A cytosolic herpes simplex virus protein inhibits antigen presentation to CD8+ T lymphocytes

IA York, C Roop, DW Andrews, SR Riddell, FL Graham… - Cell, 1994 - cell.com
IA York, C Roop, DW Andrews, SR Riddell, FL Graham, DC Johnson
Cell, 1994cell.com
Herpes simplex virus (HSV) infection of human fibroblasts rapidly renders the cells resistant
to lysis by HSV-specific CDS+ cytotoxic T lymphocytes (CTLs), which normally recognize cell
surface major histocompatibillty complex (MHC) class I proteins presenting viral peptides.
Within 3 hr of infection with HSV, MHC class I protein complexes are retained in the
endoplasmic reticulum (ER)/cis Golgi and show properties of complexes lacking antigenic
peptide. The HSV immediate-early protein ICP47 is both necessary and sufficlent to block …
Summary
Herpes simplex virus (HSV) infection of human fibroblasts rapidly renders the cells resistant to lysis by HSV-specific CDS+ cytotoxic T lymphocytes (CTLs), which normally recognize cell surface major histocompatibillty complex (MHC) class I proteins presenting viral peptides. Within 3 hr of infection with HSV, MHC class I protein complexes are retained in the endoplasmic reticulum (ER)/cis Golgi and show properties of complexes lacking antigenic peptide. The HSV immediate-early protein ICP47 is both necessary and sufficlent to block transport of class I proteinsand to inhibit lysis by CD8+ CTLs. The target for ICP47 is not known, but since ICP47 does not associate with membranes, it appears that ICP47 inhibits the production or stabilization of antigenic peptides or their translocation into the ER/cis Golgi. Thus, by expressing ICP47, HSV can evade detection by CD8+ T lymphocytes, perhaps explaining the predominance of CD4+ rather than CD8+ HSV-specific CTLs in vivo.
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