Human herpesvirus 7 u21 downregulates classical and nonclassical class I major histocompatibility complex molecules from the cell surface. J Virol 2010 Apr;84(8):3738-51
Date
01/29/2010Pubmed ID
20106916Pubmed Central ID
PMC2849505DOI
10.1128/JVI.01782-09Scopus ID
2-s2.0-77950482035 (requires institutional sign-in at Scopus site) 23 CitationsAbstract
Herpesviruses have evolved numerous strategies to evade detection by the immune system. Notably, most of the herpesviruses interfere with viral antigen presentation to cytotoxic T lymphocytes (CTLs) by removing class I major histocompatibility complex (MHC) molecules from the infected cell surface. Clearly, since the herpesviruses have evolved an extensive array of mechanisms to remove class I MHC molecules from the cell surface, this strategy serves them well. However, class I MHC molecules often serve as inhibitory ligands for NK cells, so viral downregulation of all class I MHC molecules should leave the infected cell open to NK cell attack. Some viruses solve this problem by selectively downregulating certain class I MHC products, leaving other class I products at the cell surface to serve as inhibitory NK cell ligands. Here, we show that human herpesvirus 7 (HHV-7) U21 binds to and downregulates all of the human class I MHC gene products, as well as the murine class I molecule H-2K(b). HHV-7-infected cells must therefore possess other means of escaping NK cell detection.
Author List
May NA, Glosson NL, Hudson AWMESH terms used to index this publication - Major topics in bold
AnimalsCarrier Proteins
Cell Line
Cells, Cultured
Down-Regulation
Herpesvirus 7, Human
Histocompatibility Antigens Class I
Humans
Mice
Protein Binding
Protein Interaction Mapping
Viral Proteins
