scholarly journals Host-pathogen coevolution increases genetic variation in susceptibility to infection

2018 ◽  
Author(s):  
Elizabeth ML Duxbury ◽  
Jonathan P Day ◽  
Davide Maria Vespasiani ◽  
Yannik Thüringer ◽  
Ignacio Tolosana ◽  
...  

AbstractIt is common to find considerable genetic variation in susceptibility to infection in natural populations. We have investigated whether natural selection increases this variation by testing whether host populations show more genetic variation in susceptibility to pathogens that they naturally encounter than novel pathogens. In a large cross-infection experiment involving four species of Drosophila and four host-specific viruses, we always found greater genetic variation in susceptibility to viruses that had coevolved with their host. We went on to examine the genetic architecture of resistance in one host species, finding that there are more major-effect genetic variants in coevolved host-parasite interactions. We conclude that selection by pathogens increases genetic variation in host susceptibility, and much of this effect is caused by the occurrence of major-effect resistance polymorphisms within populations.

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Elizabeth ML Duxbury ◽  
Jonathan P Day ◽  
Davide Maria Vespasiani ◽  
Yannik Thüringer ◽  
Ignacio Tolosana ◽  
...  

It is common to find considerable genetic variation in susceptibility to infection in natural populations. We have investigated whether natural selection increases this variation by testing whether host populations show more genetic variation in susceptibility to pathogens that they naturally encounter than novel pathogens. In a large cross-infection experiment involving four species of Drosophila and four host-specific viruses, we always found greater genetic variation in susceptibility to viruses that had coevolved with their host. We went on to examine the genetic architecture of resistance in one host species, finding that there are more major-effect genetic variants in coevolved host-pathogen interactions. We conclude that selection by pathogens has increased genetic variation in host susceptibility, and much of this effect is caused by the occurrence of major-effect resistance polymorphisms within populations.


2020 ◽  
Vol 287 (1930) ◽  
pp. 20201017
Author(s):  
James R. Whiting ◽  
Muayad A. Mahmud ◽  
Janette E. Bradley ◽  
Andrew D. C. MacColl

Seasonal disease and parasitic infection are common across organisms, including humans, and there is increasing evidence for intrinsic seasonal variation in immune systems. Changes are orchestrated through organisms' physiological clocks using cues such as day length. Ample research in diverse taxa has demonstrated multiple immune responses are modulated by photoperiod, but to date, there have been few experimental demonstrations that photoperiod cues alter susceptibility to infection. We investigated the interactions among photoperiod history, immunity and susceptibility in laboratory-bred three-spined stickleback (a long-day breeding fish) and its external, directly reproducing monogenean parasite Gyrodactylus gasterostei . We demonstrate that previous exposure to long-day photoperiods (PLD) increases susceptibility to infection relative to previous exposure to short days (PSD), and modifies the response to infection for the mucin gene muc2 and Treg cytokine foxp3a in skin tissues in an intermediate 12 L : 12 D photoperiod experimental trial. Expression of skin muc2 is reduced in PLD fish, and negatively associated with parasite abundance. We also observe inflammatory gene expression variation associated with natural inter-population variation in resistance, but find that photoperiod modulation of susceptibility is consistent across host populations. Thus, photoperiod modulation of the response to infection is important for host susceptibility, highlighting new mechanisms affecting seasonality of host–parasite interactions.


Parasitology ◽  
1985 ◽  
Vol 90 (1) ◽  
pp. 205-216 ◽  
Author(s):  
D. J. Minchella

Over half of all living species of plants and animals are parasitic, which by definition involves intimate association with and unfavourable impact on hosts (Price, 1980). This paper will only consider parasites whose ‘unfavourable impact’ adversely affects the birth and/or mortality rates of their hosts (Anderson, 1978). Most organisms are potential hosts and must deal with the problem of parasitism. The probability of parasitic infection of a host is influenced by both environmental and genetic factors. Traditionally it was assumed that a host was either resistant or susceptible to a particular parasite and therefore the interaction between a parasite and potential host had only two possible outcomes: either the resistant host rebuffed the parasitic attack and remained uninfected or the parasite successfully invaded and significantly reduced the reproductive success of the susceptible host. This approach, however, ignored the intraspecific genetic variation present within both host and parasite populations (Wakelin, 1978). Since the outcome is determined by the interaction of a finite set of host genes and parasite genes, genetic variation in host susceptibility and parasite infectivity (Richards, 1976; Wakelin, 1978) suggests that more than two outcomes are possible. Variation in host and parasite genomes does not begin and end at the susceptibility/infectivity loci. Other genes may also influence the outcome of host–parasite interactions by altering the life-history patterns of hosts and parasites, and lead to a variety of outcomes.


1995 ◽  
Vol 25 (12) ◽  
pp. 2010-2021 ◽  
Author(s):  
Chang-Yi Xie ◽  
Cheng C. Ying

The genetic architecture and adaptive landscape of interior lodgepole pine (Pinuscontorta ssp. latifolia Engelm. ex S. Wats.) in Canada were investigated in a provenance–family plantation located in central British Columbia. Fifty-three natural populations were sampled from three geographic regions covering the entire Canadian range, and their performance in growth and survival was recorded periodically over 20 years. Test results indicate that genetic variation among regions and among populations within regions was highly significant in all the traits investigated and accounted for, respectively, 53% and 41% of the total genetic variation in growth and 41% and 54% in survival. Within-population variation was also significant in growth but not in survival. Interior lodgepole pine in the central region demonstrated less genetic variation than in the northern and southern regions at both the population and family levels. In addition, the proportion of genetic variation associated with population was lower in the central region than in the other regions. Population differentiation in both growth and survival showed discernible elevational and geographic patterns. Regression models describing these adaptive patterns accounted for more than 80% of the among-population variation, and their veracity was verified with independent data. Populations of northern, coastal–interior transition, and high-elevation origin tended to have smaller trees with higher mortality. However, the patterns were not linear but differed in slope and (or) direction among regions. The adaptedness of populations tended to decrease as they were farther away from their origin, with a few exceptions displaying broad adaptation across more than 3° of latitude. As the test proceeded, population differentiation became more evident and adaptive clines became steeper. Some practical implications of these findings have been discussed.


