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Study On Mechanism Of EV-D68 Escape The Host Innate Immune

Posted on:2018-04-23Degree:MasterType:Thesis
Country:ChinaCandidate:Z W ZhouFull Text:PDF
GTID:2334330542460481Subject:Biology
Abstract/Summary:PDF Full Text Request
Human Enterovirus D68(EV-D68)is a member of the species Enterovirus D in the genus Enterovirus of the Picornaviridae family.It was first isolated from the pediatric patients in California,USA,in 1962.After that,the virus was rarely reported.But it caused wide public concern in recent years because of the frequently outbreak around the world,the patients appeared with a severe respiratory system and central nervous system diseases.However,the pathogenic mechanism of EV-D68 is not fully understood.The reason why the virus outbreaks is unclear,there is still lack of special treatment,it is an urgent to develop specific effective prevention and treatment to contain the virus.So word hard to studythe virus of molecular biology,replication mechanism,pathogenesis and related research,to clarify the molecular mechanisms of virus infection and immunity,will be beneficial for human to understand the EV-D68,provides the theory basis for doctor to design effective drugs and accurate diagnostic method,provides a new train of thought for developed the antiviral drugs,has very important theoretical value and practical significance.This study found a new way that the EV-D68 escape the host innate immune interferon signaling pathways,further expounds the action mode of EV-D68 inhibit the interferon signaling pathways,and to determine the way and function structure domain of virus protein interact with host immune factors.The experiments proved that bothEV-D68 and nonstructural protein 2A have an adverse effect on the product of IFN-?.On this basis,select the immune factor of interferon signaling pathways adjusted by EV-D68,namely the nonstructural protein 2Ahost target protein TRAF3,and determine the active site of interaction,which include the host targeting proteins enzyme loci and the key of the viral protein enzyme activity sites.At the same time,preliminary findings the structure proteinVP3 can inhibit the interferon signaling pathways and able to interact with IRF7,for subsequent protein structure research provides a new train of thought,provide a new method for the prevention of EV-D68 and antiviral drug development.
Keywords/Search Tags:EV-D68, 2A, VP3, Innate immunity
PDF Full Text Request
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