Fasting or fear: disentangling the roles of predation risk and food deprivation in the nitrogen metabolism of consumers.

Predators can alter nutrient cycles simply by inducing stress in prey. This stress accelerates prey's protein catabolism, nitrogen waste production, and nitrogen cycling. Yet predators also reduce the feeding rates of their prey, inducing food deprivation that is expected to slow protein catabolism and nitrogen cycling. The physiology of prey under predation risk thus balances the influences of predation risk and food deprivation, and this balance is central to understanding the role of predators in nutrient cycles. We explored the separate and combined effects of predation risk and food deprivation on prey physiology and nutrient cycling by exposing guppies (Poecilia reticulata) to predation risk and food deprivation in a 2 × 2 design. We simulated predation risk using chemical cues from a natural predator of guppies, and we created food deprivation by rationing food availability. We measured guppy response as food consumption, growth, tissue energy density, tissue carbon:nitrogen, and nitrogen (N) excretion and assimilation. We found that N-linked physiological processes (N consumption, assimilation, excretion) were strongly affected by predation risk, independent of food consumption. Guppies excreted substantially less under predation risk than they did under food deprivation or control conditions. These results suggest that predation risk, per se, triggers physiological changes in guppies that increase N retention and decrease N excretion. We suggest that slower N metabolism under predation risk is an adaptive response that minimizes protein loss in the face of predictable, predator-induced food restriction. Notably, N metabolism shares common hormonal control with food seeking behavior, and we speculate that increased N retention is a direct and immediate result of reduced food seeking under predation risk. Contrary to predation-stress-based hypotheses for how predators affect nutrient cycling by prey, our result indicates that even short-term exposure to predators may decelerate, rather than accelerate, the speed of N cycling by suppressing N turnover by prey.

Genetic variation and selection of MHC class I loci differ in two congeneric frogs.

Major histocompatibility complex (MHC) genes encode proteins in the acquired immune response pathway that often show distinctive selection-driven patterns in wild vertebrate populations. We examined genetic variation and signatures of selection in the MHC class I alpha 1 (A1)- and alpha 2 (A2)-domain encoding exons of two frog congeners [Agalychnis callidryas (n = 20) and A. lemur (n = 20)] from a single locality in Panama. We also investigated how historical demographic processes may have impacted MHC genetic diversity by analyzing a neutral mitochondrial marker. We found that both MHC domains were highly variable in both species, with both species likely expressing three loci. Our analyses revealed different signatures of selection between the two species, most notably that the A. callidryas A2 domain had experienced positive selection while the A2 domain of A. lemur had not. Diversifying selection acted on the same number of A1 and A2 allelic lineages, but on a higher percentage of A1 sites compared to A2 sites. Neutrality tests of mitochondrial haplotypes predominately indicated that the two species were at genetic equilibrium when the samples were collected. In addition, two historical tests of demography indicated both species have had relatively stable population sizes over the past 100,000 years; thus large population size changes are unlikely to have greatly influenced MHC diversity in either species during this time period. In conclusion, our results suggest that the impact of selection on MHC diversity varied between these two closely related species, likely due to a combination of distinct ecological conditions and past pathogenic pressures.

Positive selection drives the evolution of a major histocompatibility complex gene in an endangered Mexican salamander species complex.

