Volume 36 Issue 3
May  2015
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Feng-Chao LANG, Xin LI, Olga VLADMIROVA, Zhuo-Ran LI, Gui-Jun CHEN, Yu XIAO, Li-Hong LI, Dan-Feng LU, Hong-Bo HAN, Ju-Min ZHOU. Selective recruitment of host factors by HSV-1 replication centers. Zoological Research, 2015, 36(3): 142-151.
Citation: Feng-Chao LANG, Xin LI, Olga VLADMIROVA, Zhuo-Ran LI, Gui-Jun CHEN, Yu XIAO, Li-Hong LI, Dan-Feng LU, Hong-Bo HAN, Ju-Min ZHOU. Selective recruitment of host factors by HSV-1 replication centers. Zoological Research, 2015, 36(3): 142-151.

Selective recruitment of host factors by HSV-1 replication centers

Funds:  This work was supported by grants from the Yunnan Provincial Government (2013FA051; 2011HA005), the National Science Foundation of China (NSFC 81471966 to JZ and NSFC 31200964 to YX), and the common project of the Panzhihua Science and Technology Bureau from China (2012CY-S-22(9) to HH)
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  • Corresponding author: Ju-Min ZHOU
  • Received Date: 2015-03-09
  • Rev Recd Date: 2015-04-09
  • Publish Date: 2015-05-08
  • Herpes simplex virus type 1 (HSV-1) enters productive infection after infecting epithelial cells, where it controls the host nucleus to make viral proteins, starts viral DNA synthesis and assembles infectious virions. In this process, replicating viral genomes are organized into replication centers to facilitate viral growth. HSV-1 is known to use host factors, including host chromatin and host transcription regulators, to transcribe its genes; however, the invading virus also encounters host defense and stress responses to inhibit viral growth. Recently, we found that HSV-1 replication centers recruit host factor CTCF but exclude γH2A.X. Thus, HSV-1 replication centers may selectively recruit cellular factors needed for viral growth, while excluding host factors that are deleterious for viral transcription or replication. Here we report that the viral replication centers selectively excluded modified histone H3, including heterochromatin mark H3K9me3, H3S10P and active chromatin mark H3K4me3, but not unmodified H3. We found a dynamic association between the viral replication centers and host RNA polymerase II. The centers also recruited components of the DNA damage response pathway, including 53BP1, BRCA1 and host antiviral protein SP100. Importantly, we found that ATM kinase was needed for the recruitment of CTCF to the viral centers. These results suggest that the HSV-1 replication centers took advantage of host signaling pathways to actively recruit or exclude host factors to benefit viral growth.
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