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1.
The interaction of bacterial pathogens with their hosts’ innate immune systems can be extremely complex and is often difficult
to disentangle experimentally. Using mouse models of bacterial infections, several laboratories have successfully applied
genetic approaches to identify novel host genes required for innate immune defense. In addition, a variety of creative bacterial
genetic schemes have been developed to identify key bacterial genes involved in triggering or evading host immunity. In cases
where both the host and pathogen are amenable to genetic manipulation, a combination of host and pathogen genetic approaches
can be used. Focusing on bacterial infections of mice, this review summarizes the benefits and limitations of applying genetic
analysis to the study of host–pathogen interactions. In particular, we consider how prokaryotic and eukaryotic genetic strategies
can be combined, or “squared,” to yield new insights in host–pathogen biology. 相似文献
2.
Timothy L. Friesen C.-G. Chu Z. H. Liu S. S. Xu S. Halley J. D. Faris 《TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik》2009,118(8):1489-1497
Stagonospora nodorum, causal agent of Stagonospora nodorum blotch (SNB), is a destructive pathogen of wheat worldwide. As is true for many necrotrophic
host–pathogen systems, the wheat-S. nodorum system is complex and resistance to SNB is usually quantitatively inherited. We recently showed that S. nodorum produces at least four proteinaceous host-selective toxins that interact with dominant host sensitivity/susceptibility gene
products to induce SNB in seedlings. Here, we evaluated a population of wheat recombinant inbred lines that segregates for
Tsn1, Snn2, and Snn3, which confer sensitivity to the toxins SnToxA, SnTox2, and SnTox3, respectively, to determine if compatible host–toxin interactions
are associated with adult plant susceptibility to SNB foliar disease under field conditions. Artificial inoculation of the
population in 2 years and two locations with a fungal isolate known to produce SnToxA and SnTox2 indicated that compatible
SnToxA–Tsn1 and SnTox2–Snn2 interactions accounted for as much as 18 and 15% of the variation in disease severity on the flag leaf, respectively. As
previously reported for seedlings, the effects of these two interactions in conferring adult plant susceptibility were largely
additive. Additional adult plant resistance QTLs were identified on chromosomes 1B, 4B, and 5A, of which, the 1B and 5A QTLs
were previously reported to be associated with seedling resistance to SNB. Therefore, in this population, some of the same
QTLs are responsible for seedling and adult plant resistance/susceptibility. This is the first report showing that host-selective
toxins confer susceptibility of adult plants to SNB, further substantiating the importance of compatible toxin–host interactions
in the wheat-S. nodorum pathosystem.
Mention of trade names or commercial products in this article is solely for the purpose of providing specific information
and does not imply recommendation or endorsement by the US Department of Agriculture. 相似文献
3.
Although the role of host heredity in susceptibility to infectious diseases is significant, the genetic control of immunity to infection remains poorly understood. Advances in experimental and epidemiological analyses of complex genetic traits have led to the discoveries of novel genetic determinants of host resistance. New loci that control susceptibility to a number of intracellular pathogens have been identified using mouse models of infectious diseases. The contributions of individual loci, however, vary in quantitative and qualitative manner, depending on mechanisms of pathogen virulence and genetic background of the host. In this review, we discuss how genetic analysis of host resistance contributes to further understanding of host immunity and pathogenesis of intracellular infections. 相似文献
4.
5.
Pathogens and parasites can be strong agents of selection, and often exhibit some degree of genetic specificity for individual
host strains. Here we show that this host–pathogen specificity can affect the evolution of host life history traits. All else
equal, evolution should select for genes that increase individuals' reproduction rates or lifespans (and thus total reproduction
per individual). Using a simple host–pathogen model, we show that when the genetic specificity of pathogen infection is low,
host strains with higher reproduction rates or longer lifespans drive slower-reproducing or shorter-lived host strains to
extinction, as one would expect. However, when pathogens exhibit specificity for host strains with different life history
traits, the evolutionary advantages of these traits can be greatly diminished by pathogen-mediated selection. Given sufficient
host–pathogen specificity, pathogen-mediated selection can maintain polymorphism in host traits that are correlated with pathogen
resistance traits, despite large intrinsic fitness differences among host strains. These results have two important implications.
First, selection on host life history traits will be weaker than expected, whenever host fitness is significantly affected
by genotype-specific pathogen attack. Second, where polymorphism in host traits is maintained by pathogen-mediated selection,
preserving the genetic diversity of host species may require preserving their pathogens as well.
This revised version was published online in November 2006 with corrections to the Cover Date. 相似文献
6.
The process of coevolution between host and enemy has traditionally been viewed as an evolutionary arms race between resistance and counterresistance. The arms-race metaphor of coevolution is widely accepted because it explains the evolution of many characters in species involved in host–enemy interactions. However, molecular work in plant–pathogen systems suggests a coevolutionary interplay between plant recognition of an attacking pathogen and pathogen evasion from recognition. We refer to this process as information coevolution, and contrast this with arms race coevolution to show that these two processes result in very different patterns of host resistance and enemy virulence at the population level. First, information coevolution results in a lower proportion of hosts that are susceptible to enemy attack within a population. Second, information coevolution produces a pattern of local maladaptation of enemy on host, a naturally occurring phenomenon that is difficult to explain under arms race coevolution. We then conduct a literature review to survey the empirical support for either mode of coevolution using the predicted patterns of host resistance and enemy virulence. Evidence supports both modes of coevolution in plant–enemy interactions, whereas no support is found for information coevolution in vertebrate–parasite and invertebrate–parasite systems. 相似文献
7.
