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Dissection of Adult Mouse Utricle and Adenovirus-mediated Supporting-cell Infection
Published on: March 28, 2012
Mouse adenovirus type 1 infection of macrophages
Shanna L Ashley1, Amanda R Welton, Kirsten M Harwood
1Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109, USA.
Abstract:
Mouse adenovirus type 1 (MAV-1) causes acute and persistent infections in mice, with high levels of virus found in the brain, spinal cord and spleen in acute infections. MAV-1 infects endothelial cells throughout the mouse, and monocytes/macrophages have also been implicated as targets of the virus. Here we determined the extent and functional importance of macrophage infection by MAV-1. Bone marrow-derived macrophages expressed MAV-1 mRNAs and proteins upon ex vivo infection. Adherent peritoneal macrophages from infected mice expressed viral mRNAs and produced infectious virus. Infected chemokine (C-C motif) receptor 2 (CCR2) knockout mice, which are defective for macrophage recruitment, did not show differences in survival or MAV-1 load compared to controls. In contrast, macrophage depletion using clodronate-loaded liposomes resulted in increased virus replication in spleens of a MAV-1-resistant mouse strain, BALB/cJ. Thus macrophages serve both as targets of infection and as effectors of the host response.
Insights
Mouse adenovirus type 1 (MAV-1) infects macrophages, which are crucial immune cells. Macrophage depletion increased viral replication, indicating their role in controlling MAV-1 infections.
Area of Science:
- Virology
- Immunology
- Infectious Diseases
Background:
- Mouse adenovirus type 1 (MAV-1) causes severe infections in mice, affecting the brain, spinal cord, and spleen.
- MAV-1 targets endothelial cells and is suspected to infect monocytes/macrophages.
Purpose of the Study:
- To investigate the extent and functional significance of macrophage infection by MAV-1.
- To elucidate the role of macrophages in MAV-1 pathogenesis and host response.
Main Methods:
- Ex vivo infection of bone marrow-derived macrophages with MAV-1.
- Analysis of viral mRNA and protein expression in macrophages.
- Assessment of MAV-1 infection and survival in chemokine (C-C motif) receptor 2 (CCR2) knockout mice.
- Macrophage depletion using clodronate-loaded liposomes in MAV-1-resistant mice.
Main Results:
- Bone marrow-derived macrophages expressed MAV-1 mRNA and proteins upon ex vivo infection.
- Macrophages from infected mice produced infectious MAV-1.
- CCR2 knockout mice showed no difference in survival or viral load, suggesting macrophage recruitment is not critical.
- Macrophage depletion led to increased MAV-1 replication in the spleen of BALB/cJ mice.
Conclusions:
- Macrophages are confirmed targets of MAV-1 infection.
- Macrophages play a critical role in controlling MAV-1 replication and host defense, particularly in resistant mouse strains.
