ArticleProceedings. Biological sciences2021
Immune lag is a major cost of prokaryotic adaptive immunity during viral outbreaks.
Article in Proceedings. Biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Why do bacteria accumulate antiphage defence systems?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Phage provoke growth delays and SOS response induction despite CRISPR-Cas protection.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Article
- Ecological drivers of CRISPR immune systems.mSystems · 2024Article
- Article
- The coordination of anti-phage immunity mechanisms in bacterial cells.Nature communications · 2022Article
- High viral abundance and low diversity are associated with increased CRISPR-Cas prevalence across microbial ecosystems.Current biology : CB · 2022Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clustered regularly interspaced short palindromic repeat (CRISPR)-Cas adaptive immune systems enable bacteria and archaea to efficiently respond to viral pathogens by creating a genomic record of previous encounters. These systems are broadly distributed across prokaryotic taxa, yet are surprisingly absent in a majority of organisms, suggesting that the benefits of adaptive immunity frequently do not outweigh the costs. Here, combining experiments and models, we show that a delayed immune response which allows viruses to transiently redirect cellular resources to reproduction, which we call 'immune lag', is extremely costly during viral outbreaks, even to completely immune hosts. Critically, the costs of lag are only revealed by examining the early, transient dynamics of a host-virus system occurring immediately after viral challenge. Lag is a basic parameter of microbial defence, relevant to all intracellular, post-infection antiviral defence systems, that has to-date been largely ignored by theoretical and experimental treatments of host-phage systems.
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Registered trials
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