**6. Role of genetic characteristics of the infecting strains in the pathogenesis of amoebiasis**

The outcome of an infection may depend on several factors among which the genetic characteristics of the specific pathogen have been identified as an important one. Few polymorphic genetic loci have been identified and targeted to aid in the study of the population structure of *E. histolytica* strains and their possible relationships with the parasite's virulence and disease outcome (Clark, 2006; Paul et al., 2007). Examples of these genetic markers include protein coding genes (serine – rich *E. histolytica* protein, [SREHP] and Chitinase) and non-coding DNA (Strain Specific Gene and tRNA gene linked short tandem repeats [STR]) of PCR-amplified genes (Haghighi et al., 2003; Samie et al., 2008). In a study in Bangladesh, the tRNA-linked STR genotyping system has provided evidence that the parasite genome does influence the outcome of infection. tRNA-linked STR genotyping was also behind the recent observation of differences between parasite genotypes in the intestine and the liver abscess of same patients (Ali et al., 2007). Few studies, albeit inconclusive, using the polymorphic SREHP marker have indicated that certain SREHP profiles might be responsible for the presentation of intestinal amoebic symptoms (Ayehkumi et al., 2001; Samie et al., 2008). Yet, all studies with SREHP marker did support previous findings of extensive genetic diversity among *E. histolytica* isolates from the same

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geographic origin (Ayeh-kumi et al., 2001; Simonishvili et al., 2005; Samie et al., 2008; Tanyuksel et al., 2008). Thus, it seems that the parasite genotype does play a role in the outcome of infection in humans thus linking parasite diversity and virulence. Other approaches, such as SNP identification coupled with microarray-based analysis of gene expression or proteomic comparisons among parasites will be needed to identify the actual genes responsible for these results and to help us understand the mechanism of parasite virulence and pathogenesis (Ali et al., 2008).
