ncRNAs: an unexplored cellular defense mechanism in leprosy

Front Genet. 2023 Dec 4:14:1295586. doi: 10.3389/fgene.2023.1295586. eCollection 2023.

Abstract

Leprosy is an infectious disease primarily caused by the obligate intracellular parasite Mycobacterium leprae. Although it has been considered eradicated in many countries, leprosy continues to be a health issue in developing nations. Besides the social stigma associated with it, individuals affected by leprosy may experience nerve damage leading to physical disabilities if the disease is not properly treated or early diagnosed. Leprosy is recognized as a complex disease wherein socioenvironmental factors, immune response, and host genetics interact to contribute to its development. Recently, a new field of study called epigenetics has emerged, revealing that the immune response and other mechanisms related to infectious diseases can be influenced by noncoding RNAs. This review aims to summarize the significant advancements concerning non-coding RNAs in leprosy, discussing the key perspectives on this novel approach to comprehending the pathophysiology of the disease and identifying molecular markers. In our view, investigations on non-coding RNAs in leprosy hold promise and warrant increased attention from researches in this field.

Keywords: Mycobacterium leprae; immunity; infection; leprosy; miRNAs; ncRNAs.

Publication types

  • Review

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This study was supported by the Brazilian National Research Council (CNPq) 407922/2021-0, the Coordination for Higher Education Personnel Training (CAPES) 3381/2013, the Amazonian Research Foundation (FAPESPA), the VALE S.A. 27756/2019 and by the PROPESP/PROEX/UFPA. None of these organizations had any role in the design of the study, collection or analysis of the data, the decision to publish the manuscript, or its preparation. The contents of this study are the responsibility of the authors.