Proteomic analysis of EPC cell replication effect of Hsp70 on SVCV infection at different temperatures

Xue, Jianyang; Yin, Yue; Ai-dong, Qian; Li, Yuehong

doi:10.1016/j.aquaculture.2023.739875

Cited by 2 publications

(1 citation statement)

References 34 publications

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“…Recognizing its severe impact, the World Organization for Animal Health has classi ed SVCV as a mandatory noti able piscine contagion. The outbreak of SVCV is closely correlates with water temperature, with optimal conditions for the virus falling within the range of 16-17℃ (Jiao, Wang, Qian, Li, 2023). Rarely does the disease manifest when water temperatures exceed 23℃ or fall below 10℃ (Zheng, Zhang, Li, Zhang, Chen, Wang, Zhu, 2021).…”

Section: Introductionmentioning

confidence: 99%

Effects of on TLRs/MyD88 related pathways with infected by spring viremia of carp virus (SVCV) in Common Carp

Jiao,

Guo,

Dai

et al. 2024

Preprint

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Spring Viremia of Carp (SVCV) is a highly lethal viral infection that poses a significant threat to the survival and economic value of carp populations. The innate immune system serves as a robust defense mechanism against microbial intrusions. In this study, we delve into the intricate interaction between the Toll-like receptor (TLR) signaling pathway and SVCV.Our research findings unveil a noteworthy response to SVCV infection in EPC cells, characterized by an upregulation in the mRNA expression of key TLRs, namely TLR2, TLR3, TLR4, TLR7, TLR8, and TLR9. These findings strongly suggest their pivotal role in triggering the immune response against SVCV. Furthermore, our investigation delves into the therapeutic potential of ST2825, a MyD88 inhibitor, in mitigating the impact of SVCV infection. We observe that ST2825 effectively suppresses the production of the MyD88 protein, resulting in a notable reduction in mRNA expression levels of SVCV-G. This inhibition extends to the modulation of immune-related genes such as IRAK1 and IRF7, showcasing its potential as a therapeutic intervention. Notably, the ST2825-treated group demonstrates a significant decrease in the rate of cell apoptosis, underlining its potential in mitigating the detrimental effects of SVCV infection. Additionally, our study explores the mRNA expression of TRAF6, IRAK1, IRF3, and IRF7 in renal tissue. We observe a substantial increase in their expression levels in both the ST2825 and SVCV groups when compared to the control group, shedding further light on the intricate interplay within the TLR/MyD88-associated pathways during SVCV infection. In conclusion, our research enhances our understanding of how SVCV infection influences the TLR/MyD88-associated pathways. These findings provide critical insights into SVCV development and lay the groundwork for potential disease control strategies and the development of innovative therapeutic approaches.

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Section: Introductionmentioning

confidence: 99%