Chromatin mimicry by human JC virus.
Biorxiv : the Preprint Server for Biology
|January 13, 2025
Summary
Chronically infecting viruses like JC polyomavirus manipulate nuclear structure. The virus uses Agnoprotein to alter heterochromatin, reducing nuclear stiffness and creating space for replication.
Area of Science:
- Virology
- Cell Biology
- Biophysics
Background:
- Chronically persistent viruses reside within host cells, often in the nucleus.
- Nuclear viruses must overcome physical constraints like chromatin to replicate.
- JC polyomavirus (JCV) is a widespread, potentially lethal human virus.
Purpose of the Study:
- To investigate how nuclear viruses manage spatial limitations within the host cell nucleus.
- To explore the mechanism by which JCV overcomes nuclear architecture constraints.
- To understand the role of JCV's Agnoprotein in viral replication and nuclear organization.
Main Methods:
- Investigated JC polyomavirus infection in human cells.
- Analyzed the role of viral protein Agnoprotein (Agno) in nuclear heterochromatin.
- Assessed changes in nuclear stiffness and chromatin organization using biophysical methods.
- Compared replication of wild-type and mimic-mutant JCV.
Main Results:
- JCV interferes with nuclear heterochromatin, creating virus-occupied space.
- JCV's Agnoprotein mediates heterochromatin disruption via epigenetic mimicry.
- Viral epigenetic mimicry leads to chromatin reorganization and decreased nuclear stiffness.
- Mutations in Agno's epigenetic mimics reduce JCV replication.
Conclusions:
- JCV actively remodels nuclear architecture to facilitate its lifecycle.
- Epigenetic mimicry by JCV's Agno is crucial for viral replication.
- Modulation of nuclear mechanical properties is a potential strategy for nuclear virus chronicity.
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