Polyomavirus and related diseases

This study analyzes BKPyV sequence variations in Vp1 and LTag using computational methods, finding high variability in Vp1 that may impact immune control and vaccine design, while LTag shows less variability but potential effects on T-cell epitopes.

This paper identifies MCPyV ST as the dominant transforming protein of Merkel Cell Polyomavirus and shows it localizes to the nucleus without a canonical nuclear localization signal.

This study shows JCPyV infects astrocytes, dysregulates cell biology, and affects excreted vesicles, providing insights into PML pathogenesis.

The paper identifies MCV oncoproteins' regulation of miR183 cluster and piR62011 in MCC, and screens for therapeutic molecules targeting miR182.

This study identifies two MCPyV integration patterns in MCC and links them to NHEJ and MMBIR mechanisms, showing integration preference for open chromatin and viral promoter-driven oncogene expression.

The paper presents a bioinformatics method to detect Merkel cell polyomavirus insertions in whole exome sequencing data of Merkel cell carcinoma samples, achieving 100% sensitivity and 62.5% specificity.

This paper develops a CRISPR-based diagnostic tool to detect Merkel cell polyomavirus in Merkel cell carcinomas with high sensitivity and specificity.

The paper develops an agent-based computational model of BKPyV replication and assembly in salivary gland cells, revealing that slow replication may result from capsid subunit accumulation rates and salivary gland-specific transcription factors.