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In this study, we observed that the gene\n                      <jats:italic toggle=\"yes\">arvA<\/jats:italic>\n                      is required for\n                      <jats:italic toggle=\"yes\">A. fumigatus<\/jats:italic>\n                      morphogenesis, antifungal drug susceptibility, and cell wall homeostasis. Intriguingly, our study reveals novel morphological and growth aberrations in the absence of\n                      <jats:italic toggle=\"yes\">arvA<\/jats:italic>\n                      . Loss of\n                      <jats:italic toggle=\"yes\">arvA<\/jats:italic>\n                      results in hyper-swollen conidia that give rise to stunted, polarity-deficient hyphae in numerous environmental conditions, indicating a pivotal role for\n                      <jats:italic toggle=\"yes\">arvA<\/jats:italic>\n                      in\n                      <jats:italic toggle=\"yes\">A. fumigatus<\/jats:italic>\n                      morphogenesis. Surprisingly, despite these severe\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      morphological and cell wall defects,\n                      <jats:italic toggle=\"yes\">arvA<\/jats:italic>\n                      was not required for morbidity and mortality in immunologically distinct murine models of invasive pulmonary aspergillosis. However, the mechanisms by which the\n                      <jats:italic toggle=\"yes\">arvA<\/jats:italic>\n                      mutant can cause disease differ between the two models. Growth in natural calf lung surfactant was able to somewhat normalize \u2206\n                      <jats:italic toggle=\"yes\">arvA<\/jats:italic>\n                      growth with the wild-type strain, suggesting lung surfactant may partially complement the severe\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      morphological defects of\n                      <jats:italic toggle=\"yes\">arvA<\/jats:italic>\n                      loss\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      . Taken together, our observations reveal\n                      <jats:italic toggle=\"yes\">arvA<\/jats:italic>\n                      as a mediator of\n                      <jats:italic toggle=\"yes\">A. fumigatus<\/jats:italic>\n                      antifungal drug susceptibility and highlight the complex and ill-defined pulmonary nutrient environment\u2019s role in mediating\n                      <jats:italic toggle=\"yes\">A. fumigatus<\/jats:italic>\n                      pathogenesis and disease progression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Aspergillus fumigatus<\/jats:italic>\n                      is a challenging fungal pathogen in the clinic, in part due to increasing azole drug resistance. In this study, we observed that the loss of the\n                      <jats:italic toggle=\"yes\">A. fumigatus<\/jats:italic>\n                      gene\n                      <jats:italic toggle=\"yes\">arvA<\/jats:italic>\n                      results in increased azole susceptibility and significant\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      morphological changes highlighted by hyper-swollen conidia that yield stunted and polarity-deficient hyphae. Importantly, despite these severe\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      morphological and growth abnormalities, \u2206\n                      <jats:italic toggle=\"yes\">arvA<\/jats:italic>\n                      surprisingly retains full pathogenicity and virulence in two immunologically distinct murine models of invasive pulmonary aspergillosis. These results challenge our understanding of the in-host environment and how it mediates fungal morphogenesis and pathogenesis. These results, consequently, not only enhance our understanding of the role of\n                      <jats:italic toggle=\"yes\">arvA<\/jats:italic>\n                      in\n                      <jats:italic toggle=\"yes\">A. fumigatus<\/jats:italic>\n                      morphogenesis and drug susceptibility but also further emphasize the importance of\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      animal models in fully evaluating potential antifungal drug targets.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/msphere.00853-25","type":"journal-article","created":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T13:00:21Z","timestamp":1778850021000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["Insights into\n                    <i>Aspergillus fumigatus<\/i>\n                    morphogenesis and pathogenesis through the putative lipid transporter ArvA"],"prefix":"10.1128","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9808-0701","authenticated-orcid":true,"given":"Cecilia","family":"Gutierrez-Perez","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/0232r4451","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth","place":["Hanover, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1047-9994","authenticated-orcid":false,"given":"Jane T.","family":"Jones","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/0232r4451","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth","place":["Hanover, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4402-0295","authenticated-orcid":true,"given":"Charles T. 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