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Use of In vivo Imaging to Monitor the Progression of Experimental Mouse Cytomegalovirus Infection in Neonates
05:53

Use of In vivo Imaging to Monitor the Progression of Experimental Mouse Cytomegalovirus Infection in Neonates

Published on: July 6, 2013

A mouse cytomegalovirus glycoprotein retains MHC class I complexes in the ERGIC/cis-Golgi compartments

H Ziegler1, R Thale, P Lucin

  • 1Max von Pettenkofer Institut, Ludwig-Maximilians-Universitat, Munchen, Federal Republic of Germany.

Immunity
|January 1, 1997
PubMed

Insights

Mouse cytomegalovirus uses the m152 gene to block antigen presentation. This novel mechanism arrests the export of mouse MHC class I complexes, evading cytotoxic T cell detection.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Mouse cytomegalovirus (MCMV) employs immune evasion strategies to ensure viral replication.
  • MHC class I pathway presentation is crucial for adaptive immune responses, involving antigen processing and cell surface expression.
  • Understanding viral interference with antigen presentation is key to developing antiviral therapies.

Purpose of the Study:

  • To investigate the mechanism by which MCMV inhibits antigen presentation via the MHC class I pathway.
  • To identify the specific viral gene responsible for this immune evasion.
  • To characterize the function of the identified viral protein and its impact on host cell processes.

Main Methods:

  • Gene expression analysis of MCMV genes in infected murine and human cells.
  • Protein characterization of the identified viral glycoprotein (gp40).
  • Cellular localization studies and analysis of MHC class I complex transport using immunofluorescence and biochemical assays.
  • Cytotoxic T cell lysis assays to assess immune recognition.

Main Results:

  • The MCMV gene m152 was identified as responsible for blocking antigen presentation.
  • Expression of m152, encoding a 40 kDa glycoprotein (gp40), arrested the export of mouse MHC class I complexes from the ER-Golgi intermediate compartment.
  • This arrest inhibited lysis by cytotoxic T cells, while human MHC class I transport remained unaffected.
  • Deletion of the cytoplasmic tail of gp40 did not alter its effect on MHC class I export.

Conclusions:

  • MCMV utilizes the m152 gene product, gp40, to block antigen presentation through a novel mechanism.
  • This mechanism involves arresting MHC class I complex export from the ER-Golgi intermediate compartment, distinct from known viral immune evasion strategies.
  • The findings reveal a new herpesvirus strategy for shutting off MHC class I function, offering insights into viral pathogenesis and immune evasion.

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