Impact of the experimental removal of lizards on Lyme disease risk

The distribution of vector meals in the host community is an important element of understanding and predicting vector-borne disease risk. Lizards (such as the western fence lizard; Sceloporus occidentalis) play a unique role in Lyme disease ecology in the far-western United States. Lizards rather than mammals serve as the blood meal hosts for a large fraction of larval and nymphal western black-legged ticks (Ixodes pacificus--the vector for Lyme disease in that region) but are not competent reservoirs for the pathogen, Borrelia burgdorferi. Prior studies have suggested that the net effect of lizards is to reduce risk of human exposure to Lyme disease, a hypothesis that we tested experimentally. Following experimental removal of lizards, we documented incomplete host switching by larval ticks (5.19%) from lizards to other hosts. Larval tick burdens increased on woodrats, a competent reservoir, but not on deer mice, a less competent pathogen reservoir. However, most larvae failed to find an alternate host. This resulted in significantly lower densities of nymphal ticks the following year. Unexpectedly, the removal of reservoir-incompetent lizards did not cause an increase in nymphal tick infection prevalence. The net result of lizard removal was a decrease in the density of infected nymphal ticks, and therefore a decreased risk to humans of Lyme disease. Our results indicate that an incompetent reservoir for a pathogen may, in fact, increase disease risk through the maintenance of higher vector density and therefore, higher density of infected vectors.     

The genetic architecture of disease resistance in plants and the maintenance of recombination by parasites

Parasites represent strong selection on host populations because they are ubiquitous and can drastically reduce host fitness. It has been hypothesized that parasite selection could explain the widespread occurrence of recombination because it is a coevolving force that favours new genetic combinations in the host. A review of deterministic models for the maintenance of recombination reveals that for recombination to be favoured, multiple genes that interact with each other must be under selection. To evaluate whether parasite selection can explain the maintenance of recombination, we review 85 studies that investigated the genetic architecture of plant disease resistance and discuss whether they conform to the requirements that emerge from theoretical models. General characteristics of disease resistance in plants and problems in evaluating resistance experimentally are also discussed. We found strong evidence that disease resistance in plants is determined by multiple loci. Furthermore, in most cases where loci were tested for interactions, epistasis between loci that affect resistance was found. However, we found weak support for the idea that specific allelic combinations determine resistance to different host genotypes and there was little data on whether epistasis between resistance genes is negative or positive. Thus, the current data indicate that it is possible that parasite selection can favour recombination, but more studies in natural populations that specifically address the nature of the interactions between resistance genes are necessary. The data summarized here suggest that disease resistance is a complex trait and that environmental effects and fitness trade-offs should be considered in future models of the coevolutionary dynamics of host and parasites.     

Going through the motions: incorporating movement analyses into disease research

Though epidemiology dates back to the 1700s, most mathematical representations of epidemics still use transmission rates averaged at the population scale, especially for wildlife diseases. In simplifying the contact process, we ignore the heterogeneities in host movements that complicate the real world, and overlook their impact on spatiotemporal patterns of disease burden. Movement ecology offers a set of tools that help unpack the transmission process, letting researchers more accurately model how animals within a population interact and spread pathogens. Analytical techniques from this growing field can also help expose the reverse process: how infection impacts movement behaviours, and therefore other ecological processes like feeding, reproduction, and dispersal. Here, we synthesise the contributions of movement ecology in disease research, with a particular focus on studies that have successfully used movement‐based methods to quantify individual heterogeneity in exposure and transmission risk. Throughout, we highlight the rapid growth of both disease and movement ecology and comment on promising but unexplored avenues for research at their overlap. Ultimately, we suggest, including movement empowers ecologists to pose new questions, expanding our understanding of host–pathogen dynamics and improving our predictive capacity for wildlife and even human diseases.     

