Abstract

DNA viruses can hijack and manipulate the host chromatin state to facilitate their infection. Multiple lines of evidences reveal that DNA virus infection results in the host chromatin relocation, yet there is little known about the effects of viral infection on the architecture of host chromatin. Here, a combination of epigenomic, transcriptomic and biochemical assays were conducted to investigate the temporal dynamics of chromatin accessibility in response to Bombyx mori nucleopolyhedrovirus (BmNPV) infection. The high-quality ATAC-seq data indicated that progressive chromatin remodeling took place following BmNPV infection. Viral infection resulted in a more open chromatin architecture, along with the marginalization of host genome and nucleosome disassembly. Moreover, our results revealed that chromatin accessibility in uninfected cells was regulated by euchromatic modifications, whereas the viral-induced highly accessible chromatin regions were originally associated with facultative heterochromatic modification. Overall, our findings illustrate for the first time the organization and accessibility of host chromatin in BmNPV-infected cells, which lay the foundation for future studies on epigenomic regulation mediated by DNA viruses.

Highlights

  • DNA viruses are nucleic acid-based obligate intracellular microorganisms, which commonly replicate and assemble in the host nucleus

  • Bombyx mori nucleopolyhedrovirus (BmNPV) infection results in significant host chromatin marginalization, which has been found in most DNA viruses

  • By using ATAC-seq, we show that DNA virus BmNPV infection gradually remodels the accessibility of host chromatin

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Summary

Introduction

DNA viruses are nucleic acid-based obligate intracellular microorganisms, which commonly replicate and assemble in the host nucleus. A number of viral proteins can hijack host factors to bind with the gene control elements, which result in large-scale re-organization of the host genome 3D architecture to reprogram gene expression and modulate cell state [7]. Such extensive and conserved changes contribute to modifying and adapting the host intranuclear environment toward a suitable circumstance for efficient viral replication and transcription. It is fundamental to examine the dynamic changes in host nuclear organization, especially the chromatin accessibility and architecture, for that will facilitate the understanding of the epigenomic manipulation of host chromatin by DNA viruses

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