A transcription factor that is probably redox-responsive. Probably plays a role in immunomodulation and reactivation after chronic infection. Its induction results in transcription of a number of genes including sigM, and the genes for 2 type VII secretion systems ESX-2 and ESX-4. Seems to negatively regulate its own expression. The apo-form has been shown to act as a protein disulfide reductase. The apo- but not holo-form probably binds DNA. Binds 1 [4Fe-4S] cluster per subunit. Contains 1 [2Fe-2S] cluster after reconstitution of overexpressed protein from E.coli. Following nitrosylation of the [4Fe-4S] cluster binds 1 [4Fe-8(NO)] cluster per subunit. Maximal expression during progressive infection is between 2-4 weeks, however low, stable expression during chronic infection. The Fe-S cluster can be nitrosylated by nitric oxide (NO). Upon Fe-S cluster removal intramolecular disulfide bonds are formed. Fully oxidized recombinant protein tagged at both termini. Fully reduced recombinant protein tagged at both termini. Not essential in culture. Gives an attenuated infection during both progressive and chronic mouse infections. Mice infected with the disrupted strain induce a stronger host immune response than wild-type. Growth inhibited by S-nitrosoglutathione (GSNO), a source of glutathione and nitric oxide. Mutant cells are less metabolically active. When chronic infection was reactivated by corticosterone the mutant strain was not able to resume growth, suggesting that WhiB5 might be involved with bacillary proliferation during reactivation. Belongs to the WhiB family.