Poxviral B1 kinase overcomes barrier to autointegration factor, a host defense against virus replication. Cell Host Microbe 2007 May 17;1(3):187-97
Date
11/17/2007Pubmed ID
18005698Pubmed Central ID
PMC1978190DOI
10.1016/j.chom.2007.03.007Scopus ID
2-s2.0-34248205172 (requires institutional sign-in at Scopus site) 96 CitationsAbstract
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.
Author List
Wiebe MS, Traktman PAuthor
Paula Traktman Duncan PhD Emeritus Professor in the Microbiology and Immunology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsCell Line
DNA, Viral
DNA-Binding Proteins
Host-Pathogen Interactions
Humans
Nuclear Proteins
Phosphorylation
Vaccinia virus
Viral Proteins
Virus Replication
