Transcriptomic profiling reveals that NSDV exploits autophagy as a proviral mechanism to enhance viral replication

IF 2.8 2区农林科学 Q3 MICROBIOLOGY

Veterinary microbiology Pub Date : 2026-03-01 Epub Date: 2026-01-16 DOI:10.1016/j.vetmic.2026.110895

Xue-Lian Zhang , Xiao-Wen Li , Wei-Hao Tan , Jia-Run Yang , Jie-Yue Liang , Jian-Wei Shao

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引用次数: 0

Abstract

Nairobi sheep disease virus (NSDV), a tick-borne orthonairovirus that causes lethal hemorrhagic gastroenteritis in small ruminants, has recently expanded eastward into China. However, its molecular pathogenesis remains poorly understood. In this study, time-course transcriptomic profiling of NSDV-infected BHK-21 cells revealed a progressive reprogramming of the autophagy pathway, characterized by significant up-regulation of autophagy-related genes. Enhanced autophagosome formation and accelerated autophagosome–lysosome fusion were confirmed by electron microscopy and mRFP-GFP-LC3 flux assays. Pharmacological blockade of autophagy with chloroquine markedly reduced viral RNA accumulation and concurrently enhanced type I interferon responses, indicating that NSDV actively exploits autophagy to facilitate replication and dampen innate immunity. These findings identify autophagy as a proviral mechanism essential for optimal NSDV replication and suggest that targeting this pathway could offer a novel therapeutic strategy against emerging nairoviral infections.

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转录组学分析表明，NSDV利用自噬作为一种前病毒机制来增强病毒复制。

内罗毕羊病病毒（NSDV）是一种在小反刍动物中引起致命出血性胃肠炎的蜱传正呼吸道病毒，最近已向东扩展到中国。然而，其分子发病机制仍知之甚少。在本研究中，nsdv感染的BHK-21细胞的时间过程转录组学分析揭示了自噬途径的进行性重编程，其特征是自噬相关基因的显著上调。电镜和mRFP-GFP-LC3通量测定证实了自噬体形成增强和自噬体与溶酶体融合加速。用氯喹阻断自噬可显著降低病毒RNA积累，同时增强I型干扰素应答，表明NSDV积极利用自噬促进复制并抑制先天免疫。这些发现表明自噬是优化NSDV复制所必需的一种前病毒机制，并表明靶向这一途径可能提供一种新的治疗策略来对抗新出现的纳米病毒感染。

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.