Conditions affecting the timing and magnitude of Hendra virus shedding across pteropodid bat populations in Australia.

Understanding infection dynamics in animal hosts is fundamental to managing spillover and emergence of zoonotic infections. Hendra virus is endemic in Australian pteropodid bat populations and can be lethal to horses and humans. However, we know little about the factors driving Hendra virus prevalence in resevoir bat populations, making spillover difficult to predict. We use Hendra virus prevalence data collected from 13 000 pooled bat urine samples across space and time to determine if pulses of prevalence are periodic and synchronized across sites. We also test whether site-specific precipitation and temperature affect the amplitude of the largest annual prevalence pulses. We found little evidence for a periodic signal in Hendra virus prevalence. Although the largest amplitude pulses tended to occur over winter, pulses could also occur in other seasons. We found that Hendra virus prevalence was weakly synchronized across sites over short distances, suggesting that prevalence is driven by local-scale effects. Finally, we found that drier conditions in previous seasons and the abundance of Pteropus alecto were positively correlated with the peak annual values of Hendra virus prevalence. Our results suggest that in addition to seasonal effects, bat density and local climatic conditions interact to drive Hendra virus infection dynamics.

Genotype-by-genotype interactions between an insect and its pathogen.

Genotype-by-genotype (G×G) interactions are an essential requirement for the coevolution of hosts and parasites, but have only been documented in a small number of animal model systems. G×G effects arise from interactions between host and pathogen genotypes, such that some pathogen strains are more infectious in certain hosts and some hosts are more susceptible to certain pathogen strains. We tested for G×G interactions in the gypsy moth (Lymantria dispar) and its baculovirus. We infected 21 full-sib families of gypsy moths with each of 16 isolates of baculovirus and measured the between-isolate correlations of infection rate across host families for all pairwise combinations of isolates. Mean infectiousness varied among isolates and disease susceptibility varied among host families. Between-isolate correlations of infection rate were generally less than one, indicating nonadditive effects of host and pathogen type consistent with G×G interactions. Our results support the presence of G×G effects in the gypsy moth-baculovirus interaction and provide empirical evidence that correlations in infection rates between field-collected isolates are consistent with values that mathematical models have previously shown to increase the likelihood of pathogen polymorphism.

Effects of pathogen exposure on life-history variation in the gypsy moth (Lymantria dispar).

Investment in host defences against pathogens may lead to trade-offs with host fecundity. When such trade-offs arise from genetic correlations, rates of phenotypic change by natural selection may be affected. However, genetic correlations between host survival and fecundity are rarely quantified. To understand trade-offs between immune responses to baculovirus exposure and fecundity in the gypsy moth (Lymantria dispar), we estimated genetic correlations between survival probability and traits related to fecundity, such as pupal weight. In addition, we tested whether different virus isolates have different effects on male and female pupal weight. To estimate genetic correlations, we exposed individuals of known relatedness to a single baculovirus isolate. To then evaluate the effect of virus isolate on pupal weight, we exposed a single gypsy moth strain to 16 baculovirus isolates. We found a negative genetic correlation between survival and pupal weight. In addition, virus exposure caused late-pupating females to be identical in weight to males, whereas unexposed females were 2-3 times as large as unexposed males. Finally, we found that female pupal weight is a quadratic function of host mortality across virus isolates, which is likely due to trade-offs and compensatory growth processes acting at high and low mortality levels, respectively. Overall, our results suggest that fecundity costs may strongly affect the response to selection for disease resistance. In nature, baculoviruses contribute to the regulation of gypsy moth outbreaks, as pathogens often do in forest-defoliating insects. We therefore argue that trade-offs between host life-history traits may help explain outbreak dynamics.

Direct observation of electron capture and reemission by the divacancy via charge transient positron spectroscopy.

Electron capture during forward bias and reemission at zero bias by divacancies in the depletion region of a silicon diode structure at room temperature have been studied for the first time using monoenergetic positrons. The positron response increases essentially linearly with electron current, as a result of increased positron trapping by negatively charged divacancies. The measurements indicate that ≤1% of the divacancies become negatively charged in the steady state at a forward bias of 1 V. Changes in the mean positron response when applying a square wave bias to the sample (1 V forward bias and 0 V, duty cycle 1:4, times at 0 V in the range 0.1-100 µs), were consistent with a rapid conversion of doubly to singly charged divacancies (in ∼10(1) ns), followed by slower defilling of the singly charged divacancies with a time constant of ∼10(1) µs. These ac measurements allow determination of the relative populations of singly and doubly charged divacancies. The results provide confirmation of consistency between the positron's response to the silicon divacancy and previously extracted capture and emission kinetics determined through charge transient measurements and assigned to the same defect. The possibility of combining these two, orthogonal techniques suggest a promising new and powerful approach to defect spectroscopy in which the structure and electrical properties of a defect may be determined in a single measurement.

Alternative developmental pathways and the propensity to migrate: a case study in the Atlantic salmon.

Migratory behaviour with its associated phenotypic changes is generally viewed as an adaptive strategy because it incurs survival or reproductive advantages to migrants. The development of a migrant phenotype is believed to be controlled by threshold mechanisms, where individuals emigrate only after surpassing a particular body size but delay migration if below. For such a strategy to respond to natural selection, part of the phenotypic variance in the propensity to migrate must be explained by variation in additive genetic effects. Here, we use data gathered in the field and from a common rearing experiment to test for a genetic basis associated with seaward migration in Atlantic salmon (Salmo salar L.). We document a high heritability of the liability trait underlying the propensity to emigrate in juvenile salmon, and significant differences between offspring grouped according to their sires in body-size threshold values above which emigration takes place. The presence of additive genetic variance in both the liability and thresholds makes the onset of migration a process sensitive to selection and may therefore constitute an important explanatory mechanism for the interpopulation differences in the size at seaward migration observed in this species.

The genetic basis of early-life morphological traits and their relation to alternative male reproductive tactics in Atlantic salmon.

Although heritability estimates for traits potentially under natural selection are increasingly being reported, their estimation remains a challenge if we are to understand the patterns of adaptive phenotypic change in nature. Given the potentially important role of selection on the early life phenotype, and thereby on future life history events in many fish species, we conducted a common garden experiment, using the Atlantic salmon (Salmo salar L.), with two major aims. The first objective is to determine how the site of origin, the paternal sexual tactic and additive genetic effects influence phenotypic variation of several morphological traits at hatching and emergence. The second aim is to test whether a link exists between phenotypic characteristics early in life and the incidence of male alternative tactics later in life. We found no evidence of a site or paternal effect on any morphological trait at hatching or emergence, suggesting that the spatial phenotypic differences observed in the natural river system from which these fish originated are mainly environmentally driven. However, we do find significant heritabilities and maternal effects for several traits, including body size. No direct evidence was found correlating the incidence of precocious maturation with early life characteristics. We suggest that under good growing conditions, body size and other traits at early developmental stages are not reliable cues for the surpassing of the threshold values associated with male sexual development.