scholarly journals Quantitative disease resistance: to better understand parasite-mediated selection on major histocompatibility complex

2011 ◽  
Vol 279 (1728) ◽  
pp. 577-584 ◽  
Author(s):  
Helena Westerdahl ◽  
Muhammad Asghar ◽  
Dennis Hasselquist ◽  
Staffan Bensch
Keyword(s):  
Major Histocompatibility Complex ◽  
Disease Resistance ◽  
Balancing Selection ◽  
Quantitative Resistance ◽  
Infection Intensity ◽  
Positive Association ◽  
Major Histocompatibility ◽  
Quantitative Disease Resistance ◽  
Histocompatibility Complex ◽  
Descriptive Framework

We outline a descriptive framework of how candidate alleles of the immune system associate with infectious diseases in natural populations of animals. Three kinds of alleles can be separated when both prevalence of infection and infection intensity are measured—qualitative disease resistance, quantitative disease resistance and susceptibility alleles. Our descriptive framework demonstrates why alleles for quantitative resistance and susceptibility cannot be separated based on prevalence data alone, but are distinguishable on infection intensity. We then present a case study to evaluate a previous finding of a positive association between prevalence of a severe avian malaria infection (GRW2, Plasmodium ashfordi ) and a major histocompatibility complex (MHC) class I allele (B4b) in great reed warblers Acrocephalus arundinaceus . Using the same dataset, we find that individuals with allele B4b have lower GRW2 infection intensities than individuals without this allele. Therefore, allele B4b provides quantitative resistance rather than increasing susceptibility to infection. This implies that birds carrying B4b can mount an immune response that suppresses the acute-phase GRW2 infection, while birds without this allele cannot and may die. We argue that it is important to determine whether MHC alleles related to infections are advantageous (quantitative and qualitative resistance) or disadvantageous (susceptibility) to obtain a more complete picture of pathogen-mediated balancing selection.

scholarly journals Avian major histocompatibility complex copy number variation is associated with helminth richness

2020 ◽  
Vol 16 (7) ◽  
pp. 20200194
Author(s):  
Piotr Minias ◽  
Jorge S. Gutiérrez ◽  
Peter O. Dunn
Keyword(s):  
Major Histocompatibility Complex ◽  
Copy Number Variation ◽  
Mhc Class Ii ◽  
Copy Number ◽  
Positive Association ◽  
Interspecific Variation ◽  
Major Histocompatibility ◽  
Parasite Richness ◽  
Histocompatibility Complex ◽  
Number Variation

Genes of the major histocompatibility complex (MHC) play a key role in the adaptive immunity of vertebrates, as they encode receptors responsible for antigen recognition. Evolutionary history of the MHC proceeded through numerous gene duplications, which increase the spectrum of pathogens recognized by individuals. Although pathogen-mediated selection is believed to be a primary driver of MHC expansion over evolutionary times, empirical evidence for this association is virtually lacking. Here, we used an extensive dataset on MHC class II copy number variation in non-passerine birds to test for an evolutionary correlation with helminth parasite richness. As expected, our phylogenetically-informed modelling revealed a positive association between MHC copy number and total helminth richness, even after controlling for a broad spectrum of ecological and life-history traits. Thus, total helminth richness appears to be the most important correlate of MHC copy number, supporting a leading role of pathogen-mediated selection in the evolution of MHC in birds. Our results provide some of the first, although correlative, evidence linking parasitism to interspecific variation in MHC copy number among birds.

Natural selection at the class II major histocompatibility complex loci of mammals

1994 ◽  
Vol 346 (1317) ◽  
pp. 359-367 ◽  
Keyword(s):  
Major Histocompatibility Complex ◽  
Natural Selection ◽  
Balancing Selection ◽  
Synonymous Substitution ◽  
Class Ii ◽  
Class I ◽  
Major Histocompatibility ◽  
Class I Mhc ◽  
Histocompatibility Complex ◽  
Class Ii Mhc

The role of natural selection at major histocompatibility complex (MHC) loci was studied by analysis of molecular sequence data from mammalian class II MHC loci. As found previously for the class I MHC molecule and a hypothetical model of the class II molecule, the rate of non-synonymous nucleotide substitution exceeded that of synonymous substitution in the codons encoding the antigen recognition site of polymorphic class II molecules. This pattern is evidence that the polymorphism at these loci is maintained by a form of balancing selection, such as overdominant selection. By contrast, in the case of monomorphic class II loci, no such enhancement of the rate of non-synonymous substitution was observed. Phylogenetic analysis indicates that, in contrast to monomorphic (‘non-classical’) class I MHC loci, some monomorphic class II loci of mammals are quite ancient. The DMA and DMB loci, for example, diverged before all other known mammalian class II loci, possibly before the divergence of tetrapods from bony fishes. Analysis of the patterns of sharing of polymorphic residues at class II MHC loci by mammals of different species revealed that extensive convergent evolution has occurred at these loci; but no support was found for the hypothesis that MHC polymorphisms have been maintained since before the divergence of orders of eutherian mammals.

scholarly journals Major histocompatibility complex (MHC) heterozygote superiority to natural multi-parasite infections in the water vole ( Arvicola terrestris )

2008 ◽  
Vol 276 (1659) ◽  
pp. 1119-1128 ◽  
Author(s):  
M.K Oliver ◽  
S Telfer ◽  
S.B Piertney
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class Ii ◽  
Balancing Selection ◽  
Parasite Burden ◽  
Island Population ◽  
Water Vole ◽  
Immune Recognition ◽  
Major Histocompatibility ◽  
Arvicola Terrestris ◽  
Histocompatibility Complex

The fundamental role of the major histocompatibility complex (MHC) in immune recognition has led to a general consensus that the characteristically high levels of functional polymorphism at MHC genes is maintained by balancing selection operating through host–parasite coevolution. However, the actual mechanism by which selection operates is unclear. Two hypotheses have been proposed: overdominance (or heterozygote superiority) and negative frequency-dependent selection. Evidence for these hypotheses was evaluated by examining MHC–parasite relationships in an island population of water voles ( Arvicola terrestris ). Generalized linear mixed models were used to examine whether individual variation at an MHC class II DRB locus explained variation in the individual burdens of five different parasites. MHC genotype explained a significant amount of variation in the burden of gamasid mites, fleas ( Megabothris walkeri ) and nymphs of sheep ticks ( Ixodes ricinus ). Additionally, MHC heterozygotes were simultaneously co-infected by fewer parasite types than homozygotes. In each case where an MHC-dependent effect on parasite burden was resolved, the heterozygote genotype was associated with fewer parasites, and the heterozygote outperformed each homozygote in two of three cases, suggesting an overall superiority against parasitism for MHC heterozygote genotypes. This is the first demonstration of MHC heterozygote superiority against multiple parasites in a natural population, a mechanism that could help maintain high levels of functional MHC genetic diversity in natural populations.

Sign in / Sign up

Export Citation Format

Share Document