Diversity and Plasticity of Virulent Characteristics of Entamoeba histolytica

Abstract

The complexity of clinical syndromes of amebiasis, caused by the parasite Entamoeba histolytica, stems from the intricate interplay between the host immune system, the virulence of the invading parasite, and the surrounding environment. Although there is still a relative paucity of information about the precise relationship between virulence factors and the pathogenesis of Entamoeba histolytica, by accumulating data from clinical and basic research, researchers have identified essential pathogenic factors that play a critical role in the pathogenesis of amebiasis, providing important insights into disease development through animal models. Moreover, the parasite’s genetic variability has been associated with differences in virulence and disease outcomes, making it important to fully understand the epidemiology and pathogenesis of amebiasis. Deciphering the true mechanism of disease progression in humans caused by this parasite is made more difficult through its ability to demonstrate both genomic and pathological plasticity. The objective of this article is to underscore the heterogeneous nature of disease states and the malleable virulence characteristics in experimental models, while also identifying persistent scientific issues that need to be addressed.

Crystal structure of Trichinella spiralis calreticulin and the structural basis of its complement evasion mechanism involving C1q

“…Meanwhile, TcCRT may play an important role in invading host macrophages by binding to C1q on the surface of trypomastigotes, which triggers phagocytosis ( 10 , 11 ). Entamoeba histolytica ( E. histolytica ) trophozoite–produced calreticulin (EhCRT) plays a similar role in the complement-involved opsonization and phagocytosis of erythrocytes and apoptotic lymphocytes ( 12 – 14 ). In addition to protozoa, helminths also produce CRT proteins that have a similar inhibitory effect on the activation of host complement.…”