Pathogenesis and innate immune response to the microsporidian Ecytonucleospora (Enterocytozoon) hepatopenaei (EHP) infection in shrimp

Ecytonucleospora hepatopenaei (EHP) is a microsporidian parasite that causes growth retardation and size variation, resulting in severe economic losses.In this review, we summarize the pathogenesis and host immune response to the EHP infection and highlight recent studies that are progressing our understanding on the EHP infection mechanism.EHP forms environmentally resistant spores as parts of its life cycle.The characteristics of the EHP spores vary between different shrimp hosts.EHP utilizes an invasion organelle called the polar tube to infect the host.The polar tube is used as a conduit to transfer EHP's nucleus and possibly other infectious cargos into host cytoplasm.EHP contains a compacted genome with 3.26 Mbp in size.Several metabolic genes are absent in EHP, making EHP rely solely on host for nutrients.EHP-infected shrimp are more susceptible for secondary infections.Transcriptomic and proteomic analyses of EHP-infected shrimp identified several immune genes and proteins that are differentially expressed after the parasite infection.Immune signaling pathways such as Toll, JAK/STAT pathways and the prophenoloxidase-activating cascade are mainly induced while apoptosis might be suppressed to facilitate the EHP invasion.Antimicrobial peptides such as a c-type lysozyme reduce EHP infection by inhibiting EHP spore germination while lectins promote spore aggregation.Oxidative stress contributes to the pathology of EHP and the antioxidant system balancing the excess reactive oxygen species to protect host cell damage.Further research on pathogenesis mechanisms and host-pathogen responses is required for developing and implementing strategies for prevention and control of EHP infection.