Genetic variation increases risk of leprosy: Study

A study published in the Plos One journal has revealed why certain sections of population are more prone to leprosy than others. India ranks the first in terms of both prevalence and new cases of leprosy, which is about 58 per cent of the global disease burden.

The study was led by a team of German and Indian scientists from four institutions, Institute of Tropical Medicine, University of Tübingen, Germany, Lepra - Blue Peter Public Health and Research Centre, Centre for Cellular and Molecular Biology, and School of Life Sciences, Bharathiar University, Coimbatore.

The team investigated possible contribution of variations in genes which are vital for immunological control of bacterial pathogen. A case control study design was employed with Indian leprosy patients either with a few bacteria (paucibacillary) or more bacteria (multibacillary) forms of leprosy, along with infection-free individuals from the same ethnic population.

The human body identifies this bacterial pathogen by an immune receptor molecule called nucleotide oligomerisation domain (NOD). The authors investigated into the contribution of mutations in three immune recognition genes namely the NOD2- nucleotide oligomerisation domain, RIPK2 (Receptor-interacting serine-threonine kinase 2), and LRRK2 (Leucine rich reporter kinase 2).

The study found that the mutation in the LRRK2 gene increases the risk of leprosy in the Indian population.  


“The results increase our understanding on complex molecular and cellular mechanisms that are regulated by the pathogen mycobacterium leprae during its clinical course and points to additional genetic factors that may explain the extraordinary predominance of leprosy in the Indian sub-continent,” said Thirumalaisamy Velavan, lead author of this study.

“We have investigated individuals with different genetic and immunological profiles at cellular and genetic levels and found significant genetic difference between leprosy patients and normal individuals,” said K Thangaraj of CCMB.

Comments (+)