Virology Division, National Veterinary Research and Quarantine Service, Ministry for Food, Agriculture, Forestry and Fisheries, Anyang, Gyeonggido, Republic of Korea.
Mol Immunol. 2011 May;48(9-10):1253-62. doi: 10.1016/j.molimm.2011.03.010. Epub 2011 Apr 8.
Type II interferon (IFN-γ) plays an important role in defense against viral infection. Although this cytokine is found during influenza virus infection, it seems to have no protective function against the virus, and the reasons for this are not clear. To determine how the influenza virus overcomes the antiviral effects of IFN-γ, we examined the effect of A/Puerto-Rico/8/34 (H1N1) (PR8) infection on the expression of various IFN-γ inducible genes involved in defense against virus infection. The results showed that PR8 selectively affects IFN-γ induced MHC-II and iNOS expression in both the murine macrophage-like cell line, Raw264.7, and in primary alveolar macrophages. Infection of IFN-γ treated macrophages with PR8 resulted in decreased expression of CIITA/MHC-II and increased production of iNOS/NO. These changes correlate with activation of NF-κB but not with JAK/STAT signaling. The data indicate one possible mechanism underlying the ineffectiveness of IFN-γ against influenza virus, and suggest that NF-κB may be a promising target for anti-influenza drugs.
II 型干扰素（IFN-γ）在抵抗病毒感染中起着重要作用。尽管这种细胞因子在流感病毒感染时被发现，但它似乎对病毒没有保护作用，其原因尚不清楚。为了确定流感病毒如何克服 IFN-γ 的抗病毒作用，我们研究了 A/Puerto-Rico/8/34（H1N1）（PR8）感染对参与抗病毒感染防御的各种 IFN-γ 诱导基因表达的影响。结果表明，PR8 选择性地影响了鼠巨噬细胞样细胞系 Raw264.7 中以及原代肺泡巨噬细胞中 IFN-γ 诱导的 MHC-II 和 iNOS 的表达。用 PR8 感染 IFN-γ 处理的巨噬细胞导致 CIITA/MHC-II 的表达减少和 iNOS/NO 的产生增加。这些变化与 NF-κB 的激活相关，但与 JAK/STAT 信号转导无关。数据表明了 IFN-γ 对流感病毒无效的一种可能机制，并表明 NF-κB 可能是抗流感药物的一个有前途的靶点。
