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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Galectin-3 plays a role in minute virus of mice infection
Pierre O Garcin1, Ivan R Nabi2, Nelly Panté1
1Department of Zoology, University of British Columbia, Vancouver, BC, Canada.
Abstract:
Galectin-3 has previously been found to be required by the parvovirus minute virus of mice prototype strain (MVMp) for infection of mouse fibroblast cells. Since MVMp is an oncotropic virus, and galectin-3 is a multifunctional protein implicated in cancer metastasis, we hypothesized that galectin-3 and Mgat5, the Golgi enzyme that synthesizes high-affinity glycan ligands of galectin-3, might play a role in MVMp infection. Using siRNA-mediated knockdown of galectin-3 in mouse cells transformed with polyomavirus middle T antigen and Mgat5(-/-) mouse mammary tumor cells, we found that galectin-3 and Mgat5 are both necessary for efficient MVMp cell entry and infection, but not for cell binding. Moreover, we found that human cancer cells expressing higher levels of galectin-3 were more efficiently infected with MVMp than cell lines expressing lower galectin-3 levels. We conclude that galectin-3 and Mgat5 are involved in MVMp infection, and propose that galectin-3 is a determinant of MVMp oncotropism.
Insights
Minute virus of mice (MVMp) infection requires galectin-3 and Mgat5 for efficient cell entry. Higher galectin-3 levels in human cancer cells correlate with increased MVMp infection, suggesting galectin-3 determines MVMp oncotropism.
Area of Science:
- Virology
- Glycobiology
- Cancer Biology
Background:
- Galectin-3 is essential for minute virus of mice prototype strain (MVMp) infection in mouse cells.
- MVMp exhibits oncotropism, targeting cancer cells.
- Galectin-3 is a multifunctional protein associated with cancer metastasis.
Purpose of the Study:
- To investigate the roles of galectin-3 and Mgat5 in MVMp infection.
- To determine if galectin-3 and Mgat5 influence MVMp cell entry and oncotropism.
Main Methods:
- siRNA-mediated knockdown of galectin-3 in polyomavirus middle T antigen-transformed mouse cells.
- Utilizing Mgat5(-/-) mouse mammary tumor cells.
- Assessing MVMp infection efficiency in cells with varying galectin-3 and Mgat5 levels.
- Comparing MVMp infection in human cancer cell lines with different galectin-3 expression levels.
Main Results:
- Both galectin-3 and Mgat5 are essential for efficient MVMp cell entry and infection.
- Galectin-3 and Mgat5 do not affect MVMp cell binding.
- Human cancer cells with higher galectin-3 expression show more efficient MVMp infection.
Conclusions:
- Galectin-3 and Mgat5 play critical roles in MVMp infection.
- Galectin-3 is a key determinant of MVMp oncotropism.
- These findings link viral tropism to host cell glycosylation and protein interactions.

