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H5亚型禽流感病毒通过TFE3途径诱导高尔基体应激反应以促进病毒复制。

H5 subtype avian influenza virus induces Golgi apparatus stress response via TFE3 pathway to promote virus replication.

作者信息

Yin Yuncong, Kan Xianjin, Miao Xinyu, Sun Yingjie, Chen Sujuan, Qin Tao, Ding Chan, Peng Daxin, Liu Xiufan

机构信息

College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, PR China.

Jiangsu Co-Innovation Center for the Prevention and Control of Important Animal Infectious Disease and Zoonoses, Yangzhou, Jiangsu, PR China.

出版信息

PLoS Pathog. 2024 Dec 9;20(12):e1012748. doi: 10.1371/journal.ppat.1012748. eCollection 2024 Dec.

DOI:10.1371/journal.ppat.1012748
PMID:39652582
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11627363/
Abstract

During infection, avian influenza virus (AIV) triggers endoplasmic reticulum (ER) stress, a well-established phenomenon in previous research. The Golgi apparatus, situated downstream of the ER and crucial for protein trafficking, may be impacted by AIV infection. However, it remains unclear whether this induces Golgi apparatus stress (GAS) and its implications for AIV replication. We investigated the morphological changes in the Golgi apparatus and identified GAS response pathways following infection with the H5 subtype AIV strain A/Mallard/Huadong/S/2005. The results showed that AIV infection induced significant swelling and fragmentation of the Golgi apparatus in A549 cells, indicating the presence of GAS. Among the analyzed GAS response pathways, TFE3 was significantly activated during AIV infection, while HSP47 was activated early in the infection process, and CREB3-ARF4 remained inactive. The blockade of the TFE3 pathway effectively inhibited AIV replication in A549 cells and attenuated AIV virulence in mice. Additionally, activation of the TFE3 pathway promoted endosome acidification and upregulated transcription levels of glycosylation enzymes, facilitating AIV replication. These findings highlight the crucial role of the TFE3 pathway in mediating GAS response during AIV infection, shedding light on its significance in viral replication.

摘要

在感染过程中，禽流感病毒（AIV）会引发内质网（ER）应激，这是先前研究中已明确的现象。位于内质网下游且对蛋白质运输至关重要的高尔基体，可能会受到AIV感染的影响。然而，目前尚不清楚这是否会诱导高尔基体应激（GAS）及其对AIV复制的影响。我们研究了H5亚型AIV毒株A/绿头鸭/华东/S/2005感染后高尔基体的形态变化，并确定了GAS反应途径。结果表明，AIV感染诱导A549细胞中的高尔基体显著肿胀和碎片化，表明存在GAS。在所分析的GAS反应途径中，TFE3在AIV感染期间显著激活，而HSP47在感染过程早期被激活，CREB3-ARF4则保持无活性。阻断TFE3途径可有效抑制A549细胞中的AIV复制，并减弱AIV在小鼠中的毒力。此外，激活TFE3途径可促进内体酸化并上调糖基化酶的转录水平，从而促进AIV复制。这些发现突出了TFE3途径在AIV感染期间介导GAS反应中的关键作用，揭示了其在病毒复制中的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/94c8acea2e15/ppat.1012748.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/82bad5b8542f/ppat.1012748.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/ac1d5c1af596/ppat.1012748.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/a86bb1172b2c/ppat.1012748.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/805e64c3c1a2/ppat.1012748.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/197bab78c0d1/ppat.1012748.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/50b29b9c5c4a/ppat.1012748.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/94c8acea2e15/ppat.1012748.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/82bad5b8542f/ppat.1012748.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/ac1d5c1af596/ppat.1012748.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/a86bb1172b2c/ppat.1012748.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/805e64c3c1a2/ppat.1012748.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/197bab78c0d1/ppat.1012748.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/50b29b9c5c4a/ppat.1012748.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ac/11627363/94c8acea2e15/ppat.1012748.g007.jpg

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