While the upregulation of groEL, a member of the hypoxic signature gene of M. tuberculosis [36] that codifies for a chaperon protein during the NRP1 stage, supports the expression of an adaptive response to stress in M. kumamotonense. This indicates the capacity of these bacteria to establish a dormancy-like phenotype and putatively generate latent infections. Here, HSPD1 is linked to disease arising from reactivation of latent virus.