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Diversity and collective interactions during influenza A virus infection

发布日期:2018-06-07访问次数: 信息来源:动物医学院字号:[ ]


 “Diversity and collective interactions during influenza A virus infection” and “Binding of cholesterol to HA of influenza virus is essential for virus replication effecting virus budding and membrane fusion”

 

报告题目:Diversity and collective interactions during influenza A virus infection

报告人:Christopher Byron Brooke

报告题目:Binding of cholesterol to HA of influenza virus is essential for virus replication effecting virus budding and membrane fusion

报告人:Michael Veit

报告地点:动医动科大楼B112

报告时间:201868日上午9:00

主办单位:动物医学院 

联系人:孙怡朋

电话:62733990

欢迎广大师生参加!

 

报告人简介:

Christopher Byron Brooke伊利诺伊大学厄巴纳-香槟分校分子与细胞生物学院微生物学助理教授,伊利诺伊大学Carl R. Woese基因组生物学研究所研究人员,2014年担任ESWI流感大会免疫学联合主席,2014年、2016年两次担任美国病毒学会研讨会召集人,Cell ReportsPLOS PathogensJV等杂志的审稿人。长期致力于流感病毒分子生物学、流行病学以及抗病毒疗法的开发等方面的研究。目前主要研究方向:

Dissect the influence of genome architecture on influenza virus replication and evolution.

Viral interdiction through population engineering and restructuring.

Define novel mechanisms of influenza virus gene regulation.

代表性论文:

Sun J and Brooke CB. 2018. Influenza A virus superinfection potential is regulated by viral genomic heterogeneity. PLOS Pathogens. Submitted.

Kosik I, Ince WL, Gentles L, Oler AJ, Kosikova M, Angel M, Magadan J, Xie H, Yewdell JW*, and Brooke CB*. 2017. Influenza A virus hemagglutinin glycosylation compensates for antibody escape fitness costs. PLOS Pathogens. PMID: 29346435. *Authors contributed equally

Brooke CB. 2017. Population diversity and collective interactions during influenza virus infection. J. Virol.PMID: 28855247.

Brooke CB*, Ince WL*, Wei J, Bennink JR, and Yewdell JW. 2014. Influenza A virus nucleoprotein selectivelydecreases neuraminidase gene segment packaging while enhancing fitness and transmissibility. PNAS.111(47): 16854-16859. *Authors contributed equally

Das SR, Hensley SE, Ince WL, Brooke CB, Subba A, Delboy MG, Russ G, Gibbs JS, Bennink JR, and Yewdell JW. 2013. Defining Influenza A Virus Hemagglutinin Antigenic Drift by Sequential Monoclonal Antibody Selection. Cell Host Microbe. 13(3): 314-323.

 

Michael Veit,柏林自由大学兽医学院病毒学研究所教授,长期从事动脉炎病毒、流感病毒、细胞生物学等方面的研究。目前主要研究方向为流感病毒和动脉炎病毒的进入和出芽,糖蛋白的转运和加工。目前主要研究项目:

DFG Collaborative Research Centre 740: “Functional modules in living cells”.

DFG-projects: “Processing and Function of the Gp2/3/4 Spike of PRRSV“ and “The role of the GP5-M Spike of the PRRSV for virus budding and viral persistence”.

Human Frontiers Science Program: “Molecular Patterns of Influenza Virus Envelope Adaptation”.

代表性论文:

Zhang, Krabben, Wang, Veit(2018) Glycoprotein 3 of porcine reproductive and respiratory syndrome virus exhibits an unusual hairpin-like membrane topology. J. Virol. May 16.

Thaa, Herrmann, Veit(2010) Intrinsic cytoskeleton-dependent clustering of influenza virus M2 protein with hemagglutinin assessed by FLIM-FRET. J. Virol. 84, 12445-9

Brett, Kordyukova, Serebryakova, Mintaev, Alexeevski, Veit(2014) Site-specific S-acylation of influenza virus hemagglutinin: the location of the acylation site relative to the membrane border is the decisive factor for attachment of stearate. J Biol Chem. 289, 34978-89.

Fiedler, Veit, Stamnes, Rothman (1996) Bimodal interaction of coatomer with p24. Science 273, 1396

Kümmel, Heinemann, Veit(2006) Unique self-palmitoylation activity of the transport protein particle Bet3: A mechanism required for protein stability. Proc. Natl. Acad. Sci. (USA) 103, 12701.

 

 





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