2019 ◽  
Author(s):  
A. M. Sparks ◽  
K. Watt ◽  
R. Sinclair ◽  
J. G. Pilkington ◽  
J. M. Pemberton ◽  
...  

AbstractHost-parasite interactions are powerful drivers of evolutionary and ecological dynamics in natural populations. Variation in immune responses to infection is likely to shape the outcome of these interactions, with important consequences for the fitness of both host and parasite. However, little is known about how genetic variation contributes to variation in immune responses under natural conditions. Here, we examine the genetic architecture of variation in immune traits in the Soay sheep of St Kilda, an unmanaged population of sheep infected with strongyle gastrointestinal nematodes. We assayed IgA, IgE and IgG antibodies against the prevalent nematodeTeladorsagia circumcinctain the blood plasma of > 3,000 sheep collected over 26 years. Antibody levels were significantly heritable, ranging from 0.21 to 0.39 in lambs and from 0.23 to 0.57 in adults. IgA levels were strongly associated with a region on chromosome 24 explaining 21.1% and 24.5% of heritable variation in lambs and adults, respectively; this region was adjacent to two candidate loci, the Class II Major Histocompatibility Complex Transactivator (CIITA) and C-Type Lectin Domain Containing 16A (CLEC16A). Lamb IgA levels were also associated with the immunoglobulin heavy constant loci (IGH) complex on chromosome 18. Adult IgE levels and lamb IgG levels were associated with the major histocompatibility complex (MHC) on chromosome 20. This study provides evidence of high heritability of a complex immunological trait under natural conditions and provides the first evidence from a genome-wide study that large effect genes located outside the MHC region exist for immune traits in the wild.Author summaryHost-parasite interactions are powerful drivers of evolutionary and ecological dynamics in natural populations. Variation in immune responses to infection shapes the outcome of these interactions, with important consequences for the ability of the host and parasite to survive and reproduce. However, little is known about how much genes contribute to variation in immune responses under natural conditions. Our study investigates the genetic architecture of variation in three antibody types, IgA, IgE and IgG in a wild population of Soay sheep on the St Kilda archipelago in North-West Scotland. Using data collected over 26 years, we show that antibody levels have a heritable basis in lambs and adults and are stable over lifetime of individuals. We also identify several genomic regions with large effects on immune responses. Our study offers the first insights into the genetic control of immunity in a wild population, which is essential to understand how immune profiles vary in challenging natural conditions and how natural selection maintains genetic variation in complex immune traits.


2006 ◽  
Vol 84 (5) ◽  
pp. 668-676 ◽  
Author(s):  
G.P. Brown ◽  
C.M. Shilton ◽  
R. Shine

Although much research in evolutionary ecology is based upon the premise that high levels of parasitism impair the host's functioning, the assumed link between parasitism and fitness has been assessed for relatively few kinds of animals. At our study site in tropical Australia, keelback snakes ( Tropidonophis mairii (Gray, 1841), Colubridae) are heavily infected with haemogregarine blood parasites: 90% of snakes that we tested carried the parasite, with the proportion of erythrocytes containing haemogregarines averaging 15% and ranging up to a remarkable 64%. Prevalence increased with snake body size, but intensity decreased with age. Unlike lizards studied previously, the snakes did not respond to haemogregarine infection by releasing immature erythrocytes into the circulation. In striking contrast to results from a recent study on a sympatric snake species, we did not find any empirical links between parasite numbers and several measures of host fitness (body condition, growth rate, feeding rate, antipredator behaviour, locomotor performance, reproductive status, reproductive output, and recapture rate). The association between this parasite and its host thus appears to be surprisingly benign, suggesting that host–parasite interactions sometimes may have only trivial consequences for host fitness in natural populations. Plausibly, host–parasite coevolution weakens or eliminates fitness costs of parasitism.


Parasitology ◽  
2008 ◽  
Vol 135 (7) ◽  
pp. 767-781 ◽  
Author(s):  
S. TELFER ◽  
R. BIRTLES ◽  
M. BENNETT ◽  
X. LAMBIN ◽  
S. PATERSON ◽  
...  

SUMMARYThe physiological and immunological state of an animal can be influenced by current infections and infection history. Consequently, both ongoing and previous infections can affect host susceptibility to another parasite, the biology of the subsequent infection (e.g. infection length) and the impact of infection on host morbidity (pathology). In natural populations, most animals will be infected by a succession of different parasites throughout the course of their lives, with probably frequent concomitant infections. The relative timing of different infections experienced by a host (i.e. the sequence of infection events), and the effects on factors such as host susceptibility and host survival, can only be derived from longitudinal data on individual hosts. Here we review some of the evidence for the impact of co-infection on host susceptibility, infection biology and pathology focusing on insights obtained from both longitudinal studies in humans and experiments that explicitly consider the sequence of infection. We then consider the challenges posed by longitudinal infection data collected from natural populations of animals. We illustrate their usefulness using our data of microparasite infections associated with field vole (Microtus agrestis) populations to examine impacts on susceptibility and infection length. Our primary aim is to describe an analytical approach that can be used on such data to identify interactions among the parasites. The preliminary analyses presented here indicate both synergistic and antagonistic interactions between microparasites within this community and emphasise that such interactions could have significant impacts on host-parasite fitness and dynamics.


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