Canine and feline host ranges of canine parvovirus and feline panleukopenia virus: distinct host cell tropisms of each virus in vitro and in vivo.

Canine parvovirus (CPV) emerged as an apparently new virus during the mid-1970s. The origin of CPV is unknown, but a variation from feline panleukopenia virus (FPV) or another closely related parvovirus is suspected. Here we examine the in vitro and in vivo canine and feline host ranges of CPV and FPV. Examination of three canine and six feline cell lines and mitogen-stimulated canine and feline peripheral blood lymphocytes revealed that CPV replicates in both canine and feline cells, whereas FPV replicates efficiently only in feline cells. The in vivo host ranges were unexpectedly complex and distinct from the in vitro host ranges. Inoculation of dogs with FPV revealed efficient replication in the thymus and, to some degree, in the bone marrow, as shown by virus isolation, viral DNA recovery, and Southern blotting and by strand-specific in situ hybridization. FPV replication could not be demonstrated in mesenteric lymph nodes or in the small intestine, which are important target tissues in CPV infection. Although CPV replicated well in all the feline cells tested in vitro, it did not replicate in any tissue of cats after intramuscular or intravenous inoculation. These results indicate that these viruses have complex and overlapping host ranges and that distinct tissue tropisms exist in the homologous and heterologous hosts.     

The evolution of host resistance: tolerance and control as distinct strategies

In response to parasitic infection, hosts may evolve defences that reduce the deleterious effects on survivorship. This may be interpreted as a form of resistance, as long as infected hosts are able to either recover or reproduce. Here we distinguish two important routes to this form of resistance. An infected host may either: (1) tolerate pathogen damage, or (2) control the pathogen by inhibiting its growth. A model is constructed to examine the evolutionary dynamics of tolerance and control to a free-living microparasite, where both forms of resistance are costly in terms of other life-history traits. We do not observe polymorphism of tolerant genotypes. In contrast, the evolution of control may lead to disruptive selection, and ultimately dimorphism of extreme strains. The optimal host genotype also varies with the type of resistance-individuals invest more in tolerance and pay a greater cost. The free-living framework used makes the distinction between tolerance and control explicit but the distinction applies equally to directly transmitted parasites. Due to the evolutionary differences exhibited, it is important to design experiments that distinguish between the two forms of resistance.     

The natural host range shift and subsequent evolution of canine parvovirus resulted from virus-specific binding to the canine transferrin receptor

Canine parvovirus (CPV) is a host range variant of a feline virus that acquired the ability to infect dogs through changes in its capsid protein. Canine and feline viruses both use the feline transferrin receptor (TfR) to infect feline cells, and here we show that CPV infects canine cells through its ability to specifically bind the canine TfR. Receptor binding on host cells at 37 degrees C only partially correlated with the host ranges of the viruses, and an intermediate virus strain (CPV type 2) bound to higher levels on cells than did either the feline panleukopenia virus or a later strain of CPV. During the process of adaptation to dogs the later variant strain of CPV gained the ability to more efficiently use the canine TfR for infection and also showed reduced binding to feline and canine cells compared to CPV type 2. Differences on the top and the side of the threefold spike of the capsid surface controlled specific TfR binding and the efficiency of binding to feline and canine cells, and these differences also determined the cell infection properties of the viruses.     

The evolution of parasite host range in heterogeneous host populations

Theory on the evolution of niche width argues that resource heterogeneity selects for niche breadth. For parasites, this theory predicts that parasite populations will evolve, or maintain, broader host ranges when selected in genetically diverse host populations relative to homogeneous host populations. To test this prediction, we selected the bacterial parasite Serratia marcescens to kill Caenorhabditis elegans in populations that were genetically heterogeneous (50% mix of two experimental genotypes) or homogeneous (100% of either genotype). After 20 rounds of selection, we compared the host range of selected parasites by measuring parasite fitness (i.e. virulence, the selected fitness trait) on the two focal host genotypes and on a novel host genotype. As predicted, heterogeneous host populations selected for parasites with a broader host range: these parasite populations gained or maintained virulence on all host genotypes. This result contrasted with selection in homogeneous populations of one host genotype. Here, host range contracted, with parasite populations gaining virulence on the focal host genotype and losing virulence on the novel host genotype. This pattern was not, however, repeated with selection in homogeneous populations of the second host genotype: these parasite populations did not gain virulence on the focal host genotype, nor did they lose virulence on the novel host genotype. Our results indicate that host heterogeneity can maintain broader host ranges in parasite populations. Individual host genotypes, however, vary in the degree to which they select for specialization in parasite populations.     

