as

Gene Expression RegulationInfluenza A virusOrthomyxoviridae InfectionsSwine DiseasesAnimalsDogsHumansMiceMice, KnockoutVirus ReplicationATG7autophagyGAPLINCInfluenza A virusLncRNA

Identifiers

PMID42464369
PMCPMC13377811

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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.