新城疫病毒（NDV）是危害我国养禽业的重要病毒。干扰素（IFN）在宿主抵御NDV感染过程中具有关键作用。NDV可通过多种方式拮抗宿主IFN反应。V蛋白是NDV拮抗IFN反应的重要因子，可直接抑制IFN的产生，但其机制尚不明确。甲基化转移酶（DNMT3A）作为重要的转录沉默子，可通过调控IFN信号分子甲基化水平而促进IFN表达。我们前期实验发现，V蛋白的核定位能够抑制IFN产生；NDV感染或用V基因转染均可降低DNMT3A的表达。据此我们推测，NDV V蛋白可能通过抑制DNMT3A的表达抑制IFN产生。因此，本项目以宿主DNMT3A与NDV V蛋白调控IFN表达的相互关系为研究主线，利用基因功能干扰、反向遗传和甲基化检测等手段，解析DNMT3A在NDV V蛋白抑制IFN表达中的作用及其对NDV感染致病的影响，从而丰富NDV拮抗IFN的分子机制，为进一步探索NDV的感染致病机制提供理论依据。

Newcastle disease virus (NDV) is an important pathogen that causes significant losses in the poultry industry in China. Interferon (IFN) plays a key role in the host's defense against NDV infection. NDV can antagonize the host IFN response in a variety of ways. V protein plays a important role in the process of NDV antagonizing IFN response, which can directly inhibit the production of IFN, but its mechanism is unclear. DNA methyltransferase 3A (DNMT3A) , as an important gene silencer, can change IFN expression by regulating the methylation level of IFN signaling molecules. Preliminary studies revealed that NDV infection or transfection with V reduces the expression of DNMT3A. Additionally, the V protein can enter the nucleus, indicating that DNMT3A may be involved in the inhibition of IFN production by the NDV V protein. In view of this, this project used gene function interference, reverse genetics, and methylation detection to study the potential regulatory mechanism of DNMT3A in the inhibition of interferon expression by the NDV V protein. The results of this study will enrich the molecular mechanism of NDV antagonizing IFN and provide a theoretical basis for further exploration of the pathogenic mechanism of NDV infection.