%0 Journal Article
%T Human Polymorphisms as Clinical Predictors in Leprosy
%A Ernesto Prado Montes de Oca
%J Journal of Tropical Medicine
%D 2011
%I Hindawi Publishing Corporation
%R 10.1155/2011/923943
%X Genetic and serum markers in human host can predict leprosy susceptibility per se as well as be useful in classification and/or prediction of clinical variants and immunological responses in leprosy. Adequate and timely assessment of potential risks associated with these 38 host leprosy genes could diminish epidemiological burden and improve life quality of patients with this still prevalent mycobacterial disease. 1. Introduction In recent years, evidence has accumulated for so-called human ¡°multidisease susceptibility genes¡± that play a role in several infectious and noninfectious diseases [1], and genes presumably more specific on its clinical impact when dysfunctional, that probably do not predispose to the disease per se but to a clinical phenotype when the disease is already present [2]. A decline in leprosy research, probably for the erroneous belief that the battle is won, has left unanswered questions regarding the exact mechanism of disease infection and progression. Addressing these questions could help in the final eradication of leprosy [3]. Human leprosy (or Hansen disease) is a chronic granulomatous infectious disease caused by the obligate intracellular organism Mycobacterium leprae [4, 5]. Leprosy is still an important health problem worldwide, with the highest incidences in Asia, Africa, and Latin America [6]. In 2008, ~250,000 new cases of leprosy were reported to World Health Organization [7]. The high concordance rates for leprosy infection when monozygotic and dizygotic twins are compared (84.55% versus 18.35%, resp., media of two independent reports) [7] as well as loci that are linked or associated with leprosy, reveal a strong genetic component in the susceptibility and response to the infection with M. leprae. Furthermore, complex segregation analyses suggest an oligogenic model of leprosy susceptibility, with a few major genes influencing disease and several additional genes and variations causing subtle effects on disease outcome [8]. The origin of transmission of M. leprae is mainly from untreated lepromatous patients [9] and the people most probable infected (leprosy per se) are patient¡¯s contacts whose carry susceptibility alleles in loci 20p12 [10], TNFA [11], as well as PARK2 and PACRG genes [12]. Genetic variants in human host, mainly single nucleotide polymorphisms (SNPs) can predict susceptibility to leprosy per se and to clinical variants when leprosy is already present [2, 8, 13]. Even when death due to leprosy, caused by laryngeal obstruction, is uncommon [14], adequate and opportune detection of potential risks
%U http://www.hindawi.com/journals/jtm/2011/923943/