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© Institut Pasteur/Antoinette Ryter
Salmonella spp. Bactéries à Gram négatif, aérobies ou anaérobies facultatifs à transmission orofécale. Les salmonelles majeures (sérotype typhi et sérotype paratyphi) sont responsables des fièvres typhoïde et paratyphoïde chez l'homme uniquement ; les salmonelles mineures (sérotype typhimurium et sérotype enteritidis) sont impliquées dans 30 à 60 % des gastroentérites et toxiinfections d'origine alimentaire. Image colorisée.
Publication : Communications biology

Bacterial genome-wide association study of hyper-virulent pneumococcal serotype 1 identifies genetic variation associated with neurotropism.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Communications biology - 08 Oct 2020

Chaguza C, Yang M, Cornick JE, du Plessis M, Gladstone RA, Kwambana-Adams BA, Lo SW, Ebruke C, Tonkin-Hill G, Peno C, Senghore M, Obaro SK, Ousmane S, Pluschke G, Collard JM, Sigaùque B, French N, Klugman KP, Heyderman RS, McGee L, Antonio M, Breiman RF, von Gottberg A, Everett DB, Kadioglu A, Bentley SD,

Link to Pubmed [PMID] – 33033372

Link to DOI – 55910.1038/s42003-020-01290-9

Commun Biol 2020 Oct; 3(1): 559

Hyper-virulent Streptococcus pneumoniae serotype 1 strains are endemic in Sub-Saharan Africa and frequently cause lethal meningitis outbreaks. It remains unknown whether genetic variation in serotype 1 strains modulates tropism into cerebrospinal fluid to cause central nervous system (CNS) infections, particularly meningitis. Here, we address this question through a large-scale linear mixed model genome-wide association study of 909 African pneumococcal serotype 1 isolates collected from CNS and non-CNS human samples. By controlling for host age, geography, and strain population structure, we identify genome-wide statistically significant genotype-phenotype associations in surface-exposed choline-binding (P = 5.00 × 10-08) and helicase proteins (P = 1.32 × 10-06) important for invasion, immune evasion and pneumococcal tropism to CNS. The small effect sizes and negligible heritability indicated that causation of CNS infection requires multiple genetic and other factors reflecting a complex and polygenic aetiology. Our findings suggest that certain pathogen genetic variation modulate pneumococcal survival and tropism to CNS tissue, and therefore, virulence for meningitis.