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Persistence of BK virus in human foetal pancreas cells
Abstract:
High multiplicity BK virus (BKV) infection of primary cells derived from human foetal pancreas resulted in massive cytopathology and subsequent outgrowth of cells. Intranuclear BKV T-antigen was present in all cells and viral antigen was detected in 10 to 30% of these cells. The subcultured cells yielded BKV in the supernatant (approx. 10(5) TCID50/ml) and in the cells free viral DNA was present (approx. 10% of total cellular DNA content). Analysis of the viral DNA indicated the presence of deleted and rearranged BKV DNA molecules. Although all cells continuously expressed BKV T-antigen they did not exhibit the transformed phenotype. This persistent infection of human foetal pancreas cells represents a novel type of in vitro interaction between BKV and human cells which may correspond to the in vivo findings on BKV tropism for pancreatic cells.
Insights
High multiplicity BK virus (BKV) infection of human fetal pancreatic cells caused cell damage and outgrowth. Persistent BKV infection was observed without cell transformation, suggesting a novel interaction relevant to BKV tropism.
Area of Science:
- Virology
- Cell Biology
- Human Pathology
Background:
- BK virus (BKV) is a human polyomavirus.
- BKV infection is common but typically asymptomatic in healthy individuals.
- Pancreatic cells are a potential target for BKV in vivo.
Purpose of the Study:
- To investigate the in vitro interaction between BK virus and primary human fetal pancreatic cells.
- To characterize the effects of high multiplicity BKV infection on these cells.
- To determine if BKV infection leads to cellular transformation in this model.
Main Methods:
- Infection of primary human fetal pancreatic cells with high multiplicity BK virus.
- Monitoring for cytopathology and cell outgrowth.
- Detection of BKV T-antigen and viral antigen expression.
- Quantification of BKV in cell supernatant and free viral DNA within cells.
- Analysis of BKV DNA for deletions and rearrangements.
Main Results:
- High multiplicity BKV infection induced massive cytopathology and subsequent cell outgrowth.
- Intranuclear BKV T-antigen was detected in all cells; viral antigen in 10-30%.
- Subcultured cells released BKV and contained significant free viral DNA with deleted/rearranged BKV DNA molecules.
- Cells continuously expressed BKV T-antigen but did not exhibit a transformed phenotype.
Conclusions:
- Persistent BKV infection of human fetal pancreatic cells occurs in vitro.
- This interaction involves deleted/rearranged viral DNA and T-antigen expression without transformation.
- The findings represent a novel in vitro model of BKV-human cell interaction, potentially explaining BKV tropism for pancreatic cells.