LGALS3BP/90K suppresses porcine reproductive and respiratory syndrome virus replication by enhancing GP3 degradation and stimulating innate immunity
Year: 2025
Type: article
Abstract: Porcine reproductive and respiratory syndrome virus (PRRSV) seriously affects the world pig industry, and existing vaccines are not enough to protect against PRRSV efficiently. Identifying host factors that inhibit PRRSV infection may provide potential targets for antiviral therapies. Galectin 3 binding protein (LGALS3BP), also referred to as 90K, is a multifunctional protein that plays significant roles in viral infections, but its role in PRRSV infection is not clearly defined. In this study, we found that 90K expression increased during PRRSV infection. Additionally, 90K inhibits PRRSV replication by restricting both viral RNA synthesis and viral assembly. Further studies showed that 90K can interact with various PRRSV structural proteins, such as GP2, GP3, and GP5. Moreover, 90K targets K217 in GP3 for K48-linked ubiquitination, facilitating GP3 degradation through the proteasomal pathway. Meanwhile, we found that 90K induces the expression of type I interferon (IFN) and inflammatory cytokines by activating NF-κB and IRF3. Overall, our findings suggest that 90K plays a negative role in PRRSV replication by inducing PRRSV-GP3 degradation and activating innate immune responses.
Source: Veterinary Research
Authors: Qingyu Fan, Haiyan Wang, Hanze Liu, Jinzhi Li, Juan Huang, Ying Yu, Zhi Cao, Qiaoya Zhang
Language: English
Subfield: Animal Science and Zoology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,390
Funders: Qingdao Agricultural University, National Natural Science Foundation of China, Natural Science Foundation of Shandong Province, Nanjing Agricultural University, Modern Agricultural Technology Industry System of Shandong province, Science and Technology Support Plan for Youth Innovation of Colleges and Universities of Shandong Province of China
OpenAlex ID: W4411498233
