Interaction of mycobacterium tuberculosis with the host cells: a focus in the molecular mechanism involved in trafficking and autophagy

Abstract

Tuberculosis (TB) is an ancient disease remaining a serious health threat worldwide. It is caused by Mycobacterium tuberculosis (Mtb), an acid-fast bacilli, non-sporulated, slow-growing, immobile and aerobic. The pathogenesis of the disease is based on its ability to multiply and survive within phagocytic cells of the host, particularly macrophages and monocytes. The majority (90 %) of infected humans have a ?latent infection?, meaning they efficiently contain but do not spread the bacteria; they are infected but asymptomatic and not contagious. However the remaining 10 % have a lifetime risk of reactivating the infection and developing active tuberculosis (Sakamoto, 2012). The great destructive impact on public health, the co-infection with the human immunodeficiency virus (HIV) and the appearance of drug resistant strains of Mtb are demanding the development of new tools for prevention and treatment.During the last decade a greater understanding on the human immune response to Mtb infection as well as the contribution of factors linked to the pathogenesis of the disease has been achieved. Although the knowledge about the human immune response against Mtb as well as the contribution of factors linked to the pathogenesis of the disease have markedly increased in the last year, a deeper understanding of its immunopathogenesis will lead to the identification of new drugs and the development of effective vaccines.