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Cystic echinococcosis (CE) and alveolar echinococcosis (AE) are life-threatening parasitic infections worldwide caused by  Echinococcus granulosus  ( sensu lato ) and  E. multilocularis , respectively. Very little is known about the factors affecting innate susceptibility and resistance to infection with  Echinococcus  spp. Although benzimidazolic drugs against CE and AE have definitively improved the treatment of these cestodes; however, the lack of successful control campaigns, including the EG95 vaccine, at a continental level indicates the importance of generating novel therapies. This review represents an update on the latest developments in the regulatory functions of innate immune pathways such as apoptosis, toll-like receptors (TLRs), and inflammasomes against CE and AE. We suggest that apoptosis can reciprocally play a bi-functional role among the host- Echinococcus  metabolite relationships in suppressive and survival mechanisms of CE. Based on the available information, further studies are needed to determine whether the orchestrated  in silico  strategy for designing inhibitors and interfering RNA against anti-apoptotic proteins and TLRs would be effective to improve new treatments as well as therapeutic vaccines against the  E. granulosus  and  E. multilocularis.

Recent advances on innate immune pathways related to host–parasite cross-talk in cystic and alveolar echinococcosis