Laboratory of Animal Disease Prevention & Control and Animal Model, Hunan Provincial Key Laboratory of Protein Engineering in Animal Vaccines, College of Veterinary Medicine, Hunan Agricultural University (HUNAU), Changsha 410125, China.
Toxins (Basel). 2022 Feb 6;14(2):121. doi: 10.3390/toxins14020121.
Pseudorabies, caused by pseudorabies virus (PRV), is the main highly infectious disease that severely affects the pig industry globally. T-2 toxin (T2), a significant mycotoxin, is widely spread in food and feeds and shows high toxicity to mammals. The potential mechanism of the interaction between viruses and toxins is of great research value because revealing this mechanism may provide new ideas for their joint prevention and control. In this study, we investigated the effect of T2 on PRV replication and the mechanism of action. The results showed that at a low dose (10 nM), T2 had no significant effect on porcine kidney 15 (PK15) cell viability. However, this T2 concentration alleviated PRV-induced cell injury and increased cell survival time. Additionally, the number of PK15 cells infected with PRV significantly reduced by T2 treatment. Similarly, T2 significantly decreased the copy number of PRV. Investigation of the mechanism revealed that 10 nM T2 significantly inhibits PRV replication and leads to downregulation of oxidative stress- and apoptosis-related genes. These results suggest that oxidative stress and apoptosis are involved in the inhibition of PRV replication in PK15 cells by low-concentration T2. Taken together, we demonstrated the protective effects of T2 against PRV infection. A low T2 concentration inhibited the replication of PRV in PK15 cells, and this process was accompanied by downregulation of the oxidative stress and apoptosis signaling pathways. Our findings partly explain the interaction mechanism between T2 and PRV, relating to oxidative stress and apoptosis, though further research is required.
伪狂犬病是由伪狂犬病病毒（PRV）引起的，是一种严重影响全球养猪业的高度传染性疾病。T-2 毒素（T2）是一种重要的霉菌毒素，广泛存在于食品和饲料中，对哺乳动物具有很高的毒性。研究病毒和毒素相互作用的潜在机制具有重要的研究价值，因为揭示这种机制可能为它们的联合防控提供新的思路。在本研究中，我们研究了 T2 对 PRV 复制的影响及其作用机制。结果表明，在低剂量（10 nM）下，T2 对猪肾 15（PK15）细胞活力没有显著影响。然而，该 T2 浓度缓解了 PRV 诱导的细胞损伤，增加了细胞存活时间。此外，T2 处理显著减少了感染 PRV 的 PK15 细胞数量。同样，T2 显著降低了 PRV 的拷贝数。机制研究表明，10 nM T2 显著抑制 PRV 复制，并导致氧化应激和凋亡相关基因下调。这些结果表明，氧化应激和细胞凋亡参与了低浓度 T2 抑制 PK15 细胞中 PRV 复制的过程。综上所述，我们证明了 T2 对 PRV 感染的保护作用。低浓度 T2 抑制了 PRV 在 PK15 细胞中的复制，这一过程伴随着氧化应激和凋亡信号通路的下调。我们的研究结果部分解释了 T2 与 PRV 之间的相互作用机制，涉及氧化应激和细胞凋亡，但需要进一步研究。
