Interplay between host genetic variation and parasite transmission in the Biomphalaria glabrata–Schistosoma mansoni system

Abstract

Genetic variability is often predicted to enhance host fitness in the face of parasitism, yet this idea is rarely tested in an experimental setting, particularly with animal hosts. To assess this question, we used a relatively resistant line of snail hosts (Biomphalaria glabrata) to generate inbred and outcrossed progeny that were then either exposed or sham-exposed to the trematode parasite, Schistosoma mansoni. Results showed no difference in prevalence between the groups; however, large differences appeared in other host life history traits, particularly reproduction. Outcrossed progeny produced large numbers of eggs relative to inbred progeny especially in the face of infection. Furthermore, eggs produced by outcrossed snails took less time to hatch and exhibited greater hatching success compared to their inbred counterparts. Parasite reproduction demonstrated the opposite trend, with fewer parasites emerging from outcrossed snails compared to inbred individuals. This work shows that the introduction of genetic variation into inbred snail populations can have important implications for the viability of host populations and disease transmission.

Effects of host outcrossing on the interaction between an aquatic snail and its locally adapted parasite

“…Prevalence observations reflect those from our previous experiment using a single resistant line of B. glabrata (Sandland et al 2007). Taken together, these prevalence results were somewhat unexpected given that outcrossing has been associated with reduced infection in other host-parasite systems (Meagher 1999;Acevedo-Whitehouse et al 2003).…”

“…Another possibility is that alleles dictating susceptibility in B. glabrata varied little between laboratory and field stocks, allowing for high infections in both inbred and outcrossed progeny. However, the distinct evolutionary histories between snail stocks and the relatively high levels of microsatellite heterozygosity (Sandland et al 2007) in outcrossed relative to inbred individuals make this explanation less likely.…”

“…Remaining snails from each isofemale line were used in the breeding regimes outlined below. This work focuses on the three susceptible snail lines as results from the resistant line have been published elsewhere (Sandland et al 2007). …”

“…In order to complement previous work using a resistant snail line (Sandland et al 2007), we generated inbred and outcrossed treatments using multiple susceptible isofemale lines to address three main questions: (1) do outcrossed snails exhibit reduced infection prevalence and increased hemocyte levels relative to inbred hosts? ; (2) do the lifehistory responses of outcrossed and inbred hosts differ in the presence of successful S. mansoni infection?…”

Identification of differentially expressed genes in Oncomelania hupensis chronically infected with Schistosoma japonicum

“…Over the past 10 years, many studies which have sought to decipher the schistosome-snail interaction have made much advance through proteomics (Vergote et al, 2005;Bouchut et al, 2006;Guillou et al, 2007a;Roger et al, 2008), functional genomics (Miller et al, 2001;Raghavan et al, 2003;Nowak et al, 2004;Hertel et al, 2005;Lockyer et al, 2007a;Adema et al, 2010;Ittiprasert et al, 2010), and population genetics (Brandt et al, 2007;Sandland et al, 2007;Oliveira et al, 2008). Although the current understanding of schistosome and snail biology during the infection process is still incomplete, especially regarding the snail immunity (Bayne, 2009), a variety of molecules have been identified and may be associated with schistosome survival or snail defense mechanisms, including certain proteolytic enzymes such as cysteine proteases (Lodes and Yoshino, 1989;Guillou et al, 2007a;Humphries and Yoshino, 2008;Ittiprasert et al, 2010), receptor recognition molecules (e.g., fibrinogen-related proteins (FREPs) and lectin (Johnston and Yoshino, 2001;Hertel et al, 2005;Zhang et al, 2007;Ittiprasert et al, 2010)), molecules related to cell adhesion and signaling pathways (Goodall et al, 2006;Lockyer et al, 2007b;Zhang et al, 2007;Ittiprasert et al, 2010), and immune regulation-like epitope mimics (Plows et al, 2005;Lockyer et al, 2007b;Lehr et al, 2008).…”