The role of evolutionary intermediates in the host adaptation of canine parvovirus

The adaptation of viruses to new hosts is a poorly understood process likely involving a variety of viral structures and functions that allow efficient replication and spread. Canine parvovirus (CPV) emerged in the late 1970s as a host-range variant of a virus related to feline panleukopenia virus (FPV). Within a few years of its emergence in dogs, there was a worldwide replacement of the initial virus strain (CPV type 2) by a variant (CPV type 2a) characterized by four amino acid differences in the capsid protein. However, the evolutionary processes that underlie the acquisition of these four mutations, as well as their effects on viral fitness, both singly and in combination, are still uncertain. Using a comprehensive experimental analysis of multiple intermediate mutational combinations, we show that these four capsid mutations act in concert to alter antigenicity, cell receptor binding, and relative in vitro growth in feline cells. Hence, host adaptation involved complex interactions among both surface-exposed and buried capsid mutations that together altered cell infection and immune escape properties of the viruses. Notably, most intermediate viral genotypes containing different combinations of the four key amino acids possessed markedly lower fitness than the wild-type viruses.     

Reevaluation of host ranges of feline leukemia virus subgroups

We reevaluated the host ranges of feline leukemia virus (FeLV) subgroups A, B and C using pseudotype assays based on recombinant NB-tropic murine leukemia virus, which is not usually blocked after viral entry in mammalian cells. Pseudotype viruses of FeLV-B and -C infected a variety of cell lines from many mammalian species. Unexpectedly, FeLV-A pseudotype viruses of two independent isolates from the UK and US also infected a variety of non-feline cell lines including cells from humans, rabbits, pigs and minks. Moreover, both isolates of FeLV-A productively infected human embryonic kidney 293 and mink Mv-1-Lu cells. We conclude that FeLV-A is not strictly ecotropic.     

Parasite host range and the evolution of host resistance

Parasite host range plays a pivotal role in the evolution and ecology of hosts and the emergence of infectious disease. Although the factors that promote host range and the epidemiological consequences of variation in host range are relatively well characterized, the effect of parasite host range on host resistance evolution is less well understood. In this study, we tested the impact of parasite host range on host resistance evolution. To do so, we used the host bacterium Pseudomonas fluorescens SBW25 and a diverse suite of coevolved viral parasites (lytic bacteriophage Φ2) with variable host ranges (defined here as the number of host genotypes that can be infected) as our experimental model organisms. Our results show that resistance evolution to coevolved phages occurred at a much lower rate than to ancestral phage (approximately 50% vs. 100%), but the host range of coevolved phages did not influence the likelihood of resistance evolution. We also show that the host range of both single parasites and populations of parasites does not affect the breadth of the resulting resistance range in a naïve host but that hosts that evolve resistance to single parasites are more likely to resist other (genetically) more closely related parasites as a correlated response. These findings have important implications for our understanding of resistance evolution in natural populations of bacteria and viruses and other host–parasite combinations with similar underlying infection genetics, as well as the development of phage therapy.     

The evolution of parasite manipulation of host dispersal

We investigate the evolution of manipulation of host dispersal behaviour by parasites using spatially explicit individual-based simulations. We find that when dispersal is local, parasites always gain from increasing their hosts' dispersal rate, although the evolutionary outcome is determined by the costs-to-benefits ratio. However, when dispersal can be non-local, we show that parasites investing in an intermediate dispersal distance of their hosts are favoured even when the manipulation is not costly, due to the intrinsic spatial dynamics of the host-parasite interaction. Our analysis highlights the crucial importance of ecological spatial dynamics in evolutionary processes and reveals the theoretical possibility that parasites could manipulate their hosts' dispersal.     

