{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T05:41:42Z","timestamp":1792734102648,"version":"4.5.0"},"reference-count":49,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2010,7,1]],"date-time":"2010-07-01T00:00:00Z","timestamp":1277942400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2010,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:italic>Aspergillus fumigatus<\/jats:italic>\n                    is a pathogenic mold which causes invasive, often fatal, pulmonary disease in immunocompromised individuals. Recently, proteins involved in the biosynthesis of trehalose have been linked with virulence in other pathogenic fungi. We found that the trehalose content increased during the developmental life cycle of\n                    <jats:italic>A. fumigatus<\/jats:italic>\n                    , throughout which putative trehalose synthase genes\n                    <jats:italic>tpsA<\/jats:italic>\n                    and\n                    <jats:italic>tpsB<\/jats:italic>\n                    were significantly expressed. The trehalose content of\n                    <jats:italic>A. fumigatus<\/jats:italic>\n                    hyphae also increased after heat shock but not in response to other stressors. This increase in trehalose directly correlated with an increase in expression of\n                    <jats:italic>tpsB<\/jats:italic>\n                    but not\n                    <jats:italic>tpsA<\/jats:italic>\n                    . However, deletion of both\n                    <jats:italic>tpsA<\/jats:italic>\n                    and\n                    <jats:italic>tpsB<\/jats:italic>\n                    was required to block trehalose accumulation during development and heat shock. The \u0394\n                    <jats:italic>tpsAB<\/jats:italic>\n                    double mutant had delayed germination at 37\u00b0C, suggesting a developmental defect. At 50\u00b0C, the majority of \u0394\n                    <jats:italic>tpsAB<\/jats:italic>\n                    spores were found to be nonviable, and those that were viable had severely delayed germination, growth, and subsequent sporulation. \u0394\n                    <jats:italic>tpsAB<\/jats:italic>\n                    spores were also susceptible to oxidative stress. Surprisingly, the \u0394\n                    <jats:italic>tpsAB<\/jats:italic>\n                    double mutant was hypervirulent in a murine model of invasive aspergillosis, and this increased virulence was associated with alterations in the cell wall and resistance to macrophage phagocytosis. Thus, while trehalose biosynthesis is required for a number of biological processes that both promote and inhibit virulence, in\n                    <jats:italic>A. fumigatus<\/jats:italic>\n                    the predominant effect is a reduction in pathogenicity. This finding contrasts sharply with those for other fungi, in which trehalose biosynthesis acts to enhance virulence.\n                  <\/jats:p>","DOI":"10.1128\/iai.00813-09","type":"journal-article","created":{"date-parts":[[2010,5,3]],"date-time":"2010-05-03T21:09:48Z","timestamp":1272920988000},"page":"3007-3018","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":136,"title":["Role of Trehalose Biosynthesis in\n                    <i>Aspergillus fumigatus<\/i>\n                    Development, Stress Response, and Virulence"],"prefix":"10.1128","volume":"78","author":[{"given":"Nadia","family":"Al-Bader","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ghyslaine","family":"Vanier","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Liu","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabrice N.","family":"Gravelat","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mirjam","family":"Urb","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher M.-Q.","family":"Hoareau","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paolo","family":"Campoli","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Josee\u0301","family":"Chabot","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Scott G.","family":"Filler","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California"},{"name":"David Geffen School of Medicine at UCLA, Los Angeles, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donald C.","family":"Sheppard","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1099\/00221287-148-8-2599"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/JCM.44.2.553-560.2006"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.00699-07"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.01160-06"},{"key":"e_1_3_2_6_2","first-page":"137","volume":"36","year":"1998","unstructured":"Beffa, T., F. 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