Immune gene evolution can be critical to species survival in the face of infectious disease. In particular, polymorphism in the genes of the major histocompatibility complex (MHC) helps vertebrates combat novel and diverse pathogens by increasing the number of pathogen-derived proteins that can initiate the host's acquired immune response. In this study, we used a combination of presumably adaptive and neutral markers to investigate MHC evolution in populations of five salamander species within the Ambystoma velasci complex, a group consisting of 15 recently diverged species, several of which are endangered. We isolated 31 unique MHC class II ß alleles from 75 total individuals from five species in this complex. MHC heterozygosity was significantly lower than expected for all five species, and we found no clear relationship between number of MHC alleles and species range, life history, or level of heterozygosity. We inferred a phylogeny representing the evolutionary history of Ambystoma MHC, with which we found signatures of positive selection on the overall gene, putative peptide-binding residues, and allelic lineages. We identified several instances of trans-species polymorphism, a hallmark of balancing selection observed in other groups of closely related species. In contrast, we did not detect comparable allelic diversity or signatures of selection on neutral loci. Additionally, we identified 17 supertypes among the 44 unique Ambystoma alleles, indicating that these sequences may encode functionally distinct MHC variants. We therefore have strong evidence that positive selection is a major evolutionary force driving patterns of MHC polymorphism in this recently radiated species complex.

Comparison of cellular immune responses to avian influenza virus in two genetically distinct, highly inbred chicken lines.

Low pathogenicity avian influenza causes mild disease involving the respiratory, gastrointestinal, and reproductive systems of wild and domestic birds. Avian influenza research often emphasizes the effect of the virus genetics on disease, but the influence of host genetics on resistance to infection is not well understood. The genetic determinants of enhanced resistance to influenza can be explored by using genetically distinct, highly inbred chicken lines that differ in susceptibility to influenza. In this study, we compared the mucosal cellular immune responses between the relatively resistant Fayoumi M43 chicken line and the relatively susceptible Leghorn GB2 chicken line after challenging with low pathogenicity avian influenza virus (LPAIV) H6N2. The birds were inoculated at 21 days of age with 107 50 % egg infective dose (EID50) LPAIV H6N2 via nasal and tracheal routes in two separate experiments. Clinical signs were recorded, tracheal swabs were collected to measure viral titer, and tracheas and lungs were harvested for flow cytometric analysis of macrophage, B cell, and T cell populations at 4 days post-infection (dpi) (Experiments 1 and 2) and 6 dpi (Experiment 2). Blood and tears were also collected at 7 and 14 dpi (Experiment 1) to measure antibody levels. Compared to both the non-challenged Fayoumis and the relatively susceptible Leghorn chickens, relatively resistant Fayoumi chickens challenged with LPAIV demonstrated enhanced MHC class I expression on antigen-presenting cells and increased macrophage, B cell, and T cell frequencies in the trachea, which were associated with reduced tracheal viral titers at 4 dpi. In contrast, MHC class I expression and immune cell frequencies in the trachea were not different between challenged Leghorns and non-challenged Leghorns. Furthermore, Leghorns shed higher virus titers in their trachea compared to Fayoumis. Challenged Fayoumis and Leghorns both produced AIV-specific IgY detected in the serum and tears, but AIV-specific IgA was not detected in the tears. In this study, we provide new insight into immune mechanisms of enhanced resistance to avian influenza in chickens, which may lead to improved vaccination strategies and breeding programs.

Borrelia burgdorferi Manipulates Innate and Adaptive Immunity to Establish Persistence in Rodent Reservoir Hosts.

Borrelia burgdorferi sensu lato species complex is capable of establishing persistent infections in a wide variety of species, particularly rodents. Infection is asymptomatic or mild in most reservoir host species, indicating successful co-evolution of the pathogen with its natural hosts. However, infected humans and other incidental hosts can develop Lyme disease, a serious inflammatory syndrome characterized by tissue inflammation of joints, heart, muscles, skin, and CNS. Although B. burgdorferi infection induces both innate and adaptive immune responses, they are ultimately ineffective in clearing the infection from reservoir hosts, leading to bacterial persistence. Here, we review some mechanisms by which B. burgdorferi evades the immune system of the rodent host, focusing in particular on the effects of innate immune mechanisms and recent findings suggesting that T-dependent B cell responses are subverted during infection. A better understanding of the mechanisms causing persistence in rodents may help to increase our understanding of the pathogenesis of Lyme disease and ultimately aid in the development of therapies that support effective clearance of the bacterial infection by the host's immune system.