Key result
Enterovirus A71 upregulates host ATF3 and recruits it to cytoplasm to promote viral replication.
Host activating transcription factor 3 (ATF3) is upregulated during Enterovirus A71 infection and translocates to the cytoplasm to interact with the viral 5'UTR and promote viral RNA replication.
Answers are grounded in this paper and cite their sources.
ATF3 promotes EV-A71 replication in RD cells; hypothesis-generating for host-targeted antivirals, requires in vivo validation before clinical consideration.
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.
No takes yet. Share an insight, caveat, or question.
Deng et al. (2026) studied Enterovirus A71 (EV-A71) infection in RD cells. Enterovirus A71 (EV-A71) infection and host ATF3 recruitment was evaluated on EV-A71 viral genome RNA replication and host ATF3 upregulation/translocation. Enterovirus A71 infection upregulates host ATF3 in RD cells and recruits it to the cytoplasm to bind the viral 5'UTR, promoting viral genome RNA replication.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: