Open Access Research article

Spir2; a novel QTL on chromosome 4 contributes to susceptibility to pneumococcal infection in mice

Laura Wisby1, Vitor E Fernandes2, Daniel R Neill23, Aras Kadioglu23, Peter W Andrew2 and Paul Denny1*

Author Affiliations

1 MRC Mammalian Genetics Unit, Harwell, Oxon, OX11 0RD, UK

2 Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, UK

3 Department of Clinical Infection Microbiology & Immunology, Institute of Infection & Global Health, University of Liverpool, Liverpool, UK

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BMC Genomics 2013, 14:242  doi:10.1186/1471-2164-14-242

Published: 11 April 2013



Streptococcus pneumoniae causes over one million deaths worldwide annually, despite recent developments in vaccine and antibiotic therapy. Host susceptibility to pneumococcal infection and disease is controlled by a combination of genetic and environmental influences, but current knowledge remains limited.


In order to identify novel host genetic variants as predictive risk factors or as potential targets for prophylaxis, we have looked for quantitative trait loci in a mouse model of invasive pneumococcal disease. We describe a novel locus, called Streptococcus pneumoniae infection resistance 2 (Spir2) on Chr4, which influences time to morbidity and the development of bacteraemia post-infection.


The two quantitative trait loci we have identified (Spir1 and Spir2) are linked significantly to both bacteraemia and survival time. This may mean that the principle cause of death, in our model of pneumonia, is bacteraemia and the downstream inflammatory effects it precipitates in the host.

Streptococcus pneumoniae; Host susceptibility; Host genetics; Quantitative trait loci; Model organism; Mouse; Bacterial infection; Inflammation