Related Experiment Video
Updated: May 1, 2026
Use of In vivo Imaging to Monitor the Progression of Experimental Mouse Cytomegalovirus Infection in Neonates
Published on: July 6, 2013
Mouse cytomegalovirus lacking sgg1 shows reduced import into the salivary glands
Jiawei Ma1, Kimberley Bruce1, Philip G Stevenson1
1School of Chemistry and Molecular Biosciences, University of Queensland, Brisbane, Australia.
Abstract:
Cytomegaloviruses (CMVs) transmit via chronic shedding from the salivary glands. How this relates to the broad cell tropism they exhibit in vitro is unclear. Human CMV (HCMV) infection presents only after salivary gland infection is established. Murine CMV (MCMV) is therefore useful to analyse early infection events. It reaches the salivary glands via infected myeloid cells. Three adjacent spliced genes designated as m131/129 (MCK-2), sgg1 and sgg1.1, positional homologues of the HCMV UL128/130/131 tropism determinants, are implicated. We show that a sgg1 null mutant is defective in infected myeloid cell entry into the salivary glands, a phenotype distinct from MCMV lacking MCK-2. These data point to a complex, multi-step process of salivary gland colonization.
Insights
Murine cytomegalovirus (MCMV) uses specific genes like sgg1 for salivary gland entry via myeloid cells. This reveals a complex, multi-step colonization process crucial for understanding viral transmission.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Cytomegaloviruses (CMVs) establish chronic infections through salivary gland shedding.
- Understanding the relationship between viral cell tropism and salivary gland colonization is crucial.
- Human CMV (HCMV) infection is clinically apparent only after salivary gland infection.
Purpose of the Study:
- To investigate the early events of murine CMV (MCMV) infection in salivary glands.
- To elucidate the role of specific MCMV genes (m131/129, sgg1, sgg1.1) in salivary gland colonization.
- To differentiate the functions of MCMV tropism determinants from HCMV homologues.
Main Methods:
- Utilizing a murine CMV (MCMV) model to study salivary gland infection.
- Generating and analyzing a sgg1 null mutant MCMV.
- Comparing the salivary gland colonization phenotype of sgg1 and MCK-2 (m131/129) deficient MCMV.
Main Results:
- A sgg1 null mutant MCMV exhibited a defect in infected myeloid cell entry into the salivary glands.
- This phenotype differs from MCMV lacking MCK-2, indicating distinct roles.
- The findings suggest a multi-step mechanism for salivary gland colonization by MCMV.
Conclusions:
- The MCMV sgg1 gene plays a critical role in the initial stages of salivary gland colonization by facilitating myeloid cell entry.
- MCMV salivary gland colonization involves a complex, multi-step process with distinct genetic requirements.
- These findings provide insights into CMV transmission and pathogenesis, using MCMV as a model for HCMV.
