Sindbis virus (SINV) produces the small membrane protein TF from the 6K gene via a (-1) programmed ribosomal frameshifting. While several groups have shown that TF-deficient virus exhibits reduced virulence, the mechanism(s) by which this occurs remain unknown. Here, we demonstrate a role for TF in antagonizing the host interferon response. Using wild-type and type 1 interferon receptor-deficient mice and primary cells derived from these animals, we show that TF controls the induction of the host interferon response at early times during infection. Loss of TF production leads to elevated interferon and a concurrent reduction in viral loads with a loss of pathogenicity. Palmitoylation of TF has been shown to be important for particle assembly and morphology. We find that palmitoylation of TF also contributes to the ability of TF to antagonize host interferon responses as dysregulated palmitoylation of TF reduces virulence in a manner similar to loss of TF.

Sindbis病毒（SINV）通过（-1）编程的核糖体移码从6K基因产生小膜蛋白TF。尽管几组研究表明TF缺陷型病毒表现出降低的毒力，但其发生的机制仍然未知。在这里，我们证明了TF在拮抗宿主干扰素应答中的作用。使用野生型和1型干扰素受体缺陷型小鼠和源自这些动物的原代细胞，我们显示TF在感染过程中的早期控制宿主干扰素应答的诱导。TF产生的损失会导致干扰素升高，并同时导致病毒载量减少，致病性降低。已经显示TF的棕榈酰化对于颗粒组装和形态是重要的。