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Japan’s hot spring tourism, vital for rural economies, faced major setbacks during the COVID-19 pandemic. While research on travel intentions during health crises exists, there is limited exploration of public perceptions of health risk countermeasures in hot spring tourism. This study aims to fill this gap by examining the countermeasures implemented by hot spring operators in Japan and their perceived effectiveness by the public. A case study in disaster-affected areas reveals the challenges operators faced and how countermeasures influenced travel intentions, with demographic factors playing a key role in perceptions of effectiveness. This study makes several contributions: it is the first to explore public perceptions of health countermeasures in hot spring tourism, advancing the field of adaptive tourism by highlighting the importance of health protocols in rebuilding tourism industries after a crisis. Findings suggest that sanitation measures were viewed as the most effective, and operators can better allocate resources by focusing on these areas. Moreover, clear communication about countermeasures is crucial for boosting visitor confidence and facilitating recovery. Despite its focus on Japan and reliance on self-reported data, this research provides valuable insights for hot spring managers worldwide. The study’s findings offer practical guidance on prioritizing countermeasures. 

The pioneer transcription factor (TF) PU.1 controls hematopoietic cell fate by decompacting stem cell heterochromatin and allowing nonpioneer TFs to enter otherwise inaccessible genomic sites. PU.1 deficiency fatally arrests lymphopoiesis and myelopoiesis in mice, but human congenital PU.1 disorders have not previously been described. We studied six unrelated agammaglobulinemic patients, each harboring a heterozygous mutation (four de novo, two unphased) of SPI1, the gene encoding PU.1. Affected patients lacked circulating B cells and possessed few conventional dendritic cells. Introducing disease-similar SPI1 mutations into human hematopoietic stem and progenitor cells impaired early in vitro B cell and myeloid cell differentiation. Patient SPI1 mutations encoded destabilized PU.1 proteins unable to nuclear localize or bind target DNA. In PU.1-haploinsufficient pro–B cell lines, euchromatin was less accessible to nonpioneer TFs critical for B cell development, and gene expression patterns associated with the pro– to pre–B cell transition were undermined. Our findings molecularly describe a novel form of agammaglobulinemia and underscore PU.1’s critical, dose-dependent role as a hematopoietic euchromatin gatekeeper.