Susceptibility of source plants to Sugarcane Fiji disease virus influences the acquisition and transmission of the virus by the planthopper vector Perkinsiella saccharicida

Abstract:  Fiji leaf gall (FLG) caused by Sugarcane Fiji disease virus (SCFDV) is transmitted by the planthopper Perkinsiella saccharicida . FLG is managed through the identification and exploitation of plant resistance. The glasshouse-based resistance screening produced inconsistent transmission results and the factors responsible for that are not known. A series of glasshouse trials conducted over a 2-year period was compared to identify the factors responsible for the erratic transmission results. SCFDV transmission was greater when the virus was acquired by the vector from a cultivar that was susceptible to the virus than when the virus was acquired from a resistant cultivar. Virus acquisition by the vector was also greater when the vector was exposed to the susceptible cultivars than when exposed to the resistant cultivar. Results suggest that the variation in transmission levels is due to variation in susceptibility of sugarcane cultivars to SCFDV used for virus acquisition by the vector.     

Local variation in the thistle species Cirsium grayanum affects its utilization by the herbivorous ladybird beetle Henosepilachna niponica

Host plants are the most critical environmental factor for phytophagous arthropods. Adaptation to a novel host will alter the distributional range of an herbivore to include the area the novel host covers, and might promote divergence between populations utilizing the old and new hosts. On the Oshima Peninsula, Hokkaido Island, northern Japan, the ladybird beetle Henosepilachna niponica (Lewis) (Coleoptera: Coccinellidae) usually occurs exclusively on the thistle Cirsium alpicola Nakai (Asteraceae), which is distributed in the southernmost part of the island, although some other Cirsium species often grow in sympatry. At least at one site (Assabu), however, H. niponica depends on another thistle, Cirsium grayanum (Maxim.) Nakai, the most abundant and widely distributed thistle species on the Oshima Peninsula. We examined adult feeding acceptance and preference, and larval performance, in two populations of H. niponica that utilize different species of thistles (the Assabu population occurs on C. grayanum; the Shiriuchi population, on C. alpicola) by testing three kinds of thistles (C. grayanum from Assabu, C. grayanum from Shiriuchi, and C. alpicola from Shiriuchi). Results strongly suggested that among the three plants tested, C. grayanum from Assabu was the most suitable host for H. niponica. We concluded that local differences in C. grayanum mainly explain why it is not used at Shiriuchi, but that there are also local differences in host use among the beetle populations, suggesting some degree of local adaptation. This suggests that different selective regimes associated with different host plants might promote divergence among beetle populations. We conclude that H. niponica is at present unlikely to expand its range to the whole range of C. grayanum.     

口蹄疫病毒与宿主细胞的相互作用研究进展

口蹄疫病毒（FMDV）导致了偶蹄动物口蹄疫的发生,它是一类有着自身特点的RNA病毒。首先,FMDV衣壳蛋白VP1识别结合宿主细胞膜上的整联蛋白等受体,以内吞的方式进入细胞,利用宿主细胞成分完成病毒蛋白的合成。这些新合成的L^pro、2C和3C^pro等病毒致病因子进一步抑制宿主基因的转录和翻译,诱导细胞凋亡和白噬,并抑制干扰素介导的一系列先天性和获得性免疫反应。宿主则在病毒侵染细胞的初期,利用病毒识别受体等来识别病毒并诱导合成干扰素等细胞因子,介导多种免疫反应以清除病毒。病毒和宿主两者在持续的利用和较量中完成疾病的发生和痊愈等。其次,不断发现的病毒受体、结合基序、致病因子及宿主细胞的多种免疫调节因子将成为相关领域新的研究内容。综上,开发高效安全疫苗、增强自身免疫力及利用RNAi直接抑制病毒RNA等便成为现代FMDV防治的主要内容。     

Understanding the epidemiological factors that intensify the incidence of maize rough dwarf disease in Spain

