Abstract
BackgroundParasites can either respond to differences in immune defenses that exist between individual hosts plastically or, alternatively, follow a genetically canalized (“hard wired”) program of infection. Assuming that large-scale functional plasticity would be discernible in the parasite transcriptome we have performed a dual RNA-seq study of the lifecycle of Eimeria falciformis using infected mice with different immune status as models for coccidian infections.ResultsWe compared parasite and host transcriptomes (dual transcriptome) between naïve and challenge infected mice, as well as between immune competent and immune deficient ones. Mice with different immune competence show transcriptional differences as well as differences in parasite reproduction (oocyst shedding). Broad gene categories represented by differently abundant host genes indicate enrichments for immune reaction and tissue repair functions. More specifically, TGF-beta, EGF, TNF and IL-1 and IL-6 are examples of functional annotations represented differently depending on host immune status. Much in contrast, parasite transcriptomes were neither different between Coccidia isolated from immune competent and immune deficient mice, nor between those harvested from naïve and challenge infected mice. Instead, parasite transcriptomes have distinct profiles early and late in infection, characterized largely by biosynthesis or motility associated functional gene groups, respectively. Extracellular sporozoite and oocyst stages showed distinct transcriptional profiles and sporozoite transcriptomes were found enriched for species specific genes and likely pathogenicity factors.ConclusionWe propose that the niche and host-specific parasite E. falciformis uses a genetically canalized program of infection. This program is likely fixed in an evolutionary process rather than employing phenotypic plasticity to interact with its host. This in turn might limit the potential of the parasite to adapt to new host species or niches, forcing it to coevolve with its host.
Highlights
Parasites can either respond to differences in immune defenses that exist between individual hosts plastically or, alternatively, follow a genetically canalized (“hard wired”) program of infection
We investigated parasite development and transcriptomes in a mouse strain which is severely limited in adaptive immune responses (Rag1−/−; “immunocompromised” hereafter) with Rag1−/− and the respective isogenic background strain (C57BL/6 as control) at day 5 post infection
A strong reduction of parasite 18S rRNA in the challenge infection down to 3.5% of the amount measured in naïve hosts was detected in reverse transcription quantitative PCR (RTqPCR) in NMRI hosts (Fig. 1c)
Summary
Parasites can either respond to differences in immune defenses that exist between individual hosts plastically or, alternatively, follow a genetically canalized (“hard wired”) program of infection. The presence of predators is known to alter, e.g., developmental programs of genetically identical prey animals to produce different phenotypes (reviewed in [2]). Infections by pathogens are known to alter host phenotypes: all non-constitutive immune reactions can be regarded as a manifestation of plasticity [3]. For many parasite species it remains unclear whether differences in pathology are due to parasites’ genotypic or phenotypic (plastic) differences, the latter resulting from host-parasite interactions, e.g., host immune responses. It is unclear to which extent such differences a) are passively imposed on the parasite, or b) an adaptive response of the parasite Such adaptive plasticity might be a determinant of the extent of host specialisation, the likelihood of host-switches and eliminately the degree to which co-speciation and coadaptation (together defining co-evolution) are observed
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