Journal article
Complex Formation Facilitates Endocytosis of the Varicella-Zoster Virus gE:gI Fc Receptor
Journal of virology, Vol.72(2), pp.1542-1551
02/1998
DOI: 10.1128/JVI.72.2.1542-1551.1998
PMCID: PMC124636
PMID: 9445058
Abstract
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 FcγRII. 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.
Details
- Title: Subtitle
- Complex Formation Facilitates Endocytosis of the Varicella-Zoster Virus gE:gI Fc Receptor
- Creators
- Julie K Olson - Department of Microbiology and Immunology Program, University of Iowa College of Medicine, Iowa City, Iowa 52242Charles Grose - Department of Microbiology and Immunology Program, University of Iowa College of Medicine, Iowa City, Iowa 52242
- Resource Type
- Journal article
- Publication Details
- Journal of virology, Vol.72(2), pp.1542-1551
- Publisher
- American Society for Microbiology
- DOI
- 10.1128/JVI.72.2.1542-1551.1998
- PMID
- 9445058
- PMCID
- PMC124636
- ISSN
- 0022-538X
- eISSN
- 1098-5514
- Language
- English
- Date published
- 02/1998
- Academic Unit
- Stead Family Department of Pediatrics; Infectious Disease (Pediatrics)
- Record Identifier
- 9984093314502771
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