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Findings from University of Wisconsin advance knowledge in Epstein-Barr virus



November 20th, 2007

   2007 NOV 20 -- According to recent research published in the Journal of Virology, "Latent membrane protein 1 (LMP1) of Epstein Barr virus (EBV) is important for maintaining proliferation of EBV-infected B cells. LMP1, unlike its cellular counterpart, CD40, signals without a ligand and is largely internal to the plasma membrane."

   "In order to understand how LMP1 initiates its ligand-independent signaling, we focused on a leucine heptad in LMP1's first membrane-spanning domain that was shown to be necessary for LMP1's signaling through NF-kappa B. LZ1EBV, a recombinant EBV genetically altered to express LZ1, a derivative of LMP1 in which a leucine heptad was replaced with alanines, transformed B cells with 56% of wild-type (wt) EBV's efficiency, demonstrating the importance of this heptad. To elucidate the mechanism by which this domain contributes to the functions of LMP1, the properties of the wt and LZ1 were compared in transfected cells. LZ1 failed to home to lipid rafts as efficiently as did wt LMP1. The distribution of tagged derivatives of LZ1 also differed from that of wt LMP1 in transfected cells. LZ1's defect in homing to lipid rafts and altered trafficking likely underlie the defect in transformation of LZ1EBV. While the third and fourth membrane-spanning domains of LMP1 foster its trafficking to the Golgi, the leucine heptad within the first membrane-spanning domain contributes to its trafficking, particularly to internal rafts," wrote J. Lee and colleagues, University of Wisconsin.

   The researchers concluded: "B cells that are successfully transformed by LZ1EBV have the same average number of viral genomes and the same fraction of cells with capped LZ1 at the cell surface but express 50% more of the LZ1 allele than wt infected cells."

   Lee and colleagues published their study in the Journal of Virology (Membrane leucine heptad contributes to trafficking, signaling, and transformation by latent membrane protein 1. Journal of Virology, 2007;81(17):9121-9130).

   For additional information, contact B. Sugden, University of Wisconsin, School of Medicine & Public Health, McArdle Laboratory Cancer Research, 1400 University Avenue, Madison, WI 53706, USA.

   The publisher's contact information for the Journal of Virology is: American Society Microbiology, 1752 N St. NW, Washington, DC 20036-2904, USA.

   Keywords: United States, Madison, Chronic Fatigue Syndrome, EBV, Epstein-Barr Virus, Herpes, Herpesvirus, Virology, University of Wisconsin.

   This article was prepared by Virus Weekly editors from staff and other reports. Copyright 2007, Virus Weekly via NewsRx.com.

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