scholarly journals Epidemic spreading under pathogen evolution

Author(s):  
Xiyun Zhang ◽  
Ruan Zhongyuan ◽  
Muhua Zheng ◽  
Jie Zhou ◽  
Boccaletti Stefano ◽  
...  

Abstract Battling a widespread pandemic is an arms race between our mitigation efforts, e.g., social distancing or vaccination, and the pathogen's evolving persistence. This is being observed firsthand during the current COVID-19 crisis, as novel mutations are constantly challenging our global vaccination race. To address this, we introduce here a general framework for epidemic spreading under pathogen evolution, which shows that mutations can fundamentally alter the projection of the spread. Specifically, we detect a new pandemic phase - the mutated phase - in which, despite the fact that the pathogen is initially non-pandemic (R0 < 1), it may still spread due to the emergence of a critical mutation. The boundaries of this phase portray a balance between the epidemic and the evolutionary time-scales. If the mutation rate is too low, the pathogen prevalence decays prior to the appearance of a critical mutation. On the other hand, if mutations are too rapid, the pathogen evolution becomes volatile and, once again, it fails to spread. Between these two extremes, however, a broad range of conditions exists in which an initially sub-pandemic pathogen will eventually gain prevalence. This is especially relevant during vaccination, which creates, as it progresses, increasing selection pressure towards vaccine-resistance. To overcome this, we show that vaccination campaigns must be accompanied by fierce mitigation efforts, to suppress the potential rise of a resistant mutant strain.

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Richard J. Harris ◽  
K. Anne-Isola Nekaris ◽  
Bryan G. Fry

Abstract Background Snakes and primates have a multi-layered coevolutionary history as predators, prey, and competitors with each other. Previous work has explored the Snake Detection Theory (SDT), which focuses on the role of snakes as predators of primates and argues that snakes have exerted a selection pressure for the origin of primates’ visual systems, a trait that sets primates apart from other mammals. However, primates also attack and kill snakes and so snakes must simultaneously avoid primates. This factor has been recently highlighted in regard to the movement of hominins into new geographic ranges potentially exerting a selection pressure leading to the evolution of spitting in cobras on three independent occasions. Results Here, we provide further evidence of coevolution between primates and snakes, whereby through frequent encounters and reciprocal antagonism with large, diurnally active neurotoxic elapid snakes, Afro-Asian primates have evolved an increased resistance to α-neurotoxins, which are toxins that target the nicotinic acetylcholine receptors. In contrast, such resistance is not found in Lemuriformes in Madagascar, where venomous snakes are absent, or in Platyrrhini in the Americas, where encounters with neurotoxic elapids are unlikely since they are relatively small, fossorial, and nocturnal. Within the Afro-Asian primates, the increased resistance toward the neurotoxins was significantly amplified in the last common ancestor of chimpanzees, gorillas, and humans (clade Homininae). Comparative testing of venoms from Afro-Asian and American elapid snakes revealed an increase in α-neurotoxin resistance across Afro-Asian primates, which was likely selected against cobra venoms. Through structure-activity studies using native and mutant mimotopes of the α-1 nAChR receptor orthosteric site (loop C), we identified the specific amino acids responsible for conferring this increased level of resistance in hominine primates to the α-neurotoxins in cobra venom. Conclusion We have discovered a pattern of primate susceptibility toward α-neurotoxins that supports the theory of a reciprocal coevolutionary arms-race between venomous snakes and primates.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Manisha Priyam ◽  
Sanjay K. Gupta ◽  
Biplab Sarkar ◽  
T. R. Sharma ◽  
A. Pattanayak

AbstractThe high degree of conservation of toll-like receptors (TLRs), and yet their subtle variations for better adaptation of species in the host–pathogen arms race make them worthy candidates for understanding evolution. We have attempted to track the trend of TLR evolution in the most diverse vertebrate group—teleosts, where Clarias batrachus was given emphasis, considering its traits for terrestrial adaptation. Eleven C. batrachus TLRs (TLR1, 2, 3, 5, 7, 8 9, 13, 22, 25, 26) were identified in this study which clustered in proximity to its Siluriformes relative orthologues in the phylogenetic analysis of 228 TLRs from 25 teleosts. Ten TLRs (TLR1, 2, 3, 5, 7, 8 9, 13, 21, 22) with at least 15 member orthologues for each alignment were processed for selection pressure and coevolutionary analysis. TLR1, 7, 8 and 9 were found to be under positive selection in the alignment-wide test. TLR1 also showed maximum episodic diversification in its clades while the teleost group Eupercaria showed the maximum divergence in their TLR repertoire. Episodic diversification was evident in C. batrachus TLR1 and 7 alignments. These results present a strong evidence of a divergent TLR repertoire in teleosts which may be contributing towards species-specific variation in TLR functions.


