Mycobacterium Leprae–Host-Cell Interactions and Genetic Determinants in Leprosy: an Overview

Abstract

Leprosy, also known as Hansen‘s disease, is a chronic infectious disease caused by Mycobacterium leprae in which susceptibility to the mycobacteria and its clinical manifestations are attributed to the host immune response. Even though leprosy prevalence has decreased dramatically, the high number of new cases indicates active transmission. Owing to its singular features, M. leprae infection is an attractive model for investigating the regulation of human immune responses to pathogen-induced disease. Leprosy is one of the most common causes of nontraumatic peripheral neuropathy worldwide. The proportion of patients with disabilities is affected by the type of leprosy and delay in diagnosis. This article briefly reviews the clinical features as well as the immunopathological mechanisms related to the establishment of the different polar forms of leprosy, the mechanisms related to M. leprae–host cell interactions and prophylaxis and diagnosis of this complex disease. Host genetic factors are summarized and the impact of the development of interventions that prevent, reverse or limit leprosy-related nerve impairments are discussed.

Keywords:

• leprosy
• Mycobacterium leprae
• Schwann cells
• thalidomide
• TNF-α

Financial & competing interests disclosure

This work was supported by IOC/FIOCRUZ, CNPq, Brazil, and in part by the Intramural Research Program of NIH/NIAID. The authors‘ group at the Rockefeller University, NY, USA, had a patent received for the work on thalidomide action developed in 1990/1991. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This work was supported by IOC/FIOCRUZ, CNPq, Brazil, and in part by the Intramural Research Program of NIH/NIAID. The authors‘ group at the Rockefeller University, NY, USA, had a patent received for the work on thalidomide action developed in 1990/1991. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.