Mycobacterium tuberculosis (Mtb) is a highly infectious acid-fast bacillus and is known to cause tuberculosis (TB) in humans. It is a leading cause of death from a sole infectious agent, with an estimated 1.5 million deaths yearly worldwide, and up to one third of the world's population has been infected with TB. The virulence and susceptibility of Mtb are further amplified in the presence of Human Immunodeficiency Virus (HIV). Coinfection with Mtb and HIV forms a lethal combination. Previous studies had demonstrated the synergistic effects of Mtb and HIV, with one disease accelerating the disease progression of the other through multiple mechanisms, including the modulation of the immune response to these two pathogens. The response of the endosomal pattern recognition receptors to these two pathogens, specifically toll-like receptors (TLR)-3, -7, and -9, has not been elucidated, with some studies producing mixed results. This article seeks to review the roles of TLR-3, -7, and -9 in response to Mtb infection, as well as Mtb-HIV-coinfection via Toll-interleukin 1 receptor (TIR) domain-containing adaptor inducing INF-β (TRIF)-dependent and myeloid differentiation factor 88 (MyD88)-dependent pathways.
Keywords: HIV; Mycobacterium tuberculosis; Toll-like receptor 3; Toll-like receptor 7; Toll-like receptor 9.