Enterovirus A71 upregulates and recruits host ATF3 to promote viral replication
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Updated: Nov 1, 2026

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
Zhi Deng1, Zhuoran Li1, Yani Wu1
1Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, College of Life Sciences, Nankai University, Tianjin, China.
Abstract:
To hijack cellular resources, certain viruses such as EV-A71, induce the shutoff of cellular transcription and translation systems globally for establishing infection. However, our previous studies have shown that the translation efficiency of series host proteins is upregulated during EV-A71 infection potentially, including activating transcription factor 3 (ATF3). Here, we validated in RD cells that ATF3 is mount up during EV-A71 infection significantly via increasing mRNA and cap-independent translation. Our findings highlight the critical role of ATF3 in EV-A71 replication: during EV-A71 infection, ATF3 trans-locates to the cytoplasm besides upregulated, where it interacts with the viral 5' untranslated region (5'UTR) and promotes the replication of viral genome RNA. Intriguingly, the nuclear localization signal (NLS) of ATF3 also contributes to this process, including binding to the viral genome and facilitating viral replication.
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