Diversity in CRISPR-based immunity protects susceptible genotypes by restricting phage spread and evolution

Common, Jack; Walker‐Sünderhauf, David; Houte, Stineke van; Westra, Edze R.

doi:10.1101/774349

Cited by 8 publications

(18 citation statements)

References 72 publications

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“…The drop in local adaptation with time is consistent with the overall drop in phage density we observed in most phage populations (Figure 2b). This suggests that the phages are losing the coevolutionary arms race with their hosts which is in line with previous studies showing that CRISPR immunity often yields phage extinction in this system [29][30][31]. Besides, we found some evidence that evolution of new immunities may also be due to the second active CRISPR-Cas system (CR3) in this host in which we detected spacer acquisition starting at day 3 or 4 (Table S4).…”

Section: Phage Coevolution Across Space and Timesupporting

confidence: 91%

Competition and coevolution drive the evolution and the diversification of CRISPR immunity

Guillemet

Chabas

Nicot

et al. 2021

Preprint

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The diversity of resistance fuels host adaptation to infectious diseases and challenges the ability of pathogens to exploit host populations [1–3]. Yet, how this host diversity evolves over time remains unclear because it depends on the interplay between intraspecific competition and co-evolution with pathogens. Here we study the effect of a coevolving phage population on the diversification of bacterial CRISPR immunity across space and time. We demonstrate that the negative-frequency-dependent selection generated by coevolution is a powerful force that maintains host resistance diversity and selects for new resistance mutations in the host. We also find that host evolution is driven by asymmetries in competitive abilities among different host genotypes. Even if the fittest host genotypes are targeted preferentially by the evolving phages they often escape extinctions through the acquisition of new CRISPR immunity. Together, these fluctuating selective pressures maintain diversity, but not by preserving the pre-existing host composition. Instead, we repeatedly observe the introduction of new resistance genotypes stemming from the fittest hosts in each population. These results highlight the importance of competition on the transient dynamics of host-pathogen coevolution.

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Section: Phage Coevolution Across Space and Timesupporting

confidence: 91%

Competition and coevolution drive the evolution and the diversification of CRISPR immunity

Guillemet

Chabas

Nicot

et al. 2021

Preprint

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“…The evolution of increased host range is predicted to peak at intermediate levels of host diversity: low diversity results in weak selection for increased host range, because parasites may frequently encounter the same host genotype, whereas high diversity slows the response to selection by limiting the effective population size of the parasite (Benmayor et al 2009;Chabas et al 2018). Consistent with this prediction, Common et al (2020) found that generalist phages evolved readily in bacterial populations with intermediate diversity, but less so when host diversity was low and not at all when it was maximal. Sant et al (2021) similarly found that generalist phages evolved in moderately diverse bacterial populations, where the low probability of repeatedly encountering the same host genotype selected against specialists.…”

Section: How Do Parasites Evolve In Genetically Diverse Host Populati...mentioning

confidence: 89%

Genetic diversity and disease: The past, present, and future of an old idea

Gibson

2021

Evolution

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Why do infectious diseases erupt in some host populations and not others? This question has spawned independent fields of research in evolution, ecology, public health, agriculture, and conservation. In the search for environmental and genetic factors that predict variation in parasitism, one hypothesis stands out for its generality and longevity: genetically homogeneous host populations are more likely to experience severe parasitism than genetically diverse populations. In this perspective piece, I draw on overlapping ideas from evolutionary biology, agriculture, and conservation to capture the far-reaching implications of the link between genetic diversity and disease. I first summarize the development of this hypothesis and the results of experimental tests. Given the convincing support for the protective effect of genetic diversity, I then address the following questions: (1) Where has this idea been put to use, in a basic and applied sense, and how can we better use genetic diversity to limit disease spread? (2) What new hypotheses does the established disease-diversity relationship compel us to test? I conclude that monitoring, preserving, and augmenting genetic diversity is one of our most promising evolutionarily informed strategies for buffering wild, domesticated, and human populations against future outbreaks.

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“… 2005 ; Lively 2010 ), and the protective effect of host variation has been empirically demonstrated in a number of experimental (e.g., Altermatt and Ebert 2008 ; Common et al. 2020 ) and natural systems (Ekroth et al. 2019 ), especially those in which rapid host evolution is unlikely (Gibson and Nguyen 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Mosaic vaccination: How distributing different vaccines across a population could improve epidemic control

2021

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Although vaccination has been remarkably effective against some pathogens, for others, rapid antigenic evolution results in vaccination conferring only weak and/or short‐lived protection. Consequently, considerable effort has been invested in developing more evolutionarily robust vaccines, either by targeting highly conserved components of the pathogen (universal vaccines) or by including multiple immunological targets within a single vaccine (multi‐epitope vaccines). An unexplored third possibility is to vaccinate individuals with one of a number of qualitatively different vaccines, creating a “mosaic” of individual immunity in the population. Here we explore whether a mosaic vaccination strategy can deliver superior epidemiological outcomes to “conventional” vaccination, in which all individuals receive the same vaccine. We suppose vaccine doses can be distributed between distinct vaccine “targets” (e.g., different surface proteins against which an immune response can be generated) and/or immunologically distinct variants at these targets (e.g., strains); the pathogen can undergo antigenic evolution at both targets. Using simple mathematical models, here we provide a proof‐of‐concept that mosaic vaccination often outperforms conventional vaccination, leading to fewer infected individuals, improved vaccine efficacy, and lower individual risks over the course of the epidemic.

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Diversity in CRISPR-based immunity protects susceptible genotypes by restricting phage spread and evolution

Cited by 8 publications

References 72 publications

Competition and coevolution drive the evolution and the diversification of CRISPR immunity

Competition and coevolution drive the evolution and the diversification of CRISPR immunity

Genetic diversity and disease: The past, present, and future of an old idea

Mosaic vaccination: How distributing different vaccines across a population could improve epidemic control

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