2026-06-14T05:08:10Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/174412024-11-28T18:18:04Zcom_20.500.12105_2052com_20.500.12105_2051com_20.500.12105_15322col_20.500.12105_19609col_20.500.12105_16962
Repisalud
author
Escolano-Martinez, Maria S
author
Domenech, Arnau
author
Yuste, Jose Enrique
author
Cercenado, Maria I
author
Ardanuy, Carmen
author
Liñares, Josefina
author
de la Campa, Adela G
author
Martin-Galiano, Antonio Javier
funder
Ministerio de Economía y Competitividad (España)
funder
Plan Nacional de I+D+i (España)
funder
Instituto de Salud Carlos III
funder
Ministerio de Educación (España)
2024-02-02T18:46:26Z
2024-02-02T18:46:26Z
2016-07
J Infect. 2016 Jul;73(1):71-81.
10.1016/j.jinf.2016.04.010
1532-2742
The Journal of infection
27105656
http://hdl.handle.net/20.500.12105/17441
Objectives: Many outer multidomain proteins play fundamental virulent roles in an allele-dependent manner. We aimed to investigate the influence of the outer SP1992 protein, here renamed DiiA (Dimorphic invasion-involved A), in pneumococcal disease. Methods: The presence and type of diiA allele was screened by PCR in 560 clinical isolates. Isogenic mutants carrying progressive diiA deletions were constructed and checked in mouse models of infection. DiiA binding to human molecules was carried out by surface plasmon resonance. Results: The diiA gene is exclusive of Streptococcus pneumoniae and included in the core genome. DiiA variants contain one or two imperfect repeats (R1 and R2), an unstructured region and a cell-wall anchor domain. Clonal complexes carrying both repeats were associated with invasive disease, while those carrying R2 preferentially caused non-invasive syndromes in patients with underlying risk factors. Mutants lacking both repeats were less efficient in nasopharyngeal colonization and dissemination from lungs. Moreover, the ΔdiiA defective strain suffered a severe impairment in bacterial proliferation in blood. Purified DiiA bound to collagen and lactoferrin with high affinity. Conclusions: DiiA is a distinctive pneumococcal virulence factor contributing to colonization and long-term invasion in this pathogen.
eng
Adhesine
Genomics
Hypothetical protein
Invasion
Vaccine
Virulence factor
DiiA is a novel dimorphic cell wall protein of Streptococcus pneumoniae involved in invasive disease
research article
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