PRRSV infection inhibits CSFV C-strain replication via GSDMD-mediated pyroptosis

IF 2.4 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology Pub Date : 2024-08-30 DOI:10.1016/j.vetmic.2024.110243

Ruijiao Jiang , Dengjin Chen , Yongning Zhang , Lei Zhou , Xinna Ge , Jun Han , Xin Guo , Hanchun Yang

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Abstract

Classical swine fever virus (CSFV) and porcine productive and respiratory syndrome virus (PRRSV) both are significant infectious pathogens in pigs and pose great threats to the healthy development of the pig industry. PRRSV infection often reduces the antibody level of the CSFV attenuated vaccine and even leads to immune failure. In order to elucidate the potential mechanism of CSFV proliferation inhibition by PRRSV and screen out drugs that enhance the vaccine immune effect, we conducted experiments in the PAM39 cell line that can simultaneously support both PRRSV and CSFV infection. The results showed that PRRSV infection could induce gasdermin D (GSDMD) cleavage, promote cell pyroptosis, increase IL-1β secretion, and then inhibit CSFV replication. However, Astragalus polysaccharide treatment could reverse this phenomenon. The results elucidate the molecular mechanism of CSFV vaccine immune failure caused by PRRSV co-infection from the perspective of pyroptosis and provide a scientific basis for the prevention and control of clinical co-infection diseases.

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PRRSV 感染通过 GSDMD 介导的热蛋白沉积抑制 CSFV C 株的复制

猪瘟病毒（CSFV）和猪繁殖与呼吸综合征病毒（PRRSV）都是猪的重要传染病原，对养猪业的健康发展构成巨大威胁。PRRSV 感染往往会降低 CSFV 减毒疫苗的抗体水平，甚至导致免疫失败。为了阐明PRRSV抑制CSFV增殖的潜在机制，筛选出提高疫苗免疫效果的药物，我们在可同时支持PRRSV和CSFV感染的PAM39细胞系中进行了实验。结果表明，PRRSV感染可诱导gasdermin D（GSDMD）裂解，促进细胞析出，增加IL-1β分泌，进而抑制CSFV复制。然而，黄芪多糖治疗可逆转这一现象。该研究结果从热变态反应的角度阐明了PRRSV共感染导致CSFV疫苗免疫失败的分子机制，为临床共感染疾病的防控提供了科学依据。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Veterinary microbiology 农林科学-兽医学

CiteScore

5.90

自引率

6.10%

发文量

221

审稿时长

52 days

期刊介绍： Veterinary Microbiology is concerned with microbial (bacterial, fungal, viral) diseases of domesticated vertebrate animals (livestock, companion animals, fur-bearing animals, game, poultry, fish) that supply food, other useful products or companionship. In addition, Microbial diseases of wild animals living in captivity, or as members of the feral fauna will also be considered if the infections are of interest because of their interrelation with humans (zoonoses) and/or domestic animals. Studies of antimicrobial resistance are also included, provided that the results represent a substantial advance in knowledge. Authors are strongly encouraged to read - prior to submission - the Editorials (''Scope or cope'' and ''Scope or cope II'') published previously in the journal. The Editors reserve the right to suggest submission to another journal for those papers which they feel would be more appropriate for consideration by that journal. Original research papers of high quality and novelty on aspects of control, host response, molecular biology, pathogenesis, prevention, and treatment of microbial diseases of animals are published. Papers dealing primarily with immunology, epidemiology, molecular biology and antiviral or microbial agents will only be considered if they demonstrate a clear impact on a disease. Papers focusing solely on diagnostic techniques (such as another PCR protocol or ELISA) will not be published - focus should be on a microorganism and not on a particular technique. Papers only reporting microbial sequences, transcriptomics data, or proteomics data will not be considered unless the results represent a substantial advance in knowledge. Drug trial papers will be considered if they have general application or significance. Papers on the identification of microorganisms will also be considered, but detailed taxonomic studies do not fall within the scope of the journal. Case reports will not be published, unless they have general application or contain novel aspects. Papers of geographically limited interest, which repeat what had been established elsewhere will not be considered. The readership of the journal is global.