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Infection and Immunity, September 2005, p. 6048-6054, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.6048-6054.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Brucella abortus VirB12 Is Expressed during Infection but Is Not an Essential Component of the Type IV Secretion System

Yao-Hui Sun,{dagger} Hortensia G. Rolán,{dagger} Andreas B. den Hartigh,{dagger} David Sondervan, and Renée M. Tsolis*

Texas A&M University Health Science Center, Department of Medical Microbiology & Immunology, College Station, Texas 77843-1114

Received 19 January 2005/ Returned for modification 2 March 2005/ Accepted 28 April 2005

The Brucella abortus virB operon, consisting of 11 genes, virB1 to virB11, and two putative genes, orf12 (virB12) and orf13, encodes a type IV secretion system (T4SS) that is required for intracellular replication and persistent infection in the mouse model. This study was undertaken to determine whether orf12 (virB12) encodes an essential part of the T4SS apparatus. The virB12 gene was found to encode a 17-kDa protein, which was detected in vitro in B. abortus grown to stationary phase. Mice infected with B. abortus 2308 produced an antibody response to the protein encoded by virB12, showing that this gene is expressed during infection. Expression of virB12 was not required for survival in J774 macrophages. VirB12 was also dispensable for the persistence of B. abortus, B. melitensis, and B. suis in mice up to 4 weeks after infection, since deletion mutants lacking virB12 were recovered from splenic tissue at wild-type levels. These results show that VirB12 is not essential for the persistence of the human-pathogenic Brucella spp. in the mouse and macrophage models of infection.

* Corresponding author. Present address: Department of Medical Microbiology & Immunology, University of California at Davis, Davis, CA 95616. Phone: (530) 754-8497. Fax: (530) 754-7240. E-mail: rmtsolis{at}ucdavis.edu.

Editor: D. L. Burns

{dagger} Present address: Department of Medical Microbiology & Immunology, University of California at Davis, Davis, CA 95616.

Infection and Immunity, September 2005, p. 6048-6054, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.6048-6054.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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