The surviving latent individuals will experience one of the two mutually exclusive events to leave the latent compartment, naturally progressing into infectious class, or receiving the treatment.
The adaptation to hypoxic conditions, and to nutrient starvation [14], is thought to be, at least partly, responsible for its ability to survive in a latent state for long periods in humans [9] [10], [15], [16].
Understanding the mechanisms used by MTB to enter into, survive, and reactivate from latent disease states is critical given the global burden of tuberculosis and the dwindling number of effective TB treatments to combat the emergence of multi-drug resistant (MDR) and extensively drug resistant (XDR) strains.
Patients 1 and 2 had recurrences over prolonged periods, which indicated a capacity for G. bethesdensis to survive in a clinically latent state.
The latent virus can survive in the neurons throughout the life of the host and may reactivate in response to various stimuli after the reversal of viral gene silencing [ 3, 5– 8].
It would certainly be important to determine whether the infected cells can undergo same level of lytic replication, survive and is eventually switch to latent infection and transformation or whether only a committed number of cells in the population goes lytic replication, dies but is critical for the remainder of the population to survive and B transformed.
The pathogens adapt to the stressed conditions and can survive over years in the so-called latent state.
Cytomegaloviruses (CMVs), members of the herpesvirus family, have evolved a variety of mechanisms to evade the immune response to survive in infected hosts and to establish latent infection.
After a short phase of acute toxoplasmosis the infection proceeds into its latent phase when cysts are formed and these survive for the rest of the host's life, mainly in neural and muscular tissues.
The individuals may survive 1 year, 2 years, …, or 75 years after becoming TB latent.
Latent infections caused by this organism are due to its ability to survive intracellularly in phagocytic and non-phagocytic cells for many years while avoiding host immune responses [ 4].