Currently the dominant limiting factor to maize production in Spain is caused by Maize rough dwarf virus (MRDV). This study aimed to evaluate the epidemiology factors involved in the increased incidence of MRD disease in Spain. We examined the maize planthopper dynamics and MRDV incidence throughout two maize growing seasons in six locations using a set of eight maize varieties: four Bt‐varieties (BT‐var) and their isogenic counterparts (NBT‐var). Our results indicate that MRDV incidence is greatly influenced by the first colonisation of maize by Laodelphax striatellus but not by Metadelphax propinqua and by the susceptibility of the maize varieties. No significant differences were observed between the BT‐var and NBT‐var, although BT‐var exhibited 1% less MRDV infection than NBT‐var. Cultivated wheat and Lolium perenne were found for the first time to be natural hosts of MRDV. However, wheat does not seem to be a preferred host for the development of L. striatellus. Partial sequencing of genome segments S1–S9 and full sequencing of segment S10 revealed that the Spanish MRDV isolate shares nucleotide identities ranging from 93% to 97% with the available sequences of segments S7–S10 of the Italian MRDV isolate. The highest nucleotide identities with other fijiviruses were observed with Rice black‐streaked dwarf virus. Molecular variability analysis of MRDV isolates collected over a ten years period showed high nucleotide (>97%) and amino sequence identities (>99%) on segment S10, suggesting a low temporal variability.     

Factors determining the host plant range of the phytophagous mite, Tetranychus urticae (Acari: Tetranychidae): a method for quantifying host plant acceptance

The host plant acceptance of the phytophagous mite Tetranychus urticae was experimentally quantified. Host plant acceptance is described as the proportion of adult females settling on the test plant on which they have been placed. On the other hand, the host plant suitability of T. urticae on different plant species is expressed as the mean number of eggs produced by the females within 5 days (hereafter 'fecundity'). An inbred T. urticae line was tested with regard to host plant acceptance and fecundity on 11 potential host plants. These two variables were positively correlated across host plants; host plant species on which the fecundity was low were also those on which females settled less readily compared to host plants with high fecundity. The characteristics of host plant acceptance of the T. urticae are discussed in light of their potential food resource under natural conditions.     

How should environmental stress affect the population dynamics of disease?

We modelled how stress affects the population dynamics of infectious disease. We were specifically concerned with stress that increased susceptibility of uninfected hosts when exposed to infection. If such stresses also reduced resources, fecundity and/or survivorship, there was a reduction in the host carrying capacity. This lowered the contact between infected and uninfected hosts, thereby decreasing transmission. In addition, stress that increased parasite mortality decreased disease. The opposing effects of stress on disease dynamics made it difficult to predict the response of disease to environmental stress. We found analytical solutions with negative, positive, convex and concave associations between disease and stress. Numerical simulations with randomly generated parameter values suggested that the impact of host‐specific diseases generally declined with stress while the impact of non‐specific (or open) diseases increased with stress. These results help clarify predictions about the interaction between environmental stress and disease in natural populations.     

Biochemical and physiological characterisation of Erwinia species causing tip-over disease of banana

Tip-over disease has become a serious threat to banana plantations in the past decade. The disease is reported to be caused by Erwinia carotovorasubsp. carotovora and Erwinia chrysanthemi. We compared nine Erwinia strains of diseased banana plants from different agroclimatic zones of Karnataka and Andhra Pradesh, Southern India by conventional means. On the basis of morphological, cultural, physiological and biochemical characteristics and pathogenicity tests, the seven isolates I₁ to I₆ and I₈ showed similarities to Erwinia carotovorasubsp. carotovora. Isolate I₉ from Andhra Pradesh expressed characteristics similar to that of Erwinia chrysanthemi and was identified as Erwinia chrysanthemi. The isolate I₇ which showed wider variation, neither confirmed to the characteristics of Erwinia carotovorasubsp. carotovora nor with that of Erwinia chrysanthemi, and possessed characteristics in between the two species. Further we studied the host range of the bacterium causing tip-over disease of banana.     

