{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:26:42Z","timestamp":1772162802630,"version":"3.50.1"},"reference-count":100,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"6752","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Science"],"published-print":{"date-parts":[[2025,6,12]]},"abstract":"<jats:p>\n                    Jaundice is a common presentation of\n                    <jats:italic toggle=\"yes\">Plasmodium<\/jats:italic>\n                    <jats:italic toggle=\"yes\">falciparum<\/jats:italic>\n                    malaria, which arises from the accumulation of circulating bilirubin. It is not understood whether it represents an adaptive or maladaptive response to\n                    <jats:italic toggle=\"yes\">Plasmodium<\/jats:italic>\n                    spp. infection. We found that asymptomatic\n                    <jats:italic toggle=\"yes\">P. falciparum<\/jats:italic>\n                    infection in humans was associated with a higher ratio of unconjugated over conjugated bilirubin and parasite burden compared with symptomatic malaria. Genetic suppression of bilirubin synthesis by biliverdin reductase A (BVRA) increased parasite virulence and malaria mortality in mice. Accumulation of unconjugated bilirubin in plasma, through genetic inhibition of hepatic conjugation by UDP glucuronosyltransferase family 1 member A1 (UGT1A1), was protective against malaria in mice. Unconjugated bilirubin inhibited\n                    <jats:italic toggle=\"yes\">P. falciparum<\/jats:italic>\n                    proliferation in red blood cells by a mechanism that suppressed mitochondrial pyrimidine synthesis. Moreover, unconjugated bilirubin inhibited hemozoin crystallization and compromised the parasite\u2019s food vacuole. Hence, jaundice appears to represent a metabolic response to\n                    <jats:italic toggle=\"yes\">Plasmodium<\/jats:italic>\n                    spp. infection that limits malaria severity.\n                  <\/jats:p>","DOI":"10.1126\/science.adq6741","type":"journal-article","created":{"date-parts":[[2025,6,18]],"date-time":"2025-06-18T11:30:31Z","timestamp":1750246231000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":6,"title":["A metabolite-based resistance mechanism against malaria"],"prefix":"10.1126","volume":"388","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9075-2238","authenticated-orcid":true,"given":"Ana","family":"Figueiredo","sequence":"first","affiliation":[{"name":"Gulbenkian Institute for Molecular Medicine (GIMM), Avenida Professor Egas Moniz, Lisboa, Portugal."}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2333-7170","authenticated-orcid":true,"given":"Sonia Trikha","family":"Rastogi","sequence":"additional","affiliation":[{"name":"Gulbenkian Institute for Molecular Medicine (GIMM), Avenida Professor Egas Moniz, Lisboa, Portugal."}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6356-1065","authenticated-orcid":true,"given":"Susana","family":"Ramos","sequence":"additional","affiliation":[{"name":"Gulbenkian Institute for Molecular Medicine (GIMM), Avenida Professor Egas Moniz, Lisboa, Portugal."}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0313-0778","authenticated-orcid":true,"given":"F\u00e1tima","family":"Nogueira","sequence":"additional","affiliation":[{"name":"Global Health and Tropical Medicine, Instituto de Higiene e Medicina Tropical, IHMT, Universidade NOVA de Lisboa, Rua da Junqueira 100, Lisboa, Portugal."}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2932-395X","authenticated-orcid":true,"given":"Katherine","family":"De Villiers","sequence":"additional","affiliation":[{"name":"Department of Chemistry and Polymer Science, Stellenbosch University, Stellenbosch, South Africa."}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4779-6459","authenticated-orcid":true,"given":"Ant\u00f3nio G. 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