Understanding Immunity through the Lens of Disease Ecology

Hedrick, Stephen M.

doi:10.1016/j.it.2017.08.001

Cited by 14 publications

(5 citation statements)

References 126 publications

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“…The use of controlled environments provides the benefit of structured variables and assumes that the elimination of statistical noise is the fastest track to distilling insights and tackling human disease [13–16]. caveat to this approach, however, is that repeatable phenotypes obtained from inbred strains in artificial settings may exhibit substantial context-dependence when investigated under more natural conditions [14, 15, 17, 18]. Furthermore, cell signaling mechanisms may not necessarily be conserved among organisms owing to varying selection pressures among arthropod species that differentially shape both genotype and phenotype.…”

Section: An Evolving Outlook For Arthropod Vector Immunitymentioning

confidence: 99%

Vector Immunity and Evolutionary Ecology: The Harmonious Dissonance

Shaw

Tate

Levashina

et al. 2018

Trends in Immunology

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Recent scientific breakthroughs have significantly expanded our understanding of arthropod vector immunity. Insights in the laboratory have demonstrated how the immune system provides resistance to infection, and in what manner innate defenses protect against a microbial assault. Less understood, however, is the effect of biotic and abiotic factors on microbial-vector interactions and the impact of the immune system on arthropod populations in nature. Furthermore, the influence of genetic plasticity on the immune response against vector-borne pathogens remains mostly elusive. Herein, we discuss evolutionary forces that shape arthropod vector immunity. We focus on resistance, pathogenicity and tolerance to infection. We posit that novel scientific paradigms should emerge when molecular immunologists and evolutionary ecologists work together.

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Section: An Evolving Outlook For Arthropod Vector Immunitymentioning

confidence: 99%

Vector Immunity and Evolutionary Ecology: The Harmonious Dissonance

Shaw

Tate

Levashina

et al. 2018

Trends in Immunology

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“…This response shapes the within-host ecological milieu in which pathogens proliferate and evolve and, in some cases, can directly contribute to host disease, a phenomenon known as immunopathology (1, 2). To fully understand host–parasite interactions, infection pathology, and host–parasite coevolution, we must therefore quantify the nature and dynamics of the host response to infection (3).…”

mentioning

confidence: 99%

The contribution of host cell-directed vs. parasite-directed immunity to the disease and dynamics of malaria infections

Wale

Jones

Sim

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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Hosts defend themselves against pathogens by mounting an immune response. Fully understanding the immune response as a driver of host disease and pathogen evolution requires a quantitative account of its impact on parasite population dynamics. Here, we use a data-driven modeling approach to quantify the birth and death processes underlying the dynamics of infections of the rodent malaria parasite, Plasmodium chabaudi, and the red blood cells (RBCs) it targets. We decompose the immune response into 3 components, each with a distinct effect on parasite and RBC vital rates, and quantify the relative contribution of each component to host disease and parasite density. Our analysis suggests that these components are deployed in a coordinated fashion to realize distinct resource-directed defense strategies that complement the killing of parasitized cells. Early in the infection, the host deploys a strategy reminiscent of siege and scorched-earth tactics, in which it both destroys RBCs and restricts their supply. Late in the infection, a “juvenilization” strategy, in which turnover of RBCs is accelerated, allows the host to recover from anemia while holding parasite proliferation at bay. By quantifying the impact of immunity on both parasite fitness and host disease, we reveal that phenomena often interpreted as immunopathology may in fact be beneficial to the host. Finally, we show that, across mice, the components of the host response are consistently related to each other, even when infections take qualitatively different trajectories. This suggests the existence of simple rules that govern the immune system’s deployment.

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“…Obligate pathogens need to evade or suppress host immune defences in order to hijack the host's cellular machinery. The success of the pathogen largely depends on how effectively it can enter and replicate within a host cell, and conversely, how successfully the host can inhibit, degrade or tolerate the infectious agent (Hedrick, 2017). Avoidance is often the first defence strategy against an infectious agent (Curtis, 2014;Townsend et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Deformed wing virus genotypes A and B do not elicit immunologically different responses in naïve honey bee hosts

Norton,

Buchmann,

Ashe

et al. 2023

Preprint

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Deformed wing virus(DWV), in association withVarroa destructor, is currently the leading factor associated with global honey bee deaths. With the exception of Australia, the virus and mite have a near global distribution, making it difficult to separate the effect of one from the other. Over time, the prevalence of the two main DWV genotypes (DWV-A and DWV-B) has changed, leading to the suggestion that the two strains elicit a different immune response by the host, the western honey beeApis mellifera. Here we use a honey bee population naïve to both the mite and the virus to investigate if honey bees show a different immunological response to DWV genotypes. We examined the expression of 19 immune genes by RT-qPCR and comprehensively analysed the small RNA response in honey bees after experimental injection with DWV-A and DWV-B. We found no evidence to indicate that DWV-A and DWV-B elicit a different immune response in honey bees. We found that RNA interference genes are up-regulated during DWV infection and that the small interfering RNA (siRNA) response is proportional to viral loads, yet does not inhibit the virus from accumulating to high loads. We also found that the siRNA response towards DWV was weaker than the response to another honey bee pathogen,Black queen cell virus. This suggests that DWV is comparatively better at evading antiviral host defences. There was no evidence for the production of virus-derived PIWI-RNAs in response to DWV infection. In contrast to previous studies, and in the absence ofV.destructor, we found no evidence that DWV has an immunosuppressive effect in honey bees. Overall, our results advance our understanding of the immunological effect DWV elicits in honey bees.

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Understanding Immunity through the Lens of Disease Ecology

Cited by 14 publications

References 126 publications

Vector Immunity and Evolutionary Ecology: The Harmonious Dissonance

Vector Immunity and Evolutionary Ecology: The Harmonious Dissonance

The contribution of host cell-directed vs. parasite-directed immunity to the disease and dynamics of malaria infections

Deformed wing virus genotypes A and B do not elicit immunologically different responses in naïve honey bee hosts

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