Abstract
The virulence of the mycobacteria that cause tuberculosis depends on their ability to multiply in mammalian hosts. Disruption of the bacterial erp gene, which encodes the exported repetitive protein, impaired multiplication of M. tuberculosis and M. bovis Bacille Calmette-Guérin in cultured macrophages and mice. Reintroduction of erp into the mutants restored their ability to multiply. These results indicate that erp contributes to the virulence of M. tuberculosis.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Animals
-
BCG Vaccine
-
Bacterial Proteins / analysis
-
Bacterial Proteins / genetics
-
Bacterial Proteins / physiology*
-
Cell Line
-
Genes, Bacterial
-
Genetic Complementation Test
-
Immunohistochemistry
-
Lung / microbiology
-
Macrophages / microbiology
-
Membrane Proteins / analysis
-
Membrane Proteins / genetics
-
Membrane Proteins / physiology*
-
Mice
-
Mice, Inbred BALB C
-
Mutation
-
Mycobacterium bovis / genetics
-
Mycobacterium bovis / growth & development
-
Mycobacterium tuberculosis / genetics
-
Mycobacterium tuberculosis / growth & development
-
Mycobacterium tuberculosis / metabolism
-
Mycobacterium tuberculosis / pathogenicity*
-
Phagosomes / microbiology
-
Recombinant Fusion Proteins
-
Tuberculosis / microbiology
-
Vaccines, Attenuated
-
Virulence / genetics
Substances
-
BCG Vaccine
-
Bacterial Proteins
-
ERP protein, Mycobacterium tuberculosis
-
Membrane Proteins
-
Recombinant Fusion Proteins
-
Vaccines, Attenuated