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 AWAuthor
Amy W. Hudson PhD Emeritus Professor in the Microbiology and Immunology department at Medical College of WisconsinMESH 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
