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The Trafficking of Viral Immune Evasion Protein m4/gp34 and MHC class I complexes is Facilitated by Another Viral Gene m168 in Murine Cytomegalovirus Infections
Author(s) -
Lu Xiuju,
Cho Kathy,
Hill Ann
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1067.14
Subject(s) - mhc class i , biology , gene , immune system , major histocompatibility complex , microbiology and biotechnology , cytomegalovirus , mhc class ii , virology , genetics , virus , herpesviridae , viral disease
The murine cytomegalovirus (MCMV) encodes immune evasion protein m4/gp34, which is unique among known viral genes that target MHC class I pathway of antigen presentation. It associates with MHC class I molecules at the cell surface, however, it inhibits antigen recognition without reducing cell surface class I levels. We have found that the maturation of m4/gp34 and associated MHC class I molecule Kb was impaired when m4 was expressed in a gutless adenovector Ad‐m4. The current study defined more clearly the necessity and sufficiency of MCMV environment in facilitating the export of m4‐Kb complexes and identified the MCMV gene that functions to affect the complexes transport: 1) The retention of m4/gp34‐Kb complexes in Ad‐m4 infection was not caused by differences of endogenous m4/gp34 over‐expression, nor by the differences of m4/gp34 synthetic rate between Ad‐m4 and MCMV infections; 2) Super‐infection of Ad‐m4 with m4‐deletant MCMV mutant recovers the maturation of m4‐Kb complexes, which convinced that the trafficking of m4/gp34‐Kb complexes was manipulated by MCMV; 3) MCMV gene m168 was identified facilitating the export of m4/gp34‐Kb complexes. Further study is focusing on the biological meaning of m168 in promoting m4/gp34‐Kb complexes export, and the molecular mechanisms of how m168 facilitates the export of m4/gp34‐Kb complexes.