Open Access Highly Accessed Research article

Transcriptional adaptation of pneumococci and human pharyngeal cells in the presence of a virus infection

Sheila Z Kimaro Mlacha126, Teresa C T Peret3, Nikhil Kumar2, Sandra Romero-Steiner4, Julie C Dunning Hotopp2, Nadeeza Ishmael2, Valerie Grinblat-Huse2, David R Riley2, Dean D Erdman3, George M Carlone4, Jacquelyn Sampson4, J Anthony G Scott15 and Hervé Tettelin2*

Author Affiliations

1 Kenya Medical Research Institute – Wellcome Trust Research Programme, Kilifi, Kenya

2 Department of Microbiology and Immunology, Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD, USA

3 Division of Viral Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA

4 Division of Bacterial Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA

5 Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK

6 Present address: Respiratory & Meningeal Pathogens Research Unit, University of the Witwatersrand/Medical Research Council, Johannesburg, South Africa

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BMC Genomics 2013, 14:378  doi:10.1186/1471-2164-14-378

Published: 7 June 2013



Viral upper respiratory tract infections are associated with increased colonization by Streptococcus pneumoniae but the mechanisms underlying this relationship are unclear. The objective of this study is to describe a comprehensive picture of the cellular interaction between the adhering bacteria and host cells in the presence or absence of a viral co-infection.


Gene expression profiles of Detroit-562 pharyngeal cells, which were either mock-infected or infected with human respiratory syncytial virus (RSV) or human parainfluenza virus 3 (HPIV3), were analyzed using human microarrays. Transcription response of S. pneumoniae strain TIGR4 (serotype 4) in the presence of either mock- or viral-infected cells was analyzed by pneumococcal microarray. Significantly regulated genes were identified by both significance analysis of microarray (SAM) and a ≥ 2-fold change ratio cut-off. The adherence of S. pneumoniae to human pharyngeal cells was significantly augmented in the presence of RSV or HPIV3 infection. Global gene expression profiling of the host cells during infection with RSV or HPIV3 revealed increased transcription of carcinoembryonic antigen-related cell adhesion molecules (CEACAM1), CD47, fibronectin, interferon-stimulated genes and many other host cell adhesion molecules. Pneumococci increased transcription of several genes involved in adhesive functions (psaA, pilus islet), choline uptake and incorporation (lic operon), as well as transport and binding.


We have identified a core transcriptome that represents the basic machinery required for adherence of pneumococci to D562 cells infected or not infected with a virus. These bacterial genes and cell adhesion molecules can potentially be used to control pneumococcal adherence occurring secondary to a viral infection.

Streptococcus pneumoniae; RSV; HPIV3; Gene expression; Microarray; Adherence; Bacterial-viral co-infection