Bovine leukemia virus (BLV) infection is a bovine chronic infection caused by BLV, a member of the genus Deltaretrovirus. In this study, we examined the immunomodulatory effects of GS-9620, a toll-like receptor (TLR) 7 agonist, in cattle (Bos taurus) and its therapeutic potential for treating BLV infection. GS-9620 induced cytokine production in peripheral blood mononuclear cells (PBMCs) as well as CD80 expression in CD11c⁺ cells and increased CD69 and interferon (IFN)-γ expressions in T cells. Removing CD11c⁺ cells from PBMCs decreased CD69 expression in T cells in the presence of GS-9620. These results suggest that TLR7 agonism promotes T-cell activation via CD11c⁺ cells. Analyses using PBMCs from BLV-infected cattle revealed that TLR7 expression in CD11c⁺ cells was upregulated during late-stage BLV infection. Furthermore, GS-9620 increased IFN-γ and TNF-α production and inhibited syncytium formation in vitro, suggesting that GS-9620 may be used to treat BLV infection.

牛白血病病毒 (BLV) 感染是由Deltaretrovirus属成员 BLV 引起的牛慢性感染。在这项研究中，我们检测了 GS-9620（一种 toll 样受体 (TLR) 7 激动剂）在牛 ( Bos taurus ) 中的免疫调节作用及其治疗 BLV 感染的潜力。GS-9620 诱导外周血单个核细胞 (PBMC) 中的细胞因子产生以及 CD11c ⁺细胞中的 CD80 表达，并增加 T 细胞中 CD69 和干扰素 (IFN)-γ 的表达。在 GS-9620 存在的情况下，从 PBMC 中去除 CD11c ⁺细胞会降低 T 细胞中 CD69 的表达。这些结果表明 TLR7 激动剂通过 CD11c ^{+促进 T 细胞活化}细胞。使用来自 BLV 感染牛的 PBMC 的分析表明，在晚期 BLV 感染期间，CD11c ^{+细胞中的}TLR7表达上调。此外，GS-9620在体外增加了 IFN-γ 和 TNF-α 的产生并抑制了合胞体的形成，这表明 GS-9620 可用于治疗 BLV 感染。