The Compatibility Between Biomphalaria glabrata Snails and Schistosoma mansoni (original) (raw)

This review reexamines the results obtained in recent decades regarding the compatibility polymorphism between the snail, Biomphalaria glabrata, and the pathogen, Schistosoma mansoni, which is one of the agents responsible for human schistosomiasis. Some results point to the snail's resistance as explaining the incompatibility, while others support a "matching hypothesis" between the snail's immune receptors and the schistosome's antigens. We propose here that the two hypotheses are not exclusive, and that the compatible/incompatible status of a particular host/parasite couple probably reflects the balance of multiple molecular determinants that support one hypothesis or the other. Because these genes are involved in a coevolutionary arms race, we also propose that the underlying mechanisms can vary. Finally, some recent results show that environmental factors could influence compatibility. Together, these results make the compatibility between B. glabrata and S. mansoni an increasingly complex puzzle. We need to develop more integrative approaches in order to find targets that could potentially be manipulated to control the transmission of schistosomiasis. 2 THE GENETIC DETERMINISM OF THE COMPATIBILITY/INCOMPATIBILITY OF BIOMPHALARIA GLABRATA AND SCHISTOSOMA MANSONI The low prevalence of snails with patent schistosome infection, which is usually observed in transmission foci (Anderson and May 1979; Sire et al., 1999), was first believed to be explained by the low probability of an encounter between the partners. This hypothesis cannot be excluded in the interaction between B. glabrata and S. mansoni. However, a molecular screening approach yielded interesting results regarding the interaction between Schistosoma haematobium and Bulinus globosus snails. This work showed that although patency was often very low (less than 4% shed cercariae), more than 40% of the snails were exposed to the parasite in the field (Allan et al., 2013). Thus, snails experienced high levels of parasitic exposure, but only a small proportion of infected snails reached the stage of cercarial shedding. Moreover, even if snails were penetrated by miracidia, the infections often failed to develop to patency (Allan et al., 2013). These results suggest that nonsusceptibility or incompatibility of a particular host and parasite combination is a major factor in the low prevalence observed in the field. This nonsusceptibility/incompatibility can also reflect a biochemically unfavourable intramolluscan environment for the parasite, which is termed "unsuitability" (Lie and Heyneman, 1977; Sullivan and Richards, 1981). However, the most frequently involved mechanism consists of the recognition, encapsulation and killing of the parasite by immune cells (haemocytes) of the snail (Fig. 1 A). Numerous infection-based experiments have been performed