ABSTRACT
3a and 7a are nonstructural proteins of SARSCoV, which are encoded separately by ORF 3a and ORF 7a in SARSCoV genome. The expression of 3a has been founded in cells infected by virus in vivo or in vitro. Firstly, the pGL3Control vector was reconstructed , the pGL3Enhancer vector deletious of SV40 promoter gene was obtained . Then the IFN? promoter gene was cloned into the pGL3Enhancer vector and pGLIP21, the Luciferase reporter plasmid with IFN? promoter was established. The availability of pGLIP21 was verified by NDV ,the inductor of IFN?, the Luciferase activity was assayed in cells transfected with pGLIP21 by Luminometer. In order to see the function of 3a and 7a protein of SARSCoV,CHO cells expressing 3a or 7a protein were transfected with pGLIP21, the intensity of luciferase activity was analyzed . By analysis, in vitro, 3a and 7a protein of SARSCoV had the similar ability in triggering the expression of Luceferase gene, i.e 3a and 7a protein of SARSCoV could effectively activate the promoter fragment of IFN? gene. This result will help studying the function of 3a and 7a protein and provide a method to study the nosogenesis mechanism of SARSCoV.
ABSTRACT
Interferons are potent cytokines with antiviral activity that have been founded earliest. Different types of interferons have similar bioactivity, Such as anti-viruses activity, anti-tumor activity and immune modulation. They are induced by virus infection and trigger the host defense by different mechanisms. Firstly, IFNs directly induce the expression of effector proteins with antiviral activity, thus establishing a first line of defense. Secondly, they help to shape adaptive immunity, leading to long-lasting protection. Due to the key position of IFNs in antiviral defense, viruses have evolved effective countermeasures in order to successfully invade the host. By expressing so-called IFN antagonists, viruses interfere with either IFN induction, IFN signaling, or the action of IFN effector proteins.