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J Virol, February 1998, p. 1542-1551, Vol. 72, No. 2
Department of Microbiology and Immunology
Program, University of Iowa College of Medicine, Iowa City, Iowa 52242
Open reading frames within the unique short segment of
alphaherpesvirus genomes participate in egress and cell-to-cell spread. The case of varicella-zoster virus (VZV) is of particular interest not
only because the virus is highly cell associated but also because its
most prominent cell surface protein, gE, bears semblance to the
mammalian Fc receptor Fc
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Complex Formation Facilitates Endocytosis of the
Varicella-Zoster Virus gE:gI Fc Receptor
RII. A previous study demonstrated that when
expressed alone in cells, VZV gE was endocytosed from the cell surface
through a tyrosine localization motif in its cytoplasmic tail (J. K. Olson and C. Grose, J. Virol. 71:4042-4054, 1997).
Since VZV gE is normally found in association with gI in the infected
cell, the present study was directed at defining the trafficking of the
VZV gE:gI protein complex. First, VZV gI underwent endocytosis and
recycling when it was expressed alone in cells, and interestingly, VZV
gI contained a methionine-leucine internalization motif in its
cytoplasmic tail. Second, VZV gI was found by confocal microscopy to
colocalize with VZV gE during endocytosis and recycling in cells.
Third, by a quantitative internalization assay, VZV gE:gI was shown to
undergo endocytosis more efficiently (steady state, 55 to 60%) than
either gE alone (steady state, ~32%) or gI alone (steady state,
~45%). Further, examination of endocytosis-deficient mutant proteins
demonstrated that VZV gI exerted a more pronounced effect than gE on
internalization of the complex. Most importantly, therefore, these
studies suggest that VZV gI behaves as an accessory component by
facilitating the endocytosis of the major constituent gE and thereby
modulating the trafficking of the entire cell surface gE:gI Fc receptor
complex.
*
Corresponding author. Mailing address: University
Hospital, 2501JCP, 200 Hawkins Dr., Iowa City, IA 52242. Fax: (319)
356-4855. E-mail: grose{at}blue.weeg.uiowa.edu.
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