A short intrinsically disordered domain of MCPyV ALTO regulates TBK1 signaling during MCPyV infection.

ABSTRACT: Merkel cell polyomavirus (MCPyV) is an oncogenic human polyomavirus that latently infects most adults. Although the causative link between MCPyV and Merkel cell carcinoma is well established, the molecular mechanisms that govern viral latency and prevent oncogenic progression remain poorly understood. We previously reported that the MCPyV early protein ALTO is a key modulator of the STING-TBK1 signaling axis, enabling the virus to co-opt innate immune pathways to suppress excessive viral replication and promote latency over transformation. In this study, we expand on this model by identifying a short, essential domain within ALTO that is required for TBK1 activation. This domain, which we term LIT (Lost in Tau), is necessary for ALTO-TBK1 interaction but dispensable for ALTO trafficking an

SUBMITTER: Senay TE 

PROVIDER: S-EPMC12724334 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature