{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T12:07:05Z","timestamp":1788869225894,"version":"build-2803163510"},"reference-count":200,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T00:00:00Z","timestamp":1788825600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:p>\n                    Typhoidal\n                    <jats:italic>Salmonella<\/jats:italic>\n                    (\n                    <jats:italic>Salmonella enterica<\/jats:italic>\n                    serovars Typhi and Paratyphi A) continue to impose a significant global health burden, particularly in regions characterized by inadequate sanitation and rising antimicrobial resistance. Although recent reviews have comprehensively addressed epidemiology, antimicrobial resistance, vaccination strategies, and host-pathogen interactions, virulence determinants are often described in a pathway-specific manner. Consequently, a cohesive macromolecular framework integrating these determinants remains insufficiently developed. In this review, we adopt a protein-centric perspective to systematically elucidate the molecular and structural architecture underlying typhoidal\n                    <jats:italic>Salmonella<\/jats:italic>\n                    pathogenesis. Diverse virulence determinants, including Type III Secretion System (T3SS) effectors, outer membrane proteins, adhesins, toxin subunits, stress-response regulators, and metabolic proteins, are integrated into a unified structural and functional network in which their three-dimensional architectures, protein\u2013protein interaction interfaces, receptor-binding surfaces, catalytic domains, and active-site configurations collectively govern host-cell invasion, intracellular survival, immune evasion, nutrient acquisition, and systemic dissemination. Furthermore, we present a comparative analysis of\n                    <jats:italic>S<\/jats:italic>\n                    . Typhi and\n                    <jats:italic>S<\/jats:italic>\n                    . Paratyphi A, emphasizing differences in protein repertoires and regulatory adaptations that drive their distinct pathogenic mechanisms. Collectively, these structural insights establish a mechanistic bridge between protein architecture and pathogenic function and identify molecular interfaces, catalytic pockets, and receptor-binding surfaces as opportunities for diagnostics, vaccines, and anti-virulence therapeutics. Integration of structural biology with artificial intelligence-assisted drug discovery, protein engineering, single-cell infection models, and host-directed approaches may further accelerate the development of next-generation interventions against typhoidal\n                    <jats:italic>Salmonella.<\/jats:italic>\n                  <\/jats:p>","DOI":"10.3389\/fcimb.2026.1914114","type":"journal-article","created":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T11:09:33Z","timestamp":1788865773000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Protein-centric mechanisms of typhoidal Salmonella pathogenicity: emerging opportunities for diagnostics and anti-virulence therapeutics"],"prefix":"10.3389","volume":"16","author":[{"given":"Subhash Chandra","family":"Pani","sequence":"first","affiliation":[{"name":"Centre for Bio-separation Technology, Vellore Institute of Technology","place":["Vellore, Tamil Nadu, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Immanuel","family":"Dhanasingh","sequence":"additional","affiliation":[{"name":"Centre for Bio-separation Technology, Vellore Institute of Technology","place":["Vellore, Tamil Nadu, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,8]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"2110","DOI":"10.1074\/mcp.M700105-MCP200","article-title":"A comparative analysis of perturbations caused by a gene knock-out, a dominant negative allele, and a set of peptide aptamers","volume":"6","author":"Abed","year":"2007","journal-title":"Mol. 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