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1 April 2005

Volume 191, Number 7
The Journal of Infectious Diseases 2005;191:1068–1071
© 2005 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2005/19107-0008$15.00
DOI: 10.1086/428593
BRIEF REPORT

Host Susceptibility and Clinical Outcomes in Toll‐like Receptor 5–Deficient Patients with Typhoid Fever in Vietnam

Sarah J. Dunstan,1,4

Thomas R. Hawn,7,8

Nguyen Thi Hue,1,2

Christopher P. Parry,1,5

Vo An Ho,3

Ha Vinh,2

To Song Diep,2

Deborah House,6

John Wain,6

Alan Aderem,8

Tran Tinh Hien,2 and

Jeremy J. Farrar1,4

1Oxford University Clinical Research Unit and 2Hospital for Tropical Diseases, Ho Chi Minh City, and 3Dong Thap Provincial Hospital, Cao Lanh, Dong Thap Province, Vietnam; 4Center for Tropical Medicine, Nuffield Department of Clinical Medicine, Oxford University, Oxford, 5Department of Medical Microbiology and Genitourinary Medicine, University of Liverpool, Liverpool, and 6The Wellcome Trust Sanger Institute, Hinxton, Cambridge, United Kingdom; 7University of Washington Medical Center and 8Institute for Systems Biology, Seattle

Toll‐like receptor 5 (TLR5) mediates innate immune responses to bacterial pathogens by binding to flagellin. A polymorphism in the TLR5 gene introduces a premature stop codon (TLR5392STOP) that is associated with susceptibility to legionnaires disease. Here we investigated whether TLR5392STOP was associated with typhoid fever. The frequency of TLR5392STOP was not significantly different in 565 patients with typhoid fever and 281 ethnically matched control subjects. Furthermore, TLR5 deficiency had no measurable effect on a number of clinical parameters associated with typhoid fever, including fever clearance time, pathogen burden, disease severity, or age at acquisition of disease. TLR5 may not play an important role in TLR‐stimulated innate immune responses to human infection with Salmonella enterica serovar Typhi. Initiation of these responses may rely on other TLRs that recognize different bacterial ligands.

Received 29 August 2004; accepted 27 October 2004; electronically published 28 February 2005.

Reprints or correspondence: Dr. Sarah J. Dunstan, Oxford University Clinical Research Unit, Hospital for Tropical Diseases, 190 Ben Ham Tu, Quan 5, Ho Chi Minh City, Vietnam ().

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  • Financial support: The Wellcome Trust.

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