Infection and Immunity, February 2009, p. 927, Vol. 77, No. 2
0019-9567/09/$08.00+0 doi:10.1128/IAI.01368-08
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Laboratory of Infection Biology, The Rockefeller University, Weill Medical College of Cornell University, New York, New York; Department of Microbiology and Immunology, University of California, San Francisco, California; and Howard Hughes Medical Institute, Albert Einstein College of Medicine, Bronx, New York
Volume 72, no. 9, pages 5315-5321, 2004. During follow-up studies, we have discovered that the three counterimmune mutant strains described in this article had lost the ability to produce phthiocerol dimycocerosate (PDIM), a complex lipid required for full virulence of Mycobacterium tuberculosis in mice. We now believe that the phenotypes originally attributed to the transposon insertions in these mutants were in fact due to the spontaneous loss of PDIM production in these strains, independent of the transposon insertions. The conclusions of this article should be reevaluated in light of this new information.
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