Parasites driving host diversity: Incidence of disease correlated with Daphnia clonal turnover*

According to the Red Queen hypothesis, clonal diversity in asexual populations could be maintained by negative frequency‐dependant selection by coevolving parasites. If common clones are selected against and rare clones gain a concomitant advantage, we expect that clonal turnover should be faster during parasite epidemics than between them. We tested this hypothesis exploring field data of the Daphnia–Caullerya host–parasite system. The clonal make‐up and turnover of the Daphnia host population was tracked with high temporal resolution from 1998 until 2013, using first allozyme and later microsatellite markers. Significant differences in the clonal composition between random and infected subsamples of Daphnia populations were detected on six of seven tested occasions, confirming genetic specificity of the host–parasite interaction in this system. We used time series analysis to compare the rates of host clonal turnover to the incidence of parasitism, and found that Caullerya prevalence was significantly associated with microsatellite‐based clonal turnover. As alternate hypotheses, we further tested whether turnover was related to a variety of biotic, abiotic, and host demographic parameters. Other significant correlates of turnover were cyanobacterial biomass and (weakly) temperature. Overall, parasitism seems to be a strong driver of host clonal turnover, in support of the Red Queen hypothesis.     

Specific resistance prevents the evolution of general resistance and facilitates disease emergence

Host-shifts, where pathogens jump from an ancestral host to a novel host, can be facilitated or impeded by standing variation in disease resistance, but only if resistance provides broad-spectrum general resistance against multiple pathogen species. Host resistance comes in many forms and includes both general resistance, as well as specific resistance, which may only be effective against a single pathogen species or even genotype. However, most evolutionary models consider only one of these forms of resistance, and we have less understanding of how these two forms of resistance evolve in tandem. Here, we develop a model that allows for the joint evolution of specific and general resistance and asks if the evolution of specific resistance drives a decrease in the evolution of general resistance. We also explore how these evolutionary outcomes affect the risk of foreign pathogen invasion and persistence. We show that in the presence of a single endemic pathogen, the two forms of resistance are strongly exclusionary. Critically, we find that specific resistance polymorphisms can prevent the evolution of general resistance, facilitating the invasion of foreign pathogens. We also show that specific resistance polymorphisms are a necessary condition for the successful establishment of foreign pathogens following invasion, as they prevent the exclusion of the foreign pathogen by the more transmissible endemic pathogen. Our results demonstrate the importance of considering the joint evolution of multiple forms of resistance when evaluating a population's susceptibility to foreign pathogens.     

Factors affecting the bionomics of the eastern African egg parasitoid Trichogramma bournieri Pintureau & Babault (Hymenoptera: Trichogrammatidae)

The trichogrammatid Trichogramma bournieri Pintureau & Babault is a polyphagous parasitoid of eggs of several cereal stemborer species in eastern Africa. The effects of host species, host age and duration of host deprivation on the performance of the parasitoid were studied in the laboratory. Host acceptance and suitability were tested using five stemborer species. The noctuids Sesamia calamistis Hampson, Sesamia nonagrioides (Lefebvre), Busseola fusca (Fuller) the crambid Chilo partellus (Swinhoe) and the pyralid Eldana saccharina Walker were successfully parasitized by T. bournieri. Parasitism, number of progeny and developmental time varied significantly with host species. The eggs of S. calamistis and B. fusca were the most suitable, whereas those of E. saccharina were the least suitable. While parasitism and number of progeny tended to decrease with age of hosts, there were no significant differences in sex ratio. Longevity of the parasitoid increased with increase in deprivation of hosts from 0 to 12 days. Average lifetime fecundity per female decreased, indicating resorption of eggs.     

Suitability of the maize weevil and angoumois grain moth as hosts for the parasitoidsAnisopteromalus calandrae andPteromalus cerealellae

Two parasitoids,Pteromalus cerealellae (Ashmead) andAnisopteromalus calandrae (Howard) (Hymenoptera: Pteromalidae), were compared for their ability to parasitize two important internally-developing insect pests of stored maize (Zea mays L.). Parasitism byP. cerealellae was greater on Angoumois grain moth,Sitotroga cerealella (Olivier), than on maize weevil,Sitophilus zeamais Motschulsky, in no-choice experiments.Anisopteromalus calandrae parasitized more maize weevils than didP. cerealellae. The former parasitoid parasitized only a few Angoumois grain moths successfully in maize, but parasitized many in wheat if the hosts were younger than 3 weeks old. Thus, both host age and type of grain affect suitability for parasitism. The effects of parental host (species on which the female developed) and experimental host (species exposed to parasitism) on parasitism rate ofP. cerealellae were tested in a host-switching experiment. Parasitism by parasitoids reared on maize weevils was 23% lower than that of parasitoids reared on Angoumois grain moth. This effect was independent of which host the filial generation of parasitoids was tested on. However, the experimental host species had a much greater effect on parasitoid fecundity than the parental host species. Female progeny had smaller body sizes when emerging from maize weevil than from Angoumois grain moth, which may explain the parental host effect on fecundity. There was also a slight intergenerational effect of host species on parasitoid body size.     