Behavior out of control: Experimental evolution of resistance to host manipulation

Many parasites alter their host's phenotype in a manner that enhances their own fitness beyond the benefits they would gain from normal exploitation. Such host manipulation is rarely consistent with the host's best interests resulting in suboptimal and often fatal behavior from the host's perspective. In this case, hosts should evolve resistance to host manipulation. The cestode Schistocephalus solidus manipulates the behavior of its first intermediate copepod host to reduce its predation susceptibility and avoid fatal premature predation before the parasite is ready for transmission to its subsequent host. Thereafter, S. solidus increases host activity to facilitate transmission. If successful, this host manipulation is necessarily fatal for the host. I selected the copepod Macrocyclops albidus, a first intermediate host of S. solidus, for resistance or susceptibility to host manipulation to investigate their evolvability. Selection on the host indeed increased host manipulation in susceptible and reduced host manipulation in resistant selection lines. Interestingly, this seemed to be at least partly due to changes in the baseline levels of the modified trait (activity) rather than actual changes in resistance or susceptibility to host manipulation. Hence, hosts seem restricted in how rapidly and efficiently they can evolve resistance to host manipulation.     

基于智能计算噬菌体的细菌宿主范围预测

针对噬菌体的细菌宿主范围预测对于深入理解噬菌体及将其作为抗生素替代用于生物疗法具有重要意义。传统生物实验方法确定噬菌体的细菌宿主范围受到极有限的噬菌体可培养性和严苛的培养条件限制,而高通量测序技术所提供的海量基因组或宏基因组序列提供了噬菌体及细菌重要的序列信息,因此智能计算为预测噬菌体的细菌宿主范围提供了可行方法。本文从智能计算的角度对噬菌体的细菌宿主范围预测研究进行系统梳理,从噬菌体感染细菌的过程入手,描述配对预测模型所依赖的特征及其生物合理性,归纳宿主范围预测的智能模型、建模原理及预测策略,总结建模训练和评估所依赖的参考数据集与真实数据及评价指标。本文特别注意挖掘和分析各信息手段、模型、方法其背后的生物合理性及其依赖的生物机理。本综述期望推动基于智能算法的噬菌体的细菌宿主范围预测研究发展,并探索将生物先验结合人工智能实现噬菌体侵袭细菌宿主的本质机理推断,同时也为基于噬菌体的临床应用提供参考与借鉴。     

Scale insect host ranges are broader in the tropics

The specificity of the interactions between plants and their consumers varies considerably. The evolutionary and ecological factors underlying this variation are unclear. Several potential explanatory factors vary with latitude, for example plant species richness and the intensity of herbivory. Here, we use comparative phylogenetic methods to test the effect of latitude on host range in scale insects. We find that, on average, scale insects that occur in lower latitudes are more polyphagous. This result is at odds with the general pattern of greater host-plant specificity of insects in the tropics. We propose that this disparity reflects a high cost for host specificity in scale insects, stemming from unusual aspects of scale insect life history, for example, passive wind-driven dispersal. More broadly, the strong evidence for pervasive effects of geography on host range across insect groups stands in stark contrast to the weak evidence for constraints on host range due to genetic trade-offs.     

Geographic distribution and host plant ranges of East African noctuid stem borers

Surveys were carried out in Kenya, Tanzania, Uganda and Zanzibar to establish geographic distribution in the main vegetation mosaics and ecological (host plant range, feeding behaviour) characteristics of the East African noctuid stem borers. 49 wild plant species belonging to Poaceae, Cyperaceae and Typhaceae were found to harbour stem borers in the six vegetation mosaics surveyed. A total of 36 noctuid species belonging to nine genera were identified from 14,318 larvae collected, out of which 17 were new to science. The species diversity varied among vegetation mosaics and host plants. Most borer species appeared to be specialised feeders with 24 species being monophagous. Species belonging to the same types (named as the Busseola Thurau 1904 and the Sesamia Guenée 1852 types) or genus harboured common ecological characteristics such as pigmentation and feeding site. The Sciomesa Tams and Bowden 1953 genus was an exception as it had a mixture of these characters.     

Transposable elements and host genome evolution

Several recent reports have challenged the idea that transposable elements (TEs) are mainly 'selfish' or 'junk' DNA with little importance for host evolution. It has been proposed that TEs have the potential to provide host genomes with the ability to enhance their own evolution. They might also be a major source of genetic diversity, allowing response to environmental changes. Because the relationships between TEs and host genomes are highly variable, and because the selfish, junk and beneficial DNA hypotheses are by no means mutually exclusive, a single label for these relationships appears to be inappropriate and potentially misleading.     

