PDF(Pubmed)
Abstract：
Senecavirus A (SVA) is an emerging virus that poses a threat to swine herds worldwide. To date, the role of tripartite motif 5 (TRIM5) in the replication of viruses has not been evaluated. Here, TRIM5 was reported to inhibit SVA replication by promoting the type I interferon (IFN) antiviral response mediated by retinoic acid-inducible gene I (RIG-I). TRIM5 expression was significantly upregulated in SVA-infected cells, and TRIM5 overexpression inhibited viral replication and promoted IFN-α, IFN-β, interleukin-1beta (IL-1β), IL-6, and IL-18 expression. Conversely, interfering with the expression of TRIM5 had the opposite effect. Viral adsorption and entry assays showed that TRIM5 did not affect the adsorption of SVA but inhibited its entry. In addition, TRIM5 promoted the expression of RIG-I and RIG-I-mediated IFNs and proinflammatory cytokines, and this effect was also proven by inhibiting the expression of TRIM5. These findings expand the scope of knowledge on host factors inhibiting the replication of SVA and indicate that targeting TRIM5 may aid in the development of new agents against SVA.
摘要：
SenecavirusA（SVA）是一种新兴的病毒，对全世界的猪群构成威胁。迄今为止,尚未评估三方基序5（TRIM5）在病毒复制中的作用。这里,据报道,TRIM5通过促进由视黄酸诱导型基因I(RIG-I)介导的I型干扰素(IFN)抗病毒应答来抑制SVA复制。TRIM5表达在SVA感染的细胞中显著上调,TRIM5过表达抑制病毒复制并促进IFN-α，IFN-β,白细胞介素-1β（IL-1β），IL-6和IL-18表达。相反，干扰TRIM5的表达具有相反的效果。病毒吸附和进入实验表明，TRIM5不影响SVA的吸附，但抑制其进入。此外,TRIM5促进RIG-I和RIG-I介导的IFN和促炎细胞因子的表达，通过抑制TRIM5的表达也证明了这种作用。这些发现扩大了有关抑制SVA复制的宿主因子的知识范围，并表明靶向TRIM5可能有助于开发针对SVA的新药物。
