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. 2020 Jul 13;5:125. doi: 10.1038/s41392-020-00233-4

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — The controversial function of Hsp27 during virus infection. Hsp27 would enhance 2A protein-mediated eIF4G cleavage, which would in turn promote IRES function and viral genome replication. It correlates with hnRNPA1 translocation from host cell nuclei to cytosol, and the consequential virus protein translation. Hsp27 is also able to suppress apoptosis via caspase 3 inhibition. On the other hand, Hsp27 could help activating IKK complex, modulating NF-κB and AP-1 to induce the expression of pro-inflammatory cytokines