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Published on: July 6, 2013
CD13/aminopeptidase N and murine cytomegalovirus infection
1Department of Microbiology and Immunology, Medical University of South Carolina, BSB-201, PO Box 250504, 173 Ashley Avenue, Charleston, SC 29425, USA. kasmanl@musc.edu
Abstract:
CD13/aminopeptidase N is a membrane-bound metalloproteinase implicated in human cytomegalovirus (HCMV) infection and pathogenesis. Anti-CD13 antibodies can neutralize HCMV infectivity, and HCMV viremia after bone marrow transplantation induces anti-CD13 autoantibodies which correlate with development of chronic graft vs. host disease. We examined whether murine CD13/APN was similarly implicated in murine cytomegalovirus (MCMV) disease. MCMV infection did induce anti-CD13 antibodies in mice in a strain-specific manner. ICR and 129S mice developed high titers of anti-CD13 antibodies and anti-MCMV antibodies after MCMV infection, whereas CBA and CBAxC57BL/6 f1 hybrid mice produced antibodies against MCMV only. Unlike HCMV, no evidence was found for a correlation between host cell CD13/APN expression and infection, or for the presence of CD13/APN on MCMV particles, although APN inhibitors decreased MCMV plaque formation. Reproduction of CD13/APN autoantibody production in the murine system should make it possible to determine if these antibodies contribute to CMV pathogenesis.
Insights
Murine cytomegalovirus (MCMV) infection induces CD13/aminopeptidase N antibodies in a strain-specific manner. This study explores the role of CD13/APN in MCMV disease, similar to its role in human cytomegalovirus (HCMV).
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- CD13/aminopeptidase N (APN) is a metalloproteinase linked to human cytomegalovirus (HCMV) infection.
- Anti-CD13 antibodies can neutralize HCMV, and HCMV viremia can induce autoantibodies correlated with chronic graft-versus-host disease.
Purpose of the Study:
- To investigate if murine CD13/APN plays a similar role in murine cytomegalovirus (MCMV) disease.
- To determine the strain-specific antibody response to CD13/APN during MCMV infection.
Main Methods:
- MCMV infection in different mouse strains (ICR, 129S, CBA, CBAxC57BL/6 f1).
- Measurement of anti-CD13 and anti-MCMV antibody titers.
- Assessment of CD13/APN expression and its presence on MCMV particles.
- Evaluation of APN inhibitor effects on MCMV plaque formation.
Main Results:
- MCMV infection induced anti-CD13 antibodies in an ICR and 129S strain-specific manner.
- CBA and CBAxC57BL/6 f1 mice produced only anti-MCMV antibodies.
- No correlation found between host cell CD13/APN expression and MCMV infection.
- APN inhibitors reduced MCMV plaque formation, but CD13/APN was not found on MCMV particles.
Conclusions:
- Murine CD13/APN autoantibody production can be reproduced in a murine model.
- This model will help determine the contribution of CD13/APN autoantibodies to cytomegalovirus pathogenesis.
