Zhao Xiong WANG, Zhao Xiong WANG, Min Hua SUN, Min Hua SUN, Yin-feng KANG

RelA/p65-mediated Innate Immune Response Affecting NDV Replication in CEF

Newcastle hastalığı virüsü (NDV) tek-parçalı ve tek-sarmallı negatif-yönlü RNA (-) SsRNA virüsüdür. Önceki çalışmalar, NDV'nin konakçıların güçlü doğal bağışıklık tepkilerini indüklediğini göstermektedir. Virüs replikasyonu nükleer kappa B (NF-kB) yolakları üzerinden daha fazla tip I (IFN) interferon ekspresyonuna, ve ayrıca IFN-uyarımlı genlerin (ISGs) aktive ederek daha fazla virüs büyümesini geciktirmek ve spesifik korumanın geliştirilmesi için hücrelerin uyarılmasına neden olabilir. Bu çalışmada, tavuk embriyo fibroblast hücreleri (CEF) virüs enfeksiyonu kullanılarak NDV replikasyonuna karşı doğal bağışıklık yanıtlarında RelA/p65'in rolü araştırıldı. Sonuç, RelA/p65'in mRNA ve protein düzeylerinin virülansları farklı NDV suşlarıyla enfekte CEF'de belirgin oranda arttığını ve RelA/p65'in sitoplazmadan çekirdeğe transloke olduğunu gösterdi. Ayrıca, araştırma spesifik siRNA'nın RelA/p65 ekspresyonunu inhibe edebildiğini, buna uygun olarak, IFN-?, IFN-? ve STAT1 mRNA düzeylerinin önemli ölçüde azaldığını ve 2 NDV'nin replikasyon kinetiğinin RelA/p65 inhibisyonu sonrası geliştirildiğini gösterdi. Sonuç olarak; CEF, NDV enfeksiyonu sonrasında RelA/p65 yolakları aracılığıyla daha fazla IFN türü sentezleyebilir ki, bu NDV replikasyonunu geciktirir ve viral enfeksiyonun erken döneminde yayılma gösterir.

CEF'teki NDV Replikasyonunu Etkileyen RelA/p65-güdümlü Doğal İmmun Tepki

Newcastle disease virus (NDV) is a non-segmented and single-stranded negative-sense RNA (-)ssRNA virus. Previous studies indicate that NDV elicit hosts to induce strongly innate immune responses. The virus replication can cause hosts to express more type I interferon (IFN) via nuclear kappa B (NF-kB) pathways and further activate IFN-stimulated genes (ISGs) to retard virus growth and induce cells for developing specific protection. This study investigated the role of RelA/p65 in innate immune responses against NDV replication by using the virus infection chicken embryo fibroblast cells (CEF). The result showed that the mRNA and protein levels of RelA/p65 increased markedly in CEF infected with strains of NDV which differed in their virulence, and RelA/p65 translocated from the cytoplasm to the nucleus. Further research indicated that specific siRNA could inhibit expression of RelA/p65, accordingly, mRNA levels of IFN-?, IFN-? and STAT1 decreased significantly and the replication kinetics of 2 NDVs were enhanced after inhibition of RelA/p65. In conclusion, CEF can synthesize more type I IFN via RelA/p65 pathways after NDV infection, which retards NDV replication and spreads in the early phase of viral infection.

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