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Receptor-binding and oncogenic properties of polyoma viruses isolated from feral mice
John Carroll1, Dilip Dey, Lori Kreisman
1Department of Pathology, Harvard Medical School, Boston, Massachusetts, United States of America.
Wild mouse polyoma virus isolates share a common Vp1 type, identical to highly tumorigenic lab strains. This Vp1 type conserves oncogenic potential by maintaining specific receptor-binding properties, highlighting the need for neonatal immune protection.
Area of Science:
- Virology
- Oncology
- Molecular Biology
Background:
- Mouse polyoma virus (MPyV) laboratory strains exhibit varied pathogenicity linked to the Vp1 protein's sialic acid binding pocket.
- Substitutions in Vp1 define prototype strains with distinct replication, tumor induction, and dissemination capabilities.
Purpose of the Study:
- To characterize the Vp1 type of novel MPyV isolates from naturally infected mice.
- To compare the receptor-binding properties and oncogenic potential of wild-type MPyV with laboratory strains.
Main Methods:
- Analysis of Vp1 coding and regulatory sequences from 15 wild-type MPyV isolates.
- Tumorigenicity assays in newborn laboratory mice following inoculation with wild-type MPyV isolates.
Main Results:
- All 15 wild-type MPyV isolates possessed a Vp1 type identical to highly tumorigenic laboratory strains.
- These isolates induced a wide range of tumors in mice, including epithelial and mesenchymal types.
- Wild-type isolates exhibited variations in regulatory sequences despite conserved Vp1 sequences, influencing receptor binding and viral spread.
Conclusions:
- The conserved Vp1 type in wild-type MPyV maintains oncogenic potential through specific sialic acid receptor interactions, avoiding lethal acute infections.
- Natural selection preserves these receptor-binding properties, underscoring the significance of neonatal immunity against natural MPyV transmission.
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