Affiliation:
1. Department of Medical Microbiology & Immunology, Texas A&M University Health Science Center
2. Department of Veterinary Pathobiology, Texas A&M University, College Station, Texas
Abstract
ABSTRACT
The
Brucella abortus virB
operon, encoding a type IV secretion system (T4SS), is required for intracellular replication and persistent infection in the mouse model. The products of the first two genes of the
virB
operon,
virB1
and
virB2
, are predicted to be localized at the bacterial surface, where they could potentially interact with host cells. Studies to date have focused on characterization of transposon mutations in these genes, which are expected to exert polar effects on downstream genes in the operon. In order to determine whether VirB1 and VirB2 are required for the function of the T4SS apparatus, we constructed and characterized nonpolar deletion mutations of
virB1
and
virB2
. Both mutants were shown to be nonpolar, as demonstrated by their ability to express the downstream gene
virB5
during stationary phase of growth in vitro. Both VirB1 and VirB2 were essential for intracellular replication in J774 macrophages. The nonpolar
virB2
mutant was unable to cause persistent infection in the mouse model, demonstrating the essential role of VirB2 in the function of the T4SS apparatus during infection. In contrast, the nonpolar
virB1
mutant persisted at wild-type levels, showing that the function of VirB1 is dispensable in the mouse model of persistent infection.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
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