Temperature is a critical factor influencing the outbreak and progression of viral diseases in organisms. Febrile temperatures have been shown to enhance immune competence and reduce viral replication in various species. However, the underlying mechanisms remain largely unknown. In this study, we investigate the molecular mechanisms by which elevated temperatures confer resistance to viral infections, focusing on the role of heat shock factor 1 (HSF1) in regulating antimicrobial effectors rather than the traditional target genes molecular chaperones. Using shrimp <i>Litopenaeus vannamei</i> as a model, we demonstrate that febrile temperatures induce HSF1, which in turn upregulates antimicrobial peptides (AMPs) that target viral envelope proteins and inhibit viral replication. Importantly, this is the first to show that HSF1 directly binds to the heat shock element (HSE) motifs of AMPs both in shrimp and <i>Drosophila</i> S2 cells, suggesting this may be a conserved regulatory mechanism in arthropods. Additionally, our findings highlight the role of HSF1 beyond the classical heat shock response, revealing its critical function in modulating innate immunity. These insights provide new avenues for managing viral infections in aquaculture and other settings by leveraging environmental temperature control.
Science Journals
The term signe de cils was introduced in the late 19th century and is attributed to Achille Souques, one of the most prominent French neurologists of his time.1 This clinical observation reflects the tradition of meticulous bedside neurological semiology of that era. It is referred to as the eyelash sign and denotes the inability to fully conceal the eyelashes during attempted forceful bilateral eye closure.2
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New England Journal of Medicine, Volume 394, Issue 19, Page 1883-1893, May 14/21, 2026.
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Science, Volume 392, Issue 6799, Page 771-779, May 2026.
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