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Infection and Immunity, June 2001, p. 3562-3568, Vol. 69, No. 6
Institut für Medizinische Mikrobiologie, Medizinische
Hochschule Hannover, 30625 Hannover, Germany1;
National Institute for Medical Research, Mill Hill, London NW7
1AA, United Kingdom2; Institute of
Molecular and Cell Biology, Singapore 117609, Republic of
Singapore3; and Institut für
Medizinische Mikrobiologie, Universität Zürich, 8028 Zürich, Switzerland4
Received 20 October 2000/Returned for modification 28 December
2000/Accepted 26 February 2001
Pathogenic microorganisms possess antioxidant defense mechanisms
for protection from reactive oxygen metabolites which are generated
during the respiratory burst of phagocytic cells. These defense
mechanisms include enzymes such as catalase, which detoxifies reactive
oxygen species, and DNA repair systems, which repair damage resulting
from oxidative stress. To (i) determine the relative importance of the
DNA repair system when oxidative stress is encountered by the
Mycobacterium tuberculosis complex during infection of the host and to (ii) provide improved mycobacterial hosts as live carriers to express foreign antigens, the recA locus was
inactivated by allelic exchange in Mycobacterium bovis
BCG. The recA mutants are sensitive to
DNA-damaging agents and show increased susceptibility to metronidazole,
the first lead compound active against the dormant M.
tuberculosis complex. Surprisingly, the recA
genotype does not affect the in vitro dormancy response, nor
does the defect in the DNA repair system lead to attenuation as
determined in a mouse infection model. The recA mutants
will be a valuable tool for further development of BCG as an antigen
delivery system to express foreign antigens and as a source of a
genetically stable vaccine against tuberculosis.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.6.3562-3568.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Mycobacterium bovis BCG recA
Deletion Mutant Shows Increased Susceptibility to DNA-Damaging Agents
but Wild-Type Survival in a Mouse Infection Model
*
Corresponding author. Mailing address: Institut
für Medizinische Mikrobiologie, Medizinische Hochschule Hannover,
Carl-Neuberg-Str. 1, 30625 Hannover, Germany. Phone: 511-532-4348. Fax:
511-532-4366. E-mail: Sander.peter{at}gmx.de.
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