2021 ◽  
Vol 8 (7) ◽  
pp. 210530
Author(s):  
Julia R. Gog ◽  
Edward M. Hill ◽  
Leon Danon ◽  
Robin N. Thompson

As a countermeasure to the SARS-CoV-2 pandemic, there has been swift development and clinical trial assessment of candidate vaccines, with subsequent deployment as part of mass vaccination campaigns. However, the SARS-CoV-2 virus has demonstrated the ability to mutate and develop variants, which can modify epidemiological properties and potentially also the effectiveness of vaccines. The widespread deployment of highly effective vaccines may rapidly exert selection pressure on the SARS-CoV-2 virus directed towards mutations that escape the vaccine-induced immune response. This is particularly concerning while infection is widespread. By developing and analysing a mathematical model of two population groupings with differing vulnerability and contact rates, we explore the impact of the deployment of vaccines among the population on the reproduction ratio, cases, disease abundance and vaccine escape pressure. The results from this model illustrate two insights: (i) vaccination aimed at reducing prevalence could be more effective at reducing disease than directly vaccinating the vulnerable; (ii) the highest risk for vaccine escape can occur at intermediate levels of vaccination. This work demonstrates a key principle: the careful targeting of vaccines towards particular population groups could reduce disease as much as possible while limiting the risk of vaccine escape.


Author(s):  
Bruce Walsh ◽  
Michael Lynch

This chapter examines the search for a pattern of repetitive adaptive substitutions over evolutionary time. In contrast with the previous chapter, only a modest number of tests toward this aim have been proposed. The HKA and McDonald-Kreitman tests contrast the polymorphism to divergence ratio between different genomic classes (such as different genes or silent versus replacement sites within the same gene). These approaches can detect an excess of substitutions, which allows one to estimate the fraction of adaptive sites. This chapter reviews the empirical data on estimates of this fraction and discusses some of the sources of bias it its estimation. Over an even longer time scale, one can contrast the rate of change of sites in a sequence over a phylogeny. These tests require a rather special type of selection, wherein the same specific site (usually a codon) experiences multiple adaptive substitutions over a phylogeny, such as might occur in arms-race genes.


2019 ◽  
Vol 16 (155) ◽  
pp. 20190165 ◽  
Author(s):  
Mary Bushman ◽  
Rustom Antia

Theoretical models suggest that mixed-strain infections, or co-infections, are an important driver of pathogen evolution. However, the within-host dynamics of co-infections vary enormously, which complicates efforts to develop a general understanding of how co-infections affect evolution. Here, we develop a general framework which condenses the within-host dynamics of co-infections into a few key outcomes, the most important of which is the overall R 0 of the co-infection. Similar to how fitness is determined by two different alleles in a heterozygote, the R 0 of a co-infection is a product of the R 0 values of the co-infecting strains, shaped by the interaction of those strains at the within-host level. Extending the analogy, we propose that the overall R 0 reflects the dominance of the co-infecting strains, and that the ability of a mutant strain to invade a population is a function of its dominance in co-infections. To illustrate the utility of these concepts, we use a within-host model to show how dominance arises from the within-host dynamics of a co-infection, and then use an epidemiological model to demonstrate that dominance is a robust predictor of the ability of a mutant strain to save a maladapted wild-type strain from extinction (evolutionary emergence).


BMC Genetics ◽  
2009 ◽  
Vol 10 (1) ◽  
Author(s):  
Simone Rost ◽  
Hans-Joachim Pelz ◽  
Sandra Menzel ◽  
Alan D MacNicoll ◽  
Vanina León ◽  
...  

F1000Research ◽  
2014 ◽  
Vol 3 ◽  
pp. 154 ◽  
Author(s):  
Kathryn Hunt ◽  
Lars Chittka

Our memory is often surprisingly inaccurate, with errors ranging from misremembering minor details of events to generating illusory memories of entire episodes. The pervasiveness of such false memories generates a puzzle: in the face of selection pressure for accuracy of memory, how could such systematic failures have persisted over evolutionary time? It is possible that memory errors are an inevitable by-product of our adaptive memories and that semantic false memories are specifically connected to our ability to learn rules and concepts and to classify objects by category memberships. Here we test this possibility using a standard experimental false memory paradigm and inter-individual variation in verbal categorisation ability. Indeed it turns out that the error scores are significantly negatively correlated, with those individuals scoring fewer errors on the categorisation test being more susceptible to false memory intrusions in a free recall test. A similar trend, though not significant, was observed between individual categorisation ability and false memory susceptibility in a word recognition task. Our results therefore indicate that false memories, to some extent, might be a by-product of our ability to learn rules, categories and concepts.


F1000Research ◽  
2014 ◽  
Vol 3 ◽  
pp. 154 ◽  
Author(s):  
Kathryn Hunt ◽  
Lars Chittka

Our memory is often surprisingly inaccurate, with errors ranging from misremembering minor details of events to generating illusory memories of entire episodes. The pervasiveness of such false memories generates a puzzle: in the face of selection pressure for accuracy of memory, how could such systematic failures have persisted over evolutionary time? It is possible that memory errors are an inevitable by-product of our adaptive memories and that semantic false memories are specifically connected to our ability to learn rules and concepts and to classify objects by category memberships. Here we test this possibility using a standard experimental false memory paradigm and inter-individual variation in verbal categorisation ability. Indeed it turns out that the error scores are significantly negatively correlated, with those individuals scoring fewer errors on the categorisation test being more susceptible to false memory intrusions in a free recall test. A similar trend, though not significant, was observed between individual categorisation ability and false memory susceptibility in a word recognition task. Our results therefore indicate that false memories, to some extent, might be a by-product of our ability to learn rules, categories and concepts.


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