Evidence map›Paper›PMID 38675838›Full record

ArticleViruses2024

Neglected Spleen Transcriptional Profile Reveals Inflammatory Disorder Conferred by Rabbit Hemorrhagic Disease Virus 2 Infection.

Jifeng Yu, Yan Li, Lu Xiao, Jing Xie, Zhiqiang Guo, Yonggang Ye, Yi Lin, Ye Cao, Xuejing Wu, Congjian Mao and 10 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Viruses, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

20 authors at 2 institutions in 1 country.

Jifeng YuSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Yan LiCollege of Animal Science and Veterinary Medicine, Southwest Minzu University, Chengdu 610041, China.
Lu XiaoSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Jing XieSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Zhiqiang GuoSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Yonggang YeSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Yi LinSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Ye CaoSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Xuejing WuSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Congjian MaoSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Xingyu LiSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Meng PanSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Jianqiang YeSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Long ZhouCollege of Animal Science and Veterinary Medicine, Southwest Minzu University, Chengdu 610041, China.ORCID 0000-0003-2369-6058
Jian HuangCollege of Animal Science and Veterinary Medicine, Southwest Minzu University, Chengdu 610041, China.
Junyan YangSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Yong WeiSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Xianhui ZhangSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Bin ZhangCollege of Animal Science and Veterinary Medicine, Southwest Minzu University, Chengdu 610041, China.ORCID 0000-0002-3893-906X
Runmin KangSichuan Provincial Key Laboratory of Animal Breeding and Genetics, Sichuan Animal Science Academy, Chengdu 610066, China.
Sichuan Animal Science Academy · CNSouthwest Minzu University · CN

Funding

the Natural Science Foundation of Sichuan Province 2022NSFSC0081the Natural Science Foundation of Sichuan Province 24NSFSC0735the Public Welfare Scientific Research Institutes Basic Research Projects SASA202302
6 · The paper itself

Abstract

Rabbit hemorrhagic disease (RHD) is an acute fatal disease caused by the rabbit hemorrhagic disease virus (RHDV). Since the first outbreaks of type 2 RHDV (RHDV2) in April 2020 in China, the persistence of this virus in the rabbit population has caused substantial economic losses in rabbit husbandry. Previous failures in preventing RHDV2 prompted us to further investigate the immune mechanisms underlying the virus's pathogenicity, particularly concerning the spleen, a vital component of the mononuclear phagocyte system (MPS). For this, a previous RHDV2 isolate, CHN/SC2020, was utilized to challenge naive adult rabbits. Then, the splenic transcriptome was determined by RNA-Seq. This study showed that the infected adult rabbits had 3148 differentially expressed genes (DEGs), which were associated with disease, signal transduction, cellular processes, and cytokine signaling categories. Of these, 100 upregulated DEGs were involved in inflammatory factors such as IL1α, IL-6, and IL-8. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that these DEGs were significantly enriched in the cytokine-cytokine receptor interaction signaling pathway, which may play a vital role in CHN/SC2020 infection. At the same time, proinflammatory cytokines and chemokines were significantly increased in the spleen at the late stages of infection. These findings suggested that RHDV2 (CHN/SC2020) might induce dysregulation of the cytokine network and compromise splenic immunity against viral infection, which expanded our understanding of RHDV2 pathogenicity.

Indexed as

Caliciviridae InfectionsCytokinesHemorrhagic Disease Virus, RabbitSpleenTranscriptomeAnimalsGene Expression ProfilingInflammationRabbitsCytokinespathogenicityrabbit hemorrhagic disease virus 2 (RHDV2)spleentranscriptomic analysis

Identifiers

PMID38675838
PMCPMC11054208
OpenAlexW4393158957

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.