Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling.

ABSTRACT: Merkel cell polyomavirus (MCPyV) is the causative agent of the majority of Merkel cell carcinomas (MCC). The virus has limited coding capacity, with its early viral proteins, large T (LT) and small T (sT), being multifunctional and contributing to infection and transformation. A fundamental difference in early viral gene expression between infection and MCPyV-driven tumorigenesis is the expression of a truncated LT (LTtr) in the tumor. In contrast, sT is expressed in both conditions and contributes significantly to oncogenesis. Here, we identified novel functions of early viral proteins by performing genome-wide transcriptome and chromatin studies in primary human fibroblasts. Due to current limitations in infection and tumorigenesis models, we mimic these conditions by ectopically express

SUBMITTER: Ohnezeit D 

PROVIDER: S-EPMC11333005 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature