As Earth's temperature rises, fungal pathogens are adapting, altering host-pathogen interactions, disease patterns, and response to the antimicrobial drugs. Here, we show that thermal adaptation to 42{degrees}C leads to reversible changes in fungal colony size, appearance, and azole drug response in the human pathogenic fungus Aspergillus fumigatus. Importantly, this adaptation is mediated by a lncRNA, afu-182, whose RNA levels negatively correlate with temperature. Growth at a lower temperature or ectopic upregulation of afu-182 RNA levels reverses the temperature adaptation. Global transcriptomic analyses show an enrichment of pathogenesis-associated genes at 37{degrees}C and 42{degrees}C compared to 25{degrees}C. Interestingly, we found that small heat shock proteins and chaperones, but not ATP-dependent heat-shock proteins, are negatively regulated by afu-182 at 37{degrees}C and 42{degrees}C at transcriptional level. Previously, we have shown that {Delta}afu-182 strains produce worse disease outcomes in a murine model of invasive pulmonary aspergillosis (IPA). Here, more importantly, we show that the overexpression of afu-182 in clinically azole-resistant isolates increased survival in a murine model of IPA. Taken together, fungal adaptation to increased temperature leads to a decrease in afu-182 RNA levels that is associated with worse disease outcomes upon azole treatment. This provides a framework to take temperature into account when analyzing the rise in azole MIC in environmental and clinical isolates.