Schistosomiasis is the second most widespread human parasitic disease after malaria. It is reported to be endemic in more than 78 countries in the tropical and subtropical areas, in Africa, Asia and Americas. Around 200 million people are estimated to be infected all over the world, with 200 000 death per year (Chitsulo et al., 2000). Infection is caused by a trematode parasite of the genus Schistosoma, which comprises 22 different species. Three of them, Schistosoma mansoni, S. heamatobium and S. japonicum are mainly responsible for human infections. S. mansoni is the causative agent of intestinal schistosomiasis and it is vectored by a freshwater snail from the genus Biomphalaria (Basch, 1976). The compatibility between the pathogen and its host is determined by two main factors, the susceptibility of the host and the infectivity of the parasite. In Biomphalaria, this host/pathogen compatibility is determined by genetic factors but can also be modulated by nongenetic factors, such as temperature (Knight et al., 2015), pollution (Ibrahim, 2006) or UV exposure (Ruelas et al., 2009), and could also be influenced by its microbiota composition. The microbiota of an organism is constituted of all microbial organisms, such as bacteria, fungi and viruses that live within the host in a mutualistic interaction. The microbiota is known to impact host evolution and adaptation by affecting several fitness parameters (Bosch and McFall-Ngai, 2011; Zilber-Rosenberg and Rosenberg, 2008). Notably, it has been shown to play a key role in the interaction between a host and its pathogens. In the mosquito Anopheles gambiae, the microbial flora can limit the infection with Plasmodium falciparum by inhibiting the development of the parasite within the host (Dong et al., 2009). More specifically, although viruses have often been characterized by their pathogenic and harmful effects, they are also an integral part of the microbiota and they can modulate host-parasite interaction in invertebrates (Martinez et al., 2015; Pradeu, 2016). For example, PolyDNA viruses are able to manipulate the immune system of parasitoid wasps (Burke and Strand, 2012), while SSRNA DcPv can modify the behavior of a ladybird parasitized by a parasitoid wasp to protect the parasitoid larvae (Dheilly et al., 2015b). More generally, it is widely accepted that viruses can control the immune system of their host for