Tuberculosis is caused by the bacterium Mycobacterium tuberculosis, which primarily infects the lungs but can spread to other organs. Research shows that much of the global population carries the bacterium without symptoms. These latent infections pose a key challenge because only a fraction progress to active disease, yet they form a vast reservoir for future cases and transmission.

Recent work has focused on how the pathogen survives for years inside the host. The bacteria can enter a dormant state within structures called granulomas, where the immune system walls off infection but rarely eliminates it. Studies show that bacterial metabolic pathways adjust to low oxygen and nutrient levels, helping them persist. Understanding these adaptations is crucial for designing drugs that can kill non‑replicating bacteria.

Drug resistance is another central research area. Multi‑drug resistant and extensively drug resistant tuberculosis have emerged through mutations that alter drug targets or increase drug efflux. Genomic analyses are mapping these mutations, enabling rapid molecular tests that guide treatment. New drug regimens are being tested to shorten therapy and overcome resistance by targeting multiple bacterial pathways simultaneously.

On the host side, researchers are dissecting immune responses that distinguish protection from disease. Specific T cell responses and inflammatory signals appear to influence whether infection is contained or progresses. This knowledge is feeding into vaccine development. New vaccine candidates aim either to prevent infection or to boost immunity in people already infected, improving on the limited protection of the existing BCG vaccine. Together, these lines of research seek to reduce tuberculosis burden and halt its spread.