Division of Microbiology and Infectious Diseases, Department of Pathology, Shiga University of Medical Science, Seta Tsukinowa-cho, Otsu, Shiga 520-2192, Japan.
J Virol. 2011 May;85(9):4606-11. doi: 10.1128/JVI.02012-10. Epub 2011 Feb 23.
Plasmacytoid dendritic cells (pDCs) do not produce alpha interferon (IFN-α) unless viruses cause a systemic infection or overcome the first-line defense provided by conventional DCs and macrophages. We show here that even paramyxoviruses, whose infections are restricted to the respiratory tract, have a V protein able to prevent Toll-like receptor 7 (TLR7)- and TLR9-dependent IFN-α induction specific to pDCs. Mutational analysis of human parainfluenza virus type 2 demonstrates that the second Trp residue of the Trp-rich motif (Trp-X(3)-Trp-X(9)-Trp) in the C-terminal domain unique to V, a determinant for IRF7 binding, is critical for the blockade of TLR7/9-dependent signaling.
浆细胞样树突状细胞（pDCs）不会产生α干扰素（IFN-α），除非病毒引起全身感染或克服常规树突状细胞和巨噬细胞提供的第一道防线。我们在这里表明，即使是副黏病毒，其感染仅限于呼吸道，也有一种 V 蛋白能够阻止特定于 pDCs 的 Toll 样受体 7（TLR7）和 TLR9 依赖性 IFN-α诱导。人副流感病毒 2 的突变分析表明，V 蛋白特有的 C 末端结构域中富含色氨酸的基序（Trp-X(3)-Trp-X(9)-Trp）中的第二个色氨酸残基是决定 IRF7 结合的关键因素，对于阻断 TLR7/9 依赖性信号至关重要。
