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Is host-schistosome coevolution going anywhere?

ABSTRACT: BACKGROUND:That pathogens and hosts coevolve is a powerful concept with broad theoretical and applied implications spanning from genetic theory to the medical and veterinary sciences, particularly in the context of infectious disease epidemiology. A substantial body of theory has been developed to explore the likelihood and consequences of coevolution, but few empirical studies have been conducted to test these theories, particularly for indirectly-transmitted pathogen-host systems. We initiated replicate longitudinal host-schistosome co-selection trials under different host genotype combinations: Schistosoma mansoni parasite lines were co-selected with populations of either previously resistant-selected Biomphalaria glabrata host genotypes, or unselected susceptible B. glabrata genotypes, or a mixed population of the two. All parasite lines were also passaged through their obligatory mammalian definitive host at each generation. RESULTS:We demonstrated variation in, and a reciprocal impact on, the fitness of both host and pathogen phenotype and genotype, an outcome dependent on the combinations of genotypes involved, and evidence of change over time. Most apparent was the observation that parasites appeared to rapidly adapt to those intermediate hosts previously selected for resistance. CONCLUSION:Our results illustrate the potential for host-schistosome coevolution and, in particular, suggest that host resistance may be a temporary phenomenon in nature due, in part, to rapid counter-adaptations by parasites.

SUBMITTER: Webster JP

PROVIDER: S-EPMC1920509 | biostudies-literature | 2007 Jun

REPOSITORIES: biostudies-literature

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Is host-schistosome coevolution going anywhere?

Webster Joanne P JP Shrivastava Jaya J Johnson Paul J PJ Blair Lynsey L

BMC evolutionary biology 20070613

<h4>Background</h4>That pathogens and hosts coevolve is a powerful concept with broad theoretical and applied implications spanning from genetic theory to the medical and veterinary sciences, particularly in the context of infectious disease epidemiology. A substantial body of theory has been developed to explore the likelihood and consequences of coevolution, but few empirical studies have been conducted to test these theories, particularly for indirectly-transmitted pathogen-host systems. We i ...[more]

PMID: 17567519

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Project description:BackgroundHytrosaviruses (SGHVs; Hytrosaviridae family) are double-stranded DNA (dsDNA) viruses that cause salivary gland hypertrophy (SGH) syndrome in flies. Two structurally and functionally distinct SGHVs are recognized; Glossina pallidipes SGHV (GpSGHV) and Musca domestica SGHV (MdSGHV), that infect the hematophagous tsetse fly and the filth-feeding housefly, respectively. Genome sizes and gene contents of GpSGHV (~ 190 kb; 160-174 genes) and MdSGHV (~ 124 kb; 108 genes) may reflect an evolution with the SGHV-hosts resulting in differences in pathobiology. Whereas GpSGHV can switch from asymptomatic to symptomatic infections in response to certain unknown cues, MdSGHV solely infects symptomatically. Overt SGH characterizes the symptomatic infections of SGHVs, but whereas MdSGHV induces both nuclear and cellular hypertrophy (enlarged non-replicative cells), GpSGHV induces cellular hyperplasia (enlarged replicative cells). Compared to GpSGHV's specificity to Glossina species, MdSGHV infects other sympatric muscids. The MdSGHV-induced total shutdown of oogenesis inhibits its vertical transmission, while the GpSGHV's asymptomatic and symptomatic infections promote vertical and horizontal transmission, respectively. This paper reviews the coevolution of the SGHVs and their hosts (housefly and tsetse fly) based on phylogenetic relatedness of immune gene orthologs/paralogs and compares this with other virus-insect models.ResultsWhereas MdSGHV is not vertically transmitted, GpSGHV is both vertically and horizontally transmitted, and the balance between the two transmission modes may significantly influence the pathogenesis of tsetse virus. The presence and absence of bacterial symbionts (Wigglesworthia and Sodalis) in tsetse and Wolbachia in the housefly, respectively, potentially contributes to the development of SGH symptoms. Unlike MdSGHV, GpSGHV contains not only host-derived proteins, but also appears to have evolutionarily recruited cellular genes from ancestral host(s) into its genome, which, although may be nonessential for viral replication, potentially contribute to the evasion of host's immune responses. Whereas MdSGHV has evolved strategies to counteract both the housefly's RNAi and apoptotic responses, the housefly has expanded its repertoire of immune effector, modulator and melanization genes compared to the tsetse fly.ConclusionsThe ecologies and life-histories of the housefly and tsetse fly may significantly influence coevolution of MdSGHV and GpSGHV with their hosts. Although there are still many unanswered questions regarding the pathogenesis of SGHVs, and the extent to which microbiota influence expression of overt SGH symptoms, SGHVs are attractive 'explorers' to elucidate the immune responses of their hosts, and the transmission modes of other large DNA viruses.

Project description:Schistosomiasis is a debilitating disease that affects over 240 million people worldwide and is considered the most important neglected tropical disease following malaria. Free-swimming freshwater cercariae, one of the six morphologically distinct schistosome life stages, infect humans by directly penetrating through the skin. Cercariae identify and seek the host by sensing chemicals released from human skin. When they reach the host, they burrow into the skin with the help of proteases and other contents released from their acetabular glands and transform into schistosomula, the subsequent larval worm stage upon skin infection. Relative to host invasion, studies have primarily focused on the nature of the acetabular gland secretions, immune response of the host upon exposure to cercariae, and cercaria-schistosomulum transformation methods. However, the molecular signaling pathways involved from host-seeking through the decision to penetrate skin are not well understood. We recently observed that heat shock factor 1 (Hsf1) is localized to the acetabular glands of infectious schistosome cercariae, prompting us to investigate a potential role for heat shock proteins (HSPs) in cercarial invasion. In this study, we report that cercarial invasion behavior, similar to the behavior of cercariae exposed to human skin lipid, is regulated through an Hsp70-dependent process, which we show by using chemical agents that target Hsp70. The observation that biologically active protein activity modulators can elicit a direct and clear behavioral change in parasitic schistosome larvae is itself interesting and has not been previously observed. This finding suggests a novel role for Hsp70 to act as a switch in the cercaria-schistosomulum transformation, and it allows us to begin elucidating the pathways associated with cercarial host invasion. In addition, because the Hsp70 protein and its structure/function is highly conserved, the model that Hsp70 acts as a behavior transitional switch could be relevant to other parasites that also undergo an invasion process and can apply more broadly to other organisms during morphological transitions. Finally, it points to a new function for HSPs in parasite/host interactions.

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Is host-schistosome coevolution going anywhere?

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Is host-schistosome coevolution going anywhere?

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