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. doi: 10.1128/JVI.01782-09. Epub 2010 Jan 27.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Carrier Proteins / physiology*
  • Cell Line
  • Cells, Cultured
  • Down-Regulation*
  • Herpesvirus 7, Human / immunology*
  • Herpesvirus 7, Human / pathogenicity*
  • Histocompatibility Antigens Class I / biosynthesis*
  • Histocompatibility Antigens Class I / immunology*
  • Humans
  • Mice
  • Protein Binding
  • Protein Interaction Mapping
  • Viral Proteins / physiology*

Substances

  • Carrier Proteins
  • Histocompatibility Antigens Class I
  • U21 glycoprotein, human herpesvirus 7
  • Viral Proteins