{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T05:55:11Z","timestamp":1786427711193,"version":"build-2736575974"},"reference-count":163,"publisher":"MDPI AG","issue":"2","license":[{"start":{"date-parts":[[2025,1,22]],"date-time":"2025-01-22T00:00:00Z","timestamp":1737504000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Direcci\u00f3n de Investigaci\u00f3n e Innovaci\u00f3n from Universidad del Rosario"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pathogens"],"abstract":"<jats:p>Chagas disease, caused by Trypanosoma cruzi, is a parasitic zoonosis with significant health impacts, particularly in Latin America. While traditionally associated with vector-borne transmission, increased migration has expanded its reach into urban and non-endemic regions. Congenital transmission has become a critical route of infection, involving intricate maternal\u2013fetal immune interactions that challenge diagnosis and treatment. This review synthesizes findings from three RNA-seq studies that explore the molecular underpinnings of congenital Chagas disease, emphasizing differentially expressed genes (DEGs) implicated in host\u2013pathogen interactions. The DAVID tool analysis highlighted the overexpression of genes associated with the innate immune response, including pro-inflammatory cytokines that drive chemotaxis and neutrophil activation. Additionally, calcium-dependent pathways critical for parasite invasion were modulated. T. cruzi exploits the maternal\u2013fetal immune axis to establish a tolerogenic environment conducive to congenital transmission. Alterations in placental angiogenesis, cellular regeneration, and metabolic processes further demonstrate the parasite\u2019s ability to manipulate host responses for its survival and persistence. These findings underscore the complex interplay between the host and pathogen that facilitates disease progression. Future research integrating transcriptomic, proteomic, and metabolomic approaches is essential to unravel the molecular mechanisms underlying congenital Chagas disease, with a particular focus on the contributions of genetic diversity and non-coding RNAs in immune evasion and disease pathogenesis.<\/jats:p>","DOI":"10.3390\/pathogens14020106","type":"journal-article","created":{"date-parts":[[2025,1,22]],"date-time":"2025-01-22T03:40:17Z","timestamp":1737517217000},"page":"106","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Understanding Host\u2013Pathogen Interactions in Congenital Chagas Disease Through Transcriptomic Approaches"],"prefix":"10.3390","volume":"14","author":[{"given":"Tatiana M.","family":"C\u00e1ceres","sequence":"first","affiliation":[{"name":"Centro de Investigaciones en Microbiolog\u00eda y Biotecnolog\u00eda-UR (CIMBIUR), Facultad de Ciencias Naturales, Universidad del Rosario, Bogot\u00e1 111221, Colombia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luz Helena","family":"Pati\u00f1o","sequence":"additional","affiliation":[{"name":"Centro de Investigaciones en Microbiolog\u00eda y Biotecnolog\u00eda-UR (CIMBIUR), Facultad de Ciencias Naturales, Universidad del Rosario, Bogot\u00e1 111221, Colombia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1344-9312","authenticated-orcid":false,"given":"Juan David","family":"Ram\u00edrez","sequence":"additional","affiliation":[{"name":"Centro de Investigaciones en Microbiolog\u00eda y Biotecnolog\u00eda-UR (CIMBIUR), Facultad de Ciencias Naturales, Universidad del Rosario, Bogot\u00e1 111221, Colombia"},{"name":"Molecular Microbiology Laboratory, Department of Pathology, Molecular and Cell-Based Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2025,1,22]]},"reference":[{"key":"ref_1","unstructured":"World Health Organization (2015). 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