scholarly journals Causation without correlation: parasite-mediated frequency-dependent selection and infection prevalence

2021 ◽  
Vol 17 (12) ◽  
Author(s):  
Curtis M. Lively ◽  
Julie Xu ◽  
Frida Ben-Ami

Parasite-mediated selection is thought to maintain host genetic diversity for resistance. We might thus expect to find a strong positive correlation between host genetic diversity and infection prevalence across natural populations. Here, we used computer simulations to examine host–parasite coevolution in 20 simi-isolated clonal populations across a broad range of values for both parasite virulence and parasite fecundity. We found that the correlation between host genetic diversity and infection prevalence can be significantly positive for intermediate values of parasite virulence and fecundity. But the correlation can also be weak and statistically non-significant, even when parasite-mediated frequency-dependent selection is the sole force maintaining host diversity. Hence correlational analyses of field populations, while useful, might underestimate the role of parasites in maintaining host diversity.

2021 ◽  
Author(s):  
Curtis M Lively ◽  
Julie Xu ◽  
Frida Ben-Ami

Parasite-mediated selection is thought to maintain host genetic diversity for resistance. We might thus expect to find a strong positive correlation between host genetic diversity and infection prevalence across natural populations. Here we used computer simulations to examine host-parasite coevolution in 20 simi-isolated clonal populations across a broad range of values for both parasite virulence and parasite fecundity. We found that the correlation between host genetic diversity and infection prevalence can be significantly positive for intermediate values of parasite virulence and fecundity. But the correlation can also be weak and statistically non-significant, even when parasite-mediated frequency-dependent selection is the sole force maintaining host diversity. Hence correlational analyses of field populations, while useful, might underestimate the role of parasites in maintaining host diversity.


The existence within natural populations of large amounts of genetic variation in molecules and morphology presents an evolutionary problem. The ‘neutralist’ solution to this problem, that the variation is usually unimportant to the organisms displaying it, has now lost much of its strength. Interpretations that assume widespread heterozygous advantage also face serious difficulties. A resolution is possible in terms of frequency-dependent selection by predators, parasites and competitors. The evidence for pervasive frequency-dependent selection is now very strong. It appears to follow naturally from the behaviour of predators, from the evolutionary lability of parasites, from the ecology of competition and, at the molecular level, from the phenomena of enzyme kinetics. Such selection can explain the maintenance not only of conventional polymorphism but also of continuous variation in both molecular and morphological characters. It can account for the occurrence of diversity within groups of haploid and self-fertilizing organisms, and for the evolution of differences between individuals in their systems of genetic control.


2017 ◽  
Author(s):  
Dustin Brisson

AbstractThis preprint has been reviewed and recommended by Peer Community in Evolutionary Biology (http://dx.doi.org/10.24072/pci.evolbiol.100024).The existence of persistent genetic variation within natural populations presents an evolutionary problem as natural selection and genetic drift tend to erode genetic diversity. Models of balancing selection were developed to account for the high and sometimes extreme levels of polymorphism found in many natural populations. Negative frequency-dependent selection may be the most powerful selective force maintaining balanced natural polymorphisms but it is also commonly misinterpreted. The aim of this review is to clarify the processes underlying negative frequency-dependent selection, describe classes of natural polymorphisms that can and cannot result from these processes, and discuss observational and experimental data that can aid in accurately identifying the processes that generated or are maintain diversity in nature. Finally, I consider the importance of accurately describing the processes affecting genetic diversity within populations as it relates to research progress.


2019 ◽  
Author(s):  
Caroline Manet ◽  
Etienne Simon-Lorière ◽  
Grégory Jouvion ◽  
David Hardy ◽  
Matthieu Prot ◽  
...  

