The Convergence of Immunodeficiency and Immunopathology: How HIV and Silocosis Independently and Cooperatively Advance TB

Abstract

Tuberculosis (TB) is an urgent global health problem today, Nine out of every ten human infections with the etiologic agent, Mycobacterium tuberculosis, are effectively controlled by host immune responses. However, as one third of the world harbors this pernicious bacterium within their bodies, this pathogen still manages to lead to an unparalleled amount of destruction. Last year alone, there were 8.6 million new cases of active TB and1.3 million fatalities, equating to one death every 22 seconds. This epidemic is sustained at such high levels in part due to the contributions of co-morbid human immunodeficiency virus(HIV) infection and silicosis accelerating the incidence of TB.HIV+ persons develop active TB at 21–34 times the rate of their non-infected counterparts. Silicosis, the most common of all occupationally-acquired diseases, is a lung condition resulting from the inhalation of silica dust. Epidemiological studies have found that, depending upon the severity of disease, silicosis increases the risk of developing TB between 2.9 and 39 times. Where silicosis and HIV are both present, risk of TB raises even higher. This investigation examined how silicosis and HIV individually and cooperatively induce increased risk of TB. Several different impacts of each HIV and silicosis upon host innate and adaptive immunity were identified to mediate increased susceptibility to TB.