Primary Faculty Mentor Name

Markus Thali

Status

Undergraduate

Student College

College of Agriculture and Life Sciences

Program/Major

Molecular Genetics

Primary Research Category

Biological Sciences

Secondary Research Category

Health Sciences

Presentation Title

Does the Cytoplasmic Tail of HIV-1 Envelope Glycoprotein Regulate Phosphorylation of Ezrin?

Time

3:00 PM

Location

Silver Maple Ballroom - Biological Sciences

Abstract

One mode of efficient Human Immunodeficiency Virus 1 (HIV-1) dissemination is the cell-to-cell transmission of viral particles between HIV-infected T cells (producers) and uninfected CD4+ T cells (targets) at transient junctions known as the virological synapse (VS). Formation of the VS is mediated by the interaction between the viral envelope glycoprotein (Env) expressed on the producer cell surface and the CD4 receptor on the target T cell. Establishment of the VS can sometimes result in membrane fusion of the two cells, forming a small multinucleated cell (syncytium). However, several host and viral factors have been identified to repress excessive cell-cell fusion, one of those being phosphorylated ezrin (p-ezrin). This F actin-binding host protein accumulates at the VS, yet the temporal regulation of ezrin phosphorylation in HIV-1 infected cells remains to be determined.

This document is currently not available here.

Share

COinS
 

Does the Cytoplasmic Tail of HIV-1 Envelope Glycoprotein Regulate Phosphorylation of Ezrin?

One mode of efficient Human Immunodeficiency Virus 1 (HIV-1) dissemination is the cell-to-cell transmission of viral particles between HIV-infected T cells (producers) and uninfected CD4+ T cells (targets) at transient junctions known as the virological synapse (VS). Formation of the VS is mediated by the interaction between the viral envelope glycoprotein (Env) expressed on the producer cell surface and the CD4 receptor on the target T cell. Establishment of the VS can sometimes result in membrane fusion of the two cells, forming a small multinucleated cell (syncytium). However, several host and viral factors have been identified to repress excessive cell-cell fusion, one of those being phosphorylated ezrin (p-ezrin). This F actin-binding host protein accumulates at the VS, yet the temporal regulation of ezrin phosphorylation in HIV-1 infected cells remains to be determined.