ABSTRACTThe explosive spread of Zika virus (ZIKV) has been associated with major variations in severe disease and congenital afflictions among infected populations, suggesting an influence of host genes. We investigated how genome-wide variants could impact susceptibility to ZIKV infection in mice. We first describe that the susceptibility of Ifnar1 knockout mice is largely influenced by their genetic background. We then show that the broad genetic diversity of Collaborative Cross mice, which receptor to type I interferon (IFNAR) was blocked by anti-IFNAR antibody, expressed phenotypes ranging from complete resistance to severe symptoms and death with large variations in the peak and rate of decrease of plasma viral load, in brain viral load, in brain histopathology and in viral replication rate in infected cells. Differences of susceptibility between CC strains were correlated between Zika, Dengue and West Nile viruses. We identified highly susceptible and resistant mouse strains as new models to investigate the mechanisms of human ZIKV disease and other flavivirus infections. Genetic analyses revealed that phenotypic variations are driven by multiple genes with small effects, reflecting the complexity of ZIKV disease susceptibility in human population. Notably, our results rule out a role of the Oas1b gene in the susceptibility to ZIKV. Altogether, this study emphasizes the role of host genes in the pathogeny of ZIKV infection and lays the foundation for further genetic and mechanistic studies.IMPORTANCEIn recent outbreaks, ZIKV has infected millions of people and induced rare but potentially severe complications, including Guillain-Barré syndrome and encephalitis in adults. While several viral sequence variants were proposed to enhance the pathogenicity of ZIKV, the influence of host genetic variants in the clinical heterogeneity remains mostly unexplored. We have addressed this question using a mouse panel which models the genetic diversity of human population and a ZIKV strain from a recent clinical isolate. Through a combination of in vitro and in vivo approaches, we demonstrate that multiple host genetic variants determine viral replication in infected cells, and clinical severity, kinetics of blood viral load and brain pathology in mice. We describe new mouse models expressing high susceptibility or resistance to ZIKV and to other flaviviruses. These models will facilitate the identification and mechanistic characterization of host genes that influence ZIKV pathogenesis.


2019 ◽  
Vol 116 (15) ◽  
pp. 7397-7402 ◽  
Author(s):  
Mark Pagel ◽  
Mark Beaumont ◽  
Andrew Meade ◽  
Annemarie Verkerk ◽  
Andreea Calude

A puzzle of language is how speakers come to use the same words for particular meanings, given that there are often many competing alternatives (e.g., “sofa,” “couch,” “settee”), and there is seldom a necessary connection between a word and its meaning. The well-known process of random drift—roughly corresponding in this context to “say what you hear”—can cause the frequencies of alternative words to fluctuate over time, and it is even possible for one of the words to replace all others, without any form of selection being involved. However, is drift alone an adequate explanation of a shared vocabulary? Darwin thought not. Here, we apply models of neutral drift, directional selection, and positive frequency-dependent selection to explain over 417,000 word-use choices for 418 meanings in two natural populations of speakers. We find that neutral drift does not in general explain word use. Instead, some form of selection governs word choice in over 91% of the meanings we studied. In cases where one word dominates all others for a particular meaning—such as is typical of the words in the core lexicon of a language—word choice is guided by positive frequency-dependent selection—a bias that makes speakers disproportionately likely to use the words that most others use. This bias grants an increasing advantage to the common form as it becomes more popular and provides a mechanism to explain how a shared vocabulary can spontaneously self-organize and then be maintained for centuries or even millennia, despite new words continually entering the lexicon.


2017 ◽  
Vol 114 (31) ◽  
pp. 8325-8329 ◽  
Author(s):  
Mathieu Chouteau ◽  
Violaine Llaurens ◽  
Florence Piron-Prunier ◽  
Mathieu Joron