CD99-dependent expansion of myeloid-derived suppressor cells and attenuation of graft-versus-host disease

CD99 is involved in many cellular events, such as the generation of Hodgkin and Reed-Sternberg cells, T cell costimulation, and leukocyte transendothelial migration. However, these studies have been limited to in vitro or in vivo experiments using CD99-deficient cell lines or anti-CD99 antibodies. In the present study, using CD99-deficient mice established by the exchangeable gene trap method, we investigated the physiologic function of murine CD99. In a B6 splenocytes → bm12 graft-versus-host disease model, wild-type cells were minimally lethal, whereas all mice that received CD99-deficient donor cells developed an early and more severe pathology. Graftversus-host disease in these mice was associated with insufficient expansion of myeloid-derived suppressor cells. This was confirmed by experiments illustrating that the injection of wild-type donor cells depleted of Mac-1(+) cells led to an almost identical disease course as the CD99-deficient donor system. Therefore, these results suggest that CD99 plays a crucial role in the attenuation of graft-versus-host disease by regulating the expansion of myeloid-derived suppressor cells.     

Advances in the treatment of acute graft‐versus‐host disease

Allogeneic hematopoietic stem cell transplantation (HSCT) has been widely used for the treatment of hematologic malignant and non‐malignant hematologic diseases and other diseases. However, acute graft‐versus‐host disease (GVHD) is a life‐threatening complication of allogeneic transplantation. Acute GVHD may occur in 30% of transplant recipients, which is a syndrome of erythematous skin eruption, cholestatic liver disease and intestinal dysfunction, resulting from the activation of donor T lymphocytes by host antigen‐presenting cells, resulting in an immune‐mediated inflammatory response. Recent scientific advances in the understanding of the pathogenesis involved in the development of acute GVHD and clinical investigation have provided more effective therapeutic strategies for acute GVHD. This review focuses on major scientific and clinical advances in the treatment of acute GVHD.     

Trade-offs and the evolution of host specialization

Summary Trade-offs in performance on different hosts are thought to promote the evolution of host specificity by blocking host shifts. Yet, in contrast, most experiments using phytophagous insects have shown performance on alternative hosts to be uncorrelated or positively correlated. Recent quantitative genetic models based on mutation—selection balance indicate that underlying constraints on the simultaneous maximization of different components of fitness may not always generate negative genetic correlations. We suggest an alternative or additional explanation for the lack of observed negative genetic correlations. If performance is polygenically controlled and some performance loci possess only antagonistically pleiotropic alleles, then the expression of trade-offs in performance will vary over time in populations. Consequently, a trade-off will be seen only in populations that have adapted to two hosts and are at or close to genetic equilibrium. Therefore, studies testing performance on a novel as compared with a normal host will generally yield non-negative genetic correlations between performance on the two hosts. The results of published studies are consistent with the predictions of this hypothesis.     

Susceptibility and resistance to pneumococcal disease in mice.

Although pneumococcus is a major pathogen of humans and, every year, the bacterium causes illness and death in millions of individuals, the genetic basis of susceptibility to the bacterium is unknown. Previous attempts to identify the gene explaining differing susceptibility to pneumococcal disease in humans have been without significant success. In order to develop new hypotheses that can be tested in humans, significant efforts have been made using mouse models of infection and disease. Indeed, the majority of the information so far obtained on pneumococcal disease in vivo has come from mouse studies. Mice differ in their response to pneumococcal disease, however, and the genetic basis of susceptibility to infection is unknown. This review summarises the current knowledge of mouse susceptibility and resistance to pneumococcal infection.