Arbidol HCl Inhibits PRRSV Infection by Downregulating CD163 and MYH9 Expression and Modulating Inflammatory Responses
4 affiliations
- 1College of Agriculture and Biology Liaocheng University Liaocheng China lcu.edu.cn
- 2Shandong Provincial General Station of Animal Husbandry Jinan 250100 China
- 3College of Animal Science and Technology Shandong Agricultural University Tai’an China sdau.edu.cn
- 4Key Laboratory of Livestock and Poultry Multi-Omics of MARA Institute of Animal Science and Veterinary Medicine Shandong Academy of Agricultural Sciences Jinan 250100 China saas.ac.cn
Abstract
Porcine reproductive and respiratory syndrome (PRRS) constitutes a major challenge for global pig production, yet effective therapeutic interventions remain elusive. Our study investigated the antiviral potency of Arbidol HCl in counteracting PRRSV infection through comprehensive in permissive cells and in vivo approaches. Our observations demonstrate that Arbidol HCl confers an obvious antiviral activity against varied PRRSV isolates in MARC‐145 cells and primary porcine alveolar macrophages (PAMs). Mechanistic studies revealed that Arbidol HCl inhibits the early stages of PRRSV infection by significantly downregulating the expression of key viral receptors cysteine‐rich scavenger receptor (CD163) and myosin heavy chain 9 (MYH9), thereby disrupting viral attachment and internalization. Subsequent validation studies indicated that Arbidol HCl attenuates proinflammatory responses caused by PRRSV via suppressing the toll‐like receptor 4 (TLR4)/nuclear factor kappa B (NF‐κB) signaling pathway. In vivo experiments using PRRSV‐infected piglets demonstrated that Arbidol HCl treatment significantly reduced viral loads in serum, alleviated lung pathological damage, and mitigated systemic inflammatory responses. These results collectively establish Arbidol HCl as a promising dual‐action therapeutic agent that combines direct antiviral effects with anti‐inflammatory properties. Our study offers hope for developing a practical therapeutic intervention that could significantly impact swine health and food security worldwide. It will provide a novel approach for PRRS prevention and treatment in swine production.
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BibTeX
@article{chen2026arbidol,
title = {{Arbidol HCl Inhibits PRRSV Infection by Downregulating CD163 and MYH9 Expression and Modulating Inflammatory Responses}},
author = {Li Chen and Mengxue Gao and Xiaoyang Zhan and Lei Kong and Shuzhen Jiang and Suimin Shang and En-xin Li and Xiaoting Peng and Qiuju Dai and Yubao Li and Yuyu Zhang and Muhammad Zahoor Khan and Liangliang Li and Jiaqiang Wu and Tongtong Wang},
journal = {Transboundary and Emerging Diseases},
year = {2026},
month = oct,
doi = {10.1155/tbed/2505057},
url = {https://doi.org/10.1155/tbed/2505057},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Arbidol HCl Inhibits PRRSV Infection by Downregulating CD163 and MYH9 Expression and Modulating Inflammatory Responses
AU - Li Chen
AU - Mengxue Gao
AU - Xiaoyang Zhan
AU - Lei Kong
AU - Shuzhen Jiang
AU - Suimin Shang
AU - En-xin Li
AU - Xiaoting Peng
AU - Qiuju Dai
AU - Yubao Li
AU - Yuyu Zhang
AU - Muhammad Zahoor Khan
AU - Liangliang Li
AU - Jiaqiang Wu
AU - Tongtong Wang
PY - 2026
DA - 2026/10/31
JO - Transboundary and Emerging Diseases
DO - 10.1155/tbed/2505057
UR - https://doi.org/10.1155/tbed/2505057
AB - Porcine reproductive and respiratory syndrome (PRRS) constitutes a major challenge for global pig production, yet effective therapeutic interventions remain elusive. Our study investigated the antiviral potency of Arbidol HCl in counteracting PRRSV infection through comprehensive in permissive cells and in vivo approaches. Our observations demonstrate that Arbidol HCl confers an obvious antiviral activity against varied PRRSV isolates in MARC‐145 cells and primary porcine alveolar macrophages (PAMs). Mechanistic studies revealed that Arbidol HCl inhibits the early stages of PRRSV infection by significantly downregulating the expression of key viral receptors cysteine‐rich scavenger receptor (CD163) and myosin heavy chain 9 (MYH9), thereby disrupting viral attachment and internalization. Subsequent validation studies indicated that Arbidol HCl attenuates proinflammatory responses caused by PRRSV via suppressing the toll‐like receptor 4 (TLR4)/nuclear factor kappa B (NF‐κB) signaling pathway. In vivo experiments using PRRSV‐infected piglets demonstrated that Arbidol HCl treatment significantly reduced viral loads in serum, alleviated lung pathological damage, and mitigated systemic inflammatory responses. These results collectively establish Arbidol HCl as a promising dual‐action therapeutic agent that combines direct antiviral effects with anti‐inflammatory properties. Our study offers hope for developing a practical therapeutic intervention that could significantly impact swine health and food security worldwide. It will provide a novel approach for PRRS prevention and treatment in swine production.
SN - 1865-1674
SN - 1865-1682
ER -