Photo: Janice Murray & Maizels Laboratory/University of Edinburgh
For example, the leading Discovery Institute (aka Liars For Power and Money, Inc.) propagandist for ID, Michael Behe, avoids completely any reference to the fact that his 'intelligently designed' E. coli flagellum appears to have only one purpose - helping E. coli make us sick.
With their evident discomfort in mind then, it gives me great pleasure to invite creationists to comment on an article and two papers published recently in Science concerning how infection by a parasitic worm (helminth) can appear to aid other parasites by helping them overcome the body's natural immune responses. In particular, I would like them to explain how this phenomenon is better explained by their intelligent-design-by-an-omnibenevolent-designer-who-did-it-all-for-humans model than it is by Darwinian evolution by Natural Selection.
The article, which links directly to the two papers, by Rick M Maizels (Institute for Immunology and Infection Research and Centre for Immunity, University of Edinburgh, Edinburgh, UK) and William C Gause (Center for Immunity and Inflammation, Department of Medicine, New Jersey Medical School, Rutgers - the State University of New Jersey, Newark, NJ, USA) explains how infection by parasitic worms can activate latent infections by herpesvirus by "an exquisite adaptation of the viral genome is a promoter sequence that recognizes STAT6 as well as the prevailing TH2 environment of a helminth-infected host".
In other words, the virus has evolved an 'exquisite' mechanism for recognising and responding to the body's defensive response to infection by another unrelated parasite. Exquisite from the point of view of someone who recognises the exquisite in nature; a malevolent mechanism to anyone who tries to see it in terms of good and evil; an incomprehensible mechanism to someone who tries to force-fit it into a model with a single, omnibenevolent, philanthropic designer. As the authors say:
The findings of Reese et al. and Osborne et al. deepen our perspective of the complexity of infectious diseases, given that multiple colonization is ubiquitous in nature and the interactions between pathogens, commensals, and immunity operate at every level, from genes to tissues and systemic cell populations.
The first paper, by Reese et al., explains how infection by helminths can reactivate herpesviruses including the one associated with Kaposi’s sarcoma because "viral promoters that have evolved to sense host immune status":
Mammals are coinfected by multiple pathogens that interact through unknown mechanisms. We found that helminth infection, characterized by the induction of the cytokine interleukin-4 (IL-4) and the activation of the transcription factor Stat6, reactivated murine γ-herpesvirus infection in vivo. IL-4 promoted viral replication and blocked the antiviral effects of interferon-γ (IFNγ) by inducing Stat6 binding to the promoter for an important viral transcriptional transactivator. IL-4 also reactivated human Kaposi’s sarcoma–associated herpesvirus from latency in cultured cells. Exogenous IL-4 plus blockade of IFNγ reactivated latent murine γ-herpesvirus infection in vivo, suggesting a "two-signal model for viral reactivation. Thus, chronic herpesvirus infection, a component of the mammalian virome, is regulated by the counterpoised actions of multiple cytokines on viral promoters that have evolved to sense host immune status.
The second paper, by Lisa C. Osborne et al., shows how parasitic worms in the intestine interact with the resident bacteria and viruses normally found there.
The mammalian intestine is colonized by beneficial commensal bacteria and is a site of infection by pathogens, including helminth parasites. Helminths induce potent immunomodulatory effects, but whether these effects are mediated by direct regulation of host immunity or indirectly through eliciting changes in the microbiota is unknown. We tested this in the context of virus-helminth coinfection. Helminth coinfection resulted in impaired antiviral immunity and was associated with changes in the microbiota and STAT6-dependent helminth-induced alternative activation of macrophages. Notably, helminth-induced impairment of antiviral immunity was evident in germ-free mice, but neutralization of Ym1, a chitinase-like molecule that is associated with alternatively activated macrophages, could partially restore antiviral immunity. These data indicate that helminth-induced immunomodulation occurs independently of changes in the microbiota but is dependent on Ym1.
In evolutionary terms, exquisite and delightful though these evolved mechanisms might be, they are entirely unsurprising and are even predictable. Since each mechanism promotes the survival and replication of the genes which promote it, and with no regard for the effects this might have on the host provided it doesn't actually kill the host too quickly, this is precisely what we would expect of 'selfish' genes being favoured by natural selection, if this produces more copies in future generations.
It is totally incomprehensible as the product of intelligent, planned design by a philanthropic, benevolent designer, however. No such designer would design parasites in the first place, then design a system for fighting them, then to design other parasites to exploit that system whilst redesigning the original parasite to overcome the host's resistance. To do anything resembling such a thing intentionally would be the very antithesis of benevolence. Perhaps, and I accept that this is probably a forlorn hope because it requires creationists to examine their assumptions and contemplate the possibility of being wrong, a creationist can explain how exactly this fits in with their 'Intelligent Design' form of biblical literalism, complete with a magic designer who does everything because it loves us.
And please don't invoke the circular 'ineffable' argument where you define 'good' as whatever your hypothetical designer does, then claim it as evidence for a benevolent designer because it's 'good', regardless of the harm it actually does, whilst settling for an unexplained mystery as your best explanation. Remember, you have to come up with something at least as complete as the current scientific explanation, together with supporting evidence, not just something different. Simply defining something that makes people sick and die betrays your moral bankruptcy and shows how you've abandoned any moral responsibility for your beliefs and actions.
* Copyright © 2014, American Association for the Advancement of Science