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Use of In vivo Imaging to Monitor the Progression of Experimental Mouse Cytomegalovirus Infection in Neonates
Published on: July 6, 2013
Stalemating a clever opportunist: lessons from murine cytomegalovirus
Matthias J Reddehase1, Christian O Simon, Jürgen Podlech
1Institute for Virology, Johannes Gutenberg-University, Mainz, Germany. Matthias.Reddehase@uni-mainz.de
Abstract:
Cytomegaloviruses and their specific hosts have come to an arrangement that avoids disease but allows the viruses to persist in the individual host and to spread in the host species. Recent work has uncovered some of the molecular details of this evolutionary "contract for mutual survival." Cytomegaloviruses encode proteins, referred to as "immunoevasins," which are specifically committed to subvert the immune defense of the host for evading virus elimination. In reply, the hosts have evolved countermeasures to overcome the viral immunoevasins and present antigenic peptides to an extent that is sufficient for confining virus replication to below a harmful level. Accordingly, cytomegalic inclusion disease is a disease only of the immunocompromised. Although the details of the contract differ between the various cytomegalovirus host pairs, the general principles are strikingly analogous. Paradigmatic findings were made in the murine model, which adds the advantage of providing proof of principle by in vivo studies. With the focus on CD8 T cells and the major histocompatibility complex class I pathway of antigen presentation, we will discuss our view on the immune surveillance of cytomegalovirus in the murine model.
Insights
Cytomegaloviruses and hosts have an evolutionary pact for survival. Viruses use immunoevasins to evade immunity, while hosts develop countermeasures to control viral replication, preventing disease except in the immunocompromised.
Area of Science:
- Virology
- Immunology
- Evolutionary Biology
Background:
- Cytomegaloviruses (CMVs) establish persistent infections without causing disease in their specific hosts.
- This host-virus relationship involves a complex interplay of viral immune evasion and host immune response.
- Viral "immunoevasins" subvert host defenses, while host countermeasures limit viral replication.
Purpose of the Study:
- To elucidate the molecular mechanisms of the evolutionary "contract for mutual survival" between cytomegaloviruses and their hosts.
- To understand the host immune surveillance strategies against cytomegalovirus, focusing on CD8 T cells and MHC class I antigen presentation.
- To highlight the analogous principles governing this interaction across different CMV-host pairs.
Main Methods:
- Review of recent molecular and immunological studies on cytomegalovirus-host interactions.
- Focus on findings from the murine model, including in vivo studies.
- Analysis of the role of CD8 T cells and the major histocompatibility complex class I (MHC-I) pathway.
Main Results:
- Cytomegaloviruses encode immunoevasins to counteract host immune defenses.
- Host immune systems have evolved countermeasures to overcome viral immunoevasins.
- Effective host immune surveillance, particularly via CD8 T cells and MHC-I, confines CMV replication to non-pathogenic levels in immunocompetent individuals.
Conclusions:
- The CMV-host interaction represents a finely tuned evolutionary balance, a "contract for mutual survival."
- Understanding these molecular details is crucial for comprehending viral persistence and host immune control.
- The murine model provides a powerful system for studying these complex immune surveillance mechanisms in vivo.
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