ArticlePLoS pathogens2022
Merkel cell polyomavirus small T antigen is a viral transcription activator that is essential for viral genome maintenance.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Viruses and the host replisome: discovering oncogenic mechanisms of small DNA tumor viruses.Journal of virology · 2026Review
- In vitro evaluation of bidirectional transcription levels of five types of non-coding control regions of Merkel cell polyomavirus.Virology journal · 2025Article
- Pharmacologic reversion of Merkel cell carcinoma via CBP/p300 inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A short intrinsically disordered domain of MCPyV ALTO regulates TBK1 signaling during MCPyV infection.Journal of virology · 2025Article
- E2F1-3 activate Merkel cell polyomavirus early transcription and replication.bioRxiv : the preprint server for biology · 2025Article
- Merkel Cell Polyomavirus Co-Infection in HIV/AIDS Individuals: Clinical Diagnosis, Consequences and Treatments.Pathogens (Basel, Switzerland) · 2025Review
- Polyomavirus ALTOs, but not MTs, downregulate viral early gene expression by activating the NF-κB pathway.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Polyomavirus ALTOs, but not MTs, downregulate viral early gene expression by activating the NF-κB pathway.bioRxiv : the preprint server for biology · 2024Article
- Characterization of molecular mechanisms driving Merkel cell polyomavirus oncogene transcription and tumorigenic potential.PLoS pathogens · 2023Article
- Regulation of Virus Replication by BK Polyomavirus Small T Antigen.Journal of virology · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Merkel cell polyomavirus (MCV) is a small DNA tumor virus that persists in human skin and causes Merkel cell carcinoma (MCC) in immunocompromised individuals. The multi-functional protein MCV small T (sT) activates viral DNA replication by stabilizing large T (LT) and promotes cell transformation through the LT stabilization domain (LTSD). Using MCVΔsT, a mutant MCV clone that ablates sT, we investigated the role of sT in MCV genome maintenance. sT was dispensable for initiation of viral DNA replication, but essential for maintenance of the MCV genome and activation of viral early and late gene expression for progression of the viral lifecycle. Furthermore, in phenotype rescue studies, exogenous sT activated viral DNA replication and mRNA expression in MCVΔsT through the LTSD. While exogenous LT expression, which mimics LT stabilization, increased viral DNA replication, it did not activate viral mRNA expression. After cataloging transcriptional regulator proteins by proximity-based MCV sT-host protein interaction analysis, we validated LTSD-dependent sT interaction with four transcriptional regulators: Cux1, c-Jun, BRD9, and CBP. Functional studies revealed Cux1 and c-Jun as negative regulators, and CBP and BRD9 as positive regulators of MCV transcription. CBP inhibitor A-485 suppressed sT-induced viral gene activation in replicating MCVΔsT and inhibited early gene expression in MCV-integrated MCC cells. These results suggest that sT promotes viral lifecycle progression by activating mRNA expression and capsid protein production through interaction with the transcriptional regulators. This activity is essential for MCV genome maintenance, suggesting a critical role of sT in MCV persistence and MCC carcinogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.