Host and Microbe Adaptations in the Evolution of Immunity

2019 ◽  
1909 ◽  
Vol 9 (2) ◽  
pp. 181-219 ◽  
Author(s):  
L. Noon

The following experiments constitute an attempt to follow out in detail the stages by which immunity is established, in the course of a generalised bacterial infection (Pseudotuberculosis of rabbits). Two aspects of immunity are considered, firstly the presence, in the circulating fluids, of specific antibacterial substances, and secondly the power of rapidly producing such substances in answer to the specific stimulus. That is to say, attention is directed, not only to the quantity of specific antibodies present on any day of the disease, but also to the response which the animal can make to various doses of bacterial vaccine. For the immune animal is both more vigorous and more sensitive than the normal, in its reaction to a renewed dose of poison (Wassermann and Citron, 1905). Naturally the facts established with regard to one disease only, cannot be predicated at once of other diseases, in other animals. Still it is hoped that the systematic study of one disease may give some help in coordinating the large but somewhat disjointed mass of clinical observation which is already available.


Complexity ◽  
2018 ◽  
Vol 2018 ◽  
pp. 1-13
Author(s):  
M. V. Barbarossa ◽  
M. Polner ◽  
G. Röst

We investigate the temporal evolution of the distribution of immunities in a population, which is determined by various epidemiological, immunological, and demographical phenomena: after a disease outbreak, recovered individuals constitute a large immune population; however, their immunity is waning in the long term and they may become susceptible again. Meanwhile, their immunity can be boosted by repeated exposure to the pathogen, which is linked to the density of infected individuals present in the population. This prolongs the length of their immunity. We consider a mathematical model formulated as a coupled system of ordinary and partial differential equations that connects all these processes and systematically compare a number of boosting assumptions proposed in the literature, showing that different boosting mechanisms lead to very different stationary distributions of the immunity at the endemic steady state. In the situation of periodic disease outbreaks, the waveforms of immunity distributions are studied and visualized. Our results show that there is a possibility to infer the boosting mechanism from the population level immune dynamics.


2012 ◽  
Vol 11 (2) ◽  
pp. 167-176 ◽  
Author(s):  
L. J. Dishaw ◽  
R. N. Haire ◽  
G. W. Litman

2007 ◽  
Vol 8 (6) ◽  
pp. 547-548 ◽  
Author(s):  
Gary W Litman ◽  
Max D Cooper

2013 ◽  
Vol 10 (80) ◽  
pp. 20120887 ◽  
Author(s):  
Alex Best ◽  
Hannah Tidbury ◽  
Andy White ◽  
Mike Boots

While invertebrates lack the machinery necessary for ‘acquired immunity’, there is increasing empirical evidence that exposure to low levels of disease may ‘prime’ an invertebrate's immune response, increasing its defence to subsequent exposure. Despite this increasing empirical data, there has been little theoretical attention paid to immune priming. Here, we investigate the evolution of immune priming, focusing on the role of the unique feedbacks generated by a newly developed susceptible–primed–infected epidemiological model. Contrasting our results with previous models on the evolution of acquired immunity, we highlight that there are important implications to the evolution of immunity through priming owing to these different epidemiological feedbacks. In particular, we find that in contrast to acquired immunity, priming is strongly selected for at high as well as intermediate pathogen virulence. We also find that priming may be greatest at either intermediate or high host lifespans depending on the severity of disease. Furthermore, hosts faced with more severe pathogens are more likely to evolve diversity in priming. Finally, we show when the evolution of priming leads to the exclusion of the pathogens or hosts experiencing population cycles. Overall the model acts as a baseline for understanding the evolution of priming in host–pathogen systems.


2010 ◽  
Vol 277 (1700) ◽  
pp. 3649-3657 ◽  
Author(s):  
Sarah M. Short ◽  
Brian P. Lazzaro

Post-mating reduction in immune defence is common in female insects, and a trade-off between mating and immunity could affect the evolution of immunity. In this work, we tested the capacity of virgin and mated female Drosophila melanogaster to defend against infection by four bacterial pathogens. We found that female D. melanogaster suffer post-mating immunosuppression in a pathogen-dependent manner. The effect of mating was seen after infection with two bacterial pathogens ( Providencia rettgeri and Providencia alcalifaciens ), though not after infection with two other bacteria ( Enterococcus faecalis and Pseudomonas aeruginosa ). We then asked whether the evolution of post-mating immunosuppression is primarily a ‘female’ or ‘male’ trait by assaying for genetic variation among females for the degree of post-mating immune suppression they experience and among males for the level of post-mating immunosuppression they elicit in their mates. We also assayed for an interaction between male and female genotypes to test the specific hypothesis that the evolution of a trade-off between mating and immune defence in females might be being driven by sexual conflict. We found that females, but not males, harbour significant genetic variation for post-mating immunosuppression, and we did not detect an interaction between female and male genotypes. We thus conclude that post-mating immune depression is predominantly a ‘female’ trait, and find no evidence that it is evolving under sexual conflict.


2007 ◽  
Vol 28 (10) ◽  
pp. 449-454 ◽  
Author(s):  
Georg Hemmrich ◽  
David J. Miller ◽  
Thomas C.G. Bosch

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Daniel Koenig ◽  
Jörg Hagmann ◽  
Rachel Li ◽  
Felix Bemm ◽  
Tanja Slotte ◽  
...  

Genetic drift is expected to remove polymorphism from populations over long periods of time, with the rate of polymorphism loss being accelerated when species experience strong reductions in population size. Adaptive forces that maintain genetic variation in populations, or balancing selection, might counteract this process. To understand the extent to which natural selection can drive the retention of genetic diversity, we document genomic variability after two parallel species-wide bottlenecks in the genus Capsella. We find that ancestral variation preferentially persists at immunity related loci, and that the same collection of alleles has been maintained in different lineages that have been separated for several million years. By reconstructing the evolution of the disease-related locus MLO2b, we find that divergence between ancient haplotypes can be obscured by referenced based re-sequencing methods, and that trans-specific alleles can encode substantially diverged protein sequences. Our data point to long-term balancing selection as an important factor shaping the genetics of immune systems in plants and as the predominant driver of genomic variability after a population bottleneck.


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