Poxviral B1 kinase overcomes barrier to autointegration factor, a host defense against virus replication

Barrier to autointegration factor (BAF) is a DNA-binding protein found in the nucleus and cytoplasm of eukaryotic cells that functions to establish nuclear architecture during mitosis. Herein, we demonstrate a cytoplasmic role for BAF in host defense during poxviral infections. Vaccinia is the proto...

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Bibliographic Details
Published in:Cell host & microbe 2007-05, Vol.1 (3), p.187-197
Main Authors: Wiebe, Matthew S, Traktman, Paula
Format: Article
Language:English
Subjects:
Animals
Cell Line
Cercopithecus aethiops
DNA, Viral - biosynthesis
DNA-Binding Proteins - antagonists & inhibitors
DNA-Binding Proteins - immunology
DNA-Binding Proteins - metabolism
Host-Pathogen Interactions - immunology
Humans
Nuclear Proteins - antagonists & inhibitors
Nuclear Proteins - immunology
Nuclear Proteins - metabolism
Phosphorylation
Vaccinia virus - enzymology
Vaccinia virus - immunology
Viral Proteins - genetics
Viral Proteins - metabolism
Virus Replication - immunology
Virus Replication - physiology
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Summary:Barrier to autointegration factor (BAF) is a DNA-binding protein found in the nucleus and cytoplasm of eukaryotic cells that functions to establish nuclear architecture during mitosis. Herein, we demonstrate a cytoplasmic role for BAF in host defense during poxviral infections. Vaccinia is the prototypic poxvirus, a family of DNA viruses that replicate exclusively in the cytoplasm of infected cells. Mutations in the vaccinia B1 kinase (B1) compromise viral DNA replication, but the mechanism by which B1 achieves this has remained elusive. We now show that BAF acts as a potent inhibitor of poxvirus replication unless its DNA-binding activity is blocked by B1-mediated phosphorylation. These data position BAF as the effector of an innate immune response that prevents replication of exogenous viral DNA in the cytoplasm. To enable the virus to evade this defense, the poxviral B1 has evolved to usurp a signaling pathway employed by the host cell.
ISSN:1931-3128
1934-6069
DOI:10.1016/j.chom.2007.03.007