The evolution of host protection by vertically transmitted parasites

Hosts are often infected by a variety of different parasites, leading to competition for hosts and coevolution between parasite species. There is increasing evidence that some vertically transmitted parasitic symbionts may protect their hosts from further infection and that this protection may be an important reason for their persistence in nature. Here, we examine theoretically when protection is likely to evolve and its selective effects on other parasites. Our key result is that protection is most likely to evolve in response to horizontally transmitted parasites that cause a significant reduction in host fecundity. The preponderance of sterilizing horizontally transmitted parasites found in arthropods may therefore explain the evolution of protection seen by their symbionts. We also find that protection is more likely to evolve in response to highly transmissible parasites that cause intermediate, rather than high, virulence (increased death rate when infected). Furthermore, intermediate levels of protection select for faster, more virulent horizontally transmitted parasites, suggesting that protective symbionts may lead to the evolution of more virulent parasites in nature. When we allow for coevolution between the symbiont and the parasite, more protection is likely to evolve in the vertically transmitted symbionts of longer lived hosts. Therefore, if protection is found to be common in nature, it has the potential to be a major selective force on host–parasite interactions.     

The evolution of host specialisation in avian brood parasites

Traditional ecological theory predicts that specialisation can promote speciation; hence, recently derived species are specialists. However, an alternative view is that new species have broad niches, which become narrower and specialised over time. Here, we test these hypotheses using avian brood parasites and three different measures of host specialisation. Brood parasites provide an ideal system in which to investigate the evolution of specialisation, because some exploit more than 40 host species and others specialise on only one. We find that young brood parasite species are smaller and specialise on a narrower range of host sizes, as expected, if specialisation is linked with the generation of new species. Moreover, we show that highly virulent parasites are more specialised, supporting findings in other host–parasite systems. Finally, we demonstrate that different measures of specialisation can lead to different conclusions, and specialisation indices should be designed taking into account the biology of each system.     

转座因子和宿主基因组的进化

转座因子主要是一些“自在”或“无功能”的DNA,其对宿主进化无关紧要的观点受到了质疑。新近的报道指出,它们有增强宿主基因组自身进化,对环境变化作出反应的潜在能力,很可能是遗传多样性的主要源泉。     

The evolution of parasite virulence, superinfection, and host resistance

We analyze the evolutionary consequences of host resistance (the ability to decrease the probability of being infected by parasites) for the evolution of parasite virulence (the deleterious effect of a parasite on its host). When only single infections occur, host resistance does not affect the evolution of parasite virulence. However, when superinfections occur, resistance tends to decrease the evolutionarily stable (ES) level of parasite virulence. We first study a simple model in which the host does not coevolve with the parasite (i.e., the frequency of resistant hosts is independent of the parasite). We show that a higher proportion of resistant host decreases the ES level of parasite virulence. Higher levels of the efficiency of host resistance, however, do not always decrease the ES parasite virulence. The implications of these results for virulence management (evolutionary consequences of public health policies) are discussed. Second, we analyze the case where host resistance is allowed to coevolve with parasite virulence using the classical gene-for-gene (GFG) model of host-parasite interaction. It is shown that GFG coevolution leads to lower parasite virulence (in comparison with a fully susceptible host population). The model clarifies and relates the different components of the cost of parasitism: infectivity (ability to infect the host) and virulence (deleterious effect) in an evolutionary perspective.     

Identification of two mosquitocidal Bacillus cereus strains showing different host ranges

Mosquitocidal bacteria, M413 and C32 have been isolated from sediment samples collected from woodland and ditch, respectively. Gas chromatographic analysis of fatty acids methyl esters (GC-FAME) and 16S rRNA gene sequence alignment results showed these isolates belong to Bacillus cereus. The SDS-PAGE analysis of sporulated cultures of both isolates showed two major bands very similar in size. Interestingly, however, M413 is mainly toxic to 4th instars of Ochlerotatus taeniorhynchus whereas C32 is to those of Culex quinquefasciatus.