Ndjamen, B. and Fraser, S. E. and Bjorkman, P. J. (2014) Distinct Intracellular Trafficking Patterns of Host IgG by Herpes Virus Fc-Receptors. In: 2014 ASCB: an International Forum for Cell Biology, December, 2014, Philadelphia, PA. https://resolver.caltech.edu/CaltechAUTHORS:20150504-125103596
![]() |
PDF
- Published Version
See Usage Policy. 63kB |
Use this Persistent URL to link to this item: https://resolver.caltech.edu/CaltechAUTHORS:20150504-125103596
Abstract
Members of both alpha and beta herpes viruses affects 50–98% of people around the world. They cause severe symptoms in congenitally infected newborns, a lifelong latent infection that is lethal in immunocompromised individuals, and are associated with several types of cancer. Human cytomegalovirus (HCMV) and herpes simplex virus type 1 (HSV-1) viruses express proteins (HCMV gp68 and gp34; HSV-1 gE-gI) that function as Fc receptors (FcRs) by binding to the Fc regions of human IgG. In addition to binding free IgG, these viral FcRs can bind to IgG complexed with an antigen to form an antibody bipolar bridged (ABB) complex. Although HCMV gp68 and HSV-1 gE-gI have an overlapping binding site on Fc, the finding that the gp68/Fc interaction is stable at pH values between 5.6 and 8.1 but that gE-gI binds only at neutral or basic pH suggests distinct pH-based downstream events after IgG is internalized via receptor-mediated endocytosis into intracellular compartments. Here we developed a cell-based in vitro model system to define the fates of ABB complexes formed by the two types of viral FcRs. We found that alpha (HSV-1) and beta (HCMV) herpes virus FcRs displayed distinct intracellular trafficking patterns to target internalized ligands: HSV-1 gE-gI dissociates from its IgG-antigen ligand in acidic endosomal compartments and recycles back to the cell surface, whereas HCMV FcRs (gp68) are transported together with IgG-antigen complexes to lysosomes for degradation. In both cases, anti-viral IgGs and their viral targets are selectively degraded, a potential immune evasion strategy allowing herpes viruses to escape from IgG-mediated immune responses.
Item Type: | Conference or Workshop Item (Poster) | ||||||
---|---|---|---|---|---|---|---|
Related URLs: |
| ||||||
ORCID: |
| ||||||
Additional Information: | © American Society for Cell Biology. POSTER PRESENTATIONS- Sunday, December 7. | ||||||
Record Number: | CaltechAUTHORS:20150504-125103596 | ||||||
Persistent URL: | https://resolver.caltech.edu/CaltechAUTHORS:20150504-125103596 | ||||||
Usage Policy: | No commercial reproduction, distribution, display or performance rights in this work are provided. | ||||||
ID Code: | 57200 | ||||||
Collection: | CaltechAUTHORS | ||||||
Deposited By: | Ruth Sustaita | ||||||
Deposited On: | 06 May 2015 17:55 | ||||||
Last Modified: | 03 Oct 2019 08:22 |
Repository Staff Only: item control page