NIH VideoCast - Reassessing Influenza Virus Antigenic Drift: A Central Role for Anibody Driven Evolution of Viral Receptor Binding Avidity

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Reassessing Influenza Virus Antigenic Drift: A Central Role for Anibody Driven Evolution of Viral Receptor Binding Avidity

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Air date:	Wednesday, December 9, 2009, 4:15:00 PM Time displayed is Eastern Time, Washington DC Local
Views:	Total views: 137 * This only includes stats from October 2011 and forward.
Category:	Immunology
Runtime:	00:53:08
Closed captioning:	Check box to display CC outside of the video Note: You can drag the captioning window around and resize it
Description:	Scott Hensley received his PhD from Penn in 2006. Working with Gundi Ertl, he explored interactions between innate and adaptive immune responses to adenovirus vaccine vectors. In the past three years as a post-doctoral fellow in the Laboratory of Viral Diseases, NIAID, Scott has made a number of valuable contributions to viral immunology, demonstrating that mouse norovirus (endemic in most experimental mouse colonies) has minimal effects on mouse T cell and antibody responses to influenza or vaccinia virus, and that immunoproteasomes play an important role in B cell activation. His focus has been to better understand how influenza A virus escapes host immunity. Antigenic drift is the principal factor for the failure to develop vaccines that provide long lasting effective immunity to influenza, and hence is responsible for the considerable morbidity and mortality caused by influenza, year in and year out. Revisiting a mouse model system developed in the 1950s (!), Scott discovered a key factor in antigenic drift: in response to a partially neutralizing antibody response, influenza escapes immune pressure by single amino acid substitutions in the hemagglutinin that increase viral avidity for host cell receptors. At the same time, these mutations decrease viral fitness in the absence of neutralizing antibodies, providing a dynamic force driving hemagglutinin evolution independently of antigenic alterations. The surprising location of these substitutions provides an explanation for a long standing puzzle in hemagglutinin evolution, and adds an important layer of complexity to understanding HA variation. These findings provide the first significant modification to the paradigm of antigenic drift in 30 years, and are broadly applicable to other viruses. Scott is a dynamic, engaging and entertaining speaker: his seminar provides an opportunity to contemplate and discuss long standing questions about antibody neutralization of viruses that have gained new importance with the drive to develop vaccines for viruses that have eluded standard empirical approaches. The Immunology Interest Group

NLM Title:	Reassessing influenza virus antigenic drift : a central role for anibody driven evolution of viral receptor binding avidity / Scott Hensley.
Author:	Hensley, Scott. National Institutes of Health (U.S.). Immunology Interest Group.
Publisher:
Abstract:	(CIT): Scott Hensley received his PhD from Penn in 2006. Working with Gundi Ertl, he explored interactions between innate and adaptive immune responses to adenovirus vaccine vectors. In the past three years as a post-doctoral fellow in the Laboratory of Viral Diseases, NIAID, Scott has made a number of valuable contributions to viral immunology, demonstrating that mouse norovirus (endemic in most experimental mouse colonies) has minimal effects on mouse T cell and antibody responses to influenza or vaccinia virus, and that immunoproteasomes play an important role in B cell activation. His focus has been to better understand how influenza A virus escapes host immunity. Antigenic drift is the principal factor for the failure to develop vaccines that provide long lasting effective immunity to influenza, and hence is responsible for the considerable morbidity and mortality caused by influenza, year in and year out. Revisiting a mouse model system developed in the 1950s (!), Scott discovered a key factor in antigenic drift: in response to a partially neutralizing antibody response, influenza escapes immune pressure by single amino acid substitutions in the hemagglutinin that increase viral avidity for host cell receptors. At the same time, these mutations decrease viral fitness in the absence of neutralizing antibodies, providing a dynamic force driving hemagglutinin evolution independently of antigenic alterations. The surprising location of these substitutions provides an explanation for a long standing puzzle in hemagglutinin evolution, and adds an important layer of complexity to understanding HA variation. These findings provide the first significant modification to the paradigm of antigenic drift in 30 years, and are broadly applicable to other viruses. Scott is a dynamic, engaging and entertaining speaker: his seminar provides an opportunity to contemplate and discuss long standing questions about antibody neutralization of viruses that have gained new importance with the drive to develop vaccines for viruses that have eluded standard empirical approaches. The Immunology Interest Group.
Subjects:	Genetic Drift Influenza, Human--immunology Orthomyxoviridae--immunology Receptors, Virus--immunology
Publication Types:	Lecture Webcast
NLM Classification:	QW 168.5.O7
NLM ID:	101522188
CIT Live ID:	8327
Permanent link:	https://videocast.nih.gov/watch=8327

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