Host-parasite relationship in cystic echinococcosis: an evolving story

Abstract

The larval stage of Echinococcus granulosus causes cystic echinococcosis, a neglected infectious disease that constitutes a major public health problem in developing countries. Despite being under constant barrage by the immune system, E. granulosus modulates antiparasite immune responses and persists in the human hosts with detectable humoral and cellular responses against the parasite. In vitro and in vivo immunological approaches, together with molecular biology and immunoproteomic technologies, provided us exciting insights into the mechanisms involved in the initiation of E. granulosus infection and the consequent induction and regulation of the immune response. Although the last decade has clarified many aspects of host-parasite relationship in human cystic echinococcosis, establishing the full mechanisms that cause the disease requires more studies. Here, we review some of the recent developments and discuss new avenues in this evolving story of E. granulosus infection in man.

Figure 1

Major components of the immune response to hydatid cyst fluid in the host: Echinococcus granulosus-derived immune modulators and the main cytokines that regulate this response. Parasite-derived molecules as AgB, EgTeg, and EgEF-1β/δ could elicit a predominant Th2 activation whereas EgTPx and other HCF components can elicit a concomitant Th1/Th2 cell activation.