2. Academic Validation
  3. The glycoprotein 5 of porcine reproductive and respiratory syndrome virus stimulates mitochondrial ROS to facilitate viral replication

The glycoprotein 5 of porcine reproductive and respiratory syndrome virus stimulates mitochondrial ROS to facilitate viral replication

  • mBio. 2023 Dec 4:e0265123. doi: 10.1128/mbio.02651-23.
Shuang Zhang # 1 2 3,  Lei Zeng # 1 2 3,  Bing-Qian Su 1 2 3,  Guo-Yu Yang 2 3 4,  Jiang Wang 1 2 3 5,  Sheng-Li Ming 1 2 3,  Bei-Bei Chu 1 2 3 4 5 6
Affiliations

Affiliations

  • 1 College of Veterinary Medicine, Henan Agricultural University, Zhengzhou, Henan Province, China.
  • 2 Key Laboratory of Animal Biochemistry and Nutrition, Ministry of Agriculture and Rural Affairs of the People's Republic of China, Zhengzhou, Henan Province, China.
  • 3 Key Laboratory of Animal Growth and Development, Zhengzhou, Henan Province, China.
  • 4 International Joint Research Center of National Animal Immunology, Henan Agricultural University, Zhengzhou, Henan Province, China.
  • 5 Ministry of Education Key Laboratory for Animal Pathogens and Biosafety, Zhengzhou, Henan Province, China.
  • 6 Longhu Advanced Immunization Laboratory, Zhengzhou, Henan Province, China.
  • # Contributed equally.
PMID: 38047681 DOI: 10.1128/mbio.02651-23
Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) presents a significant economic concern for the global swine industry due to its connection to serious production losses and increased mortality rates. There is currently no specific treatment for PRRSV. Previously, we had uncovered that PRRSV-activated lipophagy to facilitate viral replication. However, the precise mechanism that PRRSV used to trigger Autophagy remained unclear. Here, we found that PRRSV GP5 enhanced mitochondrial CA2+ uptake from ER by promoting ER-mitochondria contact, resulting in mROS release. Elevated mROS induced Autophagy, which alleviated NLRP3 inflammasome activation for optimal viral replication. Our study shed light on a novel mechanism revealing how PRRSV exploits mROS to facilitate viral replication.

Keywords

ER-mitochondria contacts; IP3R; NLRP3 inflammasome; PRRSV; VDAC1; autophagy.

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