Explaining the maintenance of adaptive diversity within populations is a long-standing goal in evolutionary biology, with important implications for conservation, medicine, and agriculture. Adaptation often leads to the fixation of beneficial alleles, and therefore it erodes local diversity so that understanding the coexistence of multiple adaptive phenotypes requires deciphering the ecological mechanisms that determine their respective benefits. Here, we show how antagonistic frequency-dependent selection (FDS), generated by natural and sexual selection acting on the same trait, maintains mimicry polymorphism in the toxic butterfly Heliconius numata. Positive FDS imposed by predators on mimetic signals favors the fixation of the most abundant and best-protected wing-pattern morph, thereby limiting polymorphism. However, by using mate-choice experiments, we reveal disassortative mate preferences of the different wing-pattern morphs. The resulting negative FDS on wing-pattern alleles is consistent with the excess of heterozygote genotypes at the supergene locus controlling wing-pattern variation in natural populations of H. numata. The combined effect of positive and negative FDS on visual signals is sufficient to maintain a diversity of morphs displaying accurate mimicry with other local prey, although some of the forms only provide moderate protection against predators. Our findings help understand how alternative adaptive phenotypes can be maintained within populations and emphasize the need to investigate interactions between selective pressures in other cases of puzzling adaptive polymorphism.


2008 ◽  
Vol 105 (46) ◽  
pp. 17872-17877 ◽  
Author(s):  
Andrew R. Weeks ◽  
Ary A. Hoffmann

Asexual organisms can be genetically variable and evolve through time, yet it is not known how genetic diversity is maintained in populations. In sexual organisms, negative frequency-dependent selection plays a role in maintaining diversity at some loci, but in asexual organisms, this mechanism could provide a general explanation for persistent genetic diversity because it acts on the whole genome and not just on some polymorphisms within a genome. Using field manipulations, we show that negative frequency-dependent selection maintains clonal diversity in an asexual mite species, and we link predicted equilibrium clonal frequencies to average frequencies in space and time. Intense frequency-dependent selection is likely to be a general mechanism for persistent genetic diversity in asexual organisms.


2010 ◽  
Vol 277 (1701) ◽  
pp. 3783-3791 ◽  
Author(s):  
Eva R. Kallio ◽  
Michael Begon ◽  
Heikki Henttonen ◽  
Esa Koskela ◽  
Tapio Mappes ◽  
...  

Infected females may transfer maternal antibodies (MatAbs) to their offspring, which may then be transiently protected against infections the mother has encountered. However, the role of maternal protection in infectious disease dynamics in wildlife has largely been neglected. Here, we investigate the effects of Puumala hantavirus (PUUV)-specific MatAbs on PUUV dynamics, using 7 years' data from a cyclic bank vole population in Finland. For the first time to our knowledge, we partition seropositivity data from a natural population into separate dynamic patterns for MatAbs and infection. The likelihood of young of the year carrying PUUV-specific MatAbs during the breeding season correlated positively with infection prevalence in the overwintered parent population in the preceding spring. The probability of PUUV infection varied between seasons (highest in spring, lowest in late summer) and depended on population structure, but was also, in late autumn, notably, negatively related to summer MatAb prevalence, as well as to infection prevalence earlier in the breeding season. Hence, our results suggest that high infection prevalence in the early breeding season leads to a high proportion of transiently immune young individuals, which causes delays in transmission. This suggests, in turn, that MatAb protection has the potential to affect infection dynamics in natural populations.


Recent studies suggest that parasites (interpreted broadly to include viruses, bacteria, protozoans and helminths) may influence the numerical magnitude or geographical distribution of their host populations; most of such studies focus on the population biology and epidemiology of the host-parasite association, taking no explicit account of the genetics. Other researchers have explored the possibility that the coevolution of hosts and parasites may be responsible for much of the genetic diversity found in natural populations, and may even be the main reason for sexual reproduction; such genetic studies rarely take accurate account of the density- and frequency-dependent effects associated with the transmission and maintenance of parasitic infections. This paper aims to combine epidemiology and genetics, reviewing the way in which earlier studies fit into a wider scheme and offering some new ideas about host-parasite coevolution. One central conclusion is that ‘successful’ parasites need not necessarily evolve to be harmless: both theory and some empirical evidence (particularly from the myxoma-rabbit system) indicate that many coevolutionary paths are possible, depending on the relation between virulence and transmissibility of the parasite or pathogen.


Sign in / Sign up

Export Citation Format

Share Document