Effects of phenotypic plasticity on pathogen transmission in the field in a Lepidoptera-NPV system 总被引:1,自引:1,他引:0
A. F. Reeson K. Wilson J. S. Cory P. Hankard J. M. Weeks D. Goulson R. S. Hails 《Oecologia》2000,124(3):373-380
In models of insect–pathogen interactions, the transmission parameter (ν) is the term that describes the efficiency with which
pathogens are transmitted between hosts. There are two components to the transmission parameter, namely the rate at which
the host encounters pathogens (contact rate) and the rate at which contact between host and pathogen results in infection
(host susceptibility). Here it is shown that in larvae of Spodoptera exempta (Lepidoptera: Noctuidae), in which rearing density triggers the expression of one of two alternative phenotypes, the high-density
morph is associated with an increase in larval activity. This response is likely to result in an increase in the contact rate
between hosts and pathogens. Rearing density is also known to affect susceptibility of S. exempta to pathogens, with the high-density morph showing increased resistance to a baculovirus. In order to determine whether density-dependent
differences observed in the laboratory might affect transmission in the wild, a field trial was carried out to estimate the
transmission parameter for S. exempta and its nuclear polyhedrosis virus (NPV). The transmission parameter was found to be significantly higher among larvae reared
in isolation than among those reared in crowds. Models of insect–pathogen interactions, in which the transmission parameter
is assumed to be constant, will therefore not fully describe the S. exempta-NPV system. The finding that crowding can influence transmission in this way has major implications for both the long-term
population dynamics and the invasion dynamics of insect–pathogen systems.
Received: 14 June 1999 / Accepted: 22 March 2000 相似文献
8.
Mycobacterium tuberculosis is an example of an intracellular pathogen that mediates the disease state through complex interactions with the host’s immune
system. Not only does this organism replicate in the hostile environment prevailing within the infected macrophage, but it
has also developed intricate mechanisms to inhibit several defence mechanisms of the host’s immune system. It is postulated
here that the mediators of these interactions with the host are products of differentially expressed genes in the pathogen.
B and T cell responses of the host are hence to be used as tools to identify such gene products from an expression library
of theMycobacterium tuberculosis genome. The various pathways of generating a productive immune response that may be targeted by the pathogen are discussed 相似文献
9.
The heterogeneity of parasitism risk among host individuals is a key factor for stabilizing or sustaining host–parasitoid
interactions. Host maturation variability, or the variation in the maturation times among host individuals, is the simplest
source of such heterogeneity, but it has often been neglected in previous theoretical studies. We developed a configuration
individual-based model (cIBM) of host–parasitoid interaction to investigate to what degree of host maturation variability
promotes the persistence of host–parasitoid interactions. We ran simulations with various degrees of host maturation variability
for different lengths of unsusceptible period. The result showed that low host maturation variability could sustain host–parasitoid
dynamics when the host-unsusceptible period was short. Conversely, high levels of variability could sustain host–parasitoid
dynamics when the host-unsusceptible period was about half of the total larval period. This suggests that the balance between
variability and unsusceptible period is important for the persistence of host–parasitoid interaction. We conclude that maturation
variability is a factor that can contribute to the sustainment of host–parasitoid interactions. 相似文献
10.
A growing body of evidence points towards epigenetic mechanisms being responsible for a wide range of biological phenomena, from the plasticity of plant growth and development to the nutritional control of caste determination in honeybees and the etiology of human disease (e.g., cancer). With the (partial) elucidation of the molecular basis of epigenetic variation and the heritability of certain of these changes, the field of evolutionary epigenetics is flourishing. Despite this, the role of epigenetics in shaping host–pathogen interactions has received comparatively little attention. Yet there is plenty of evidence supporting the implication of epigenetic mechanisms in the modulation of the biological interaction between hosts and pathogens. The phenotypic plasticity of many key parasite life-history traits appears to be under epigenetic control. Moreover, pathogen-induced effects in host phenotype may have transgenerational consequences, and the bases of these changes and their heritability probably have an epigenetic component. The significance of epigenetic modifications may, however, go beyond providing a mechanistic basis for host and pathogen plasticity. Epigenetic epidemiology has recently emerged as a promising area for future research on infectious diseases. In addition, the incorporation of epigenetic inheritance and epigenetic plasticity mechanisms to evolutionary models and empirical studies of host–pathogen interactions will provide new insights into the evolution and coevolution of these associations. Here, we review the evidence available for the role epigenetics on host–pathogen interactions, and the utility and versatility of the epigenetic technologies available that can be cross-applied to host–pathogen studies. We conclude with recommendations and directions for future research on the burgeoning field of epigenetics as applied to host–pathogen interactions. 相似文献
11.
The role of evolutionary dynamics in understanding host–parasitoid interactions is interlinked with the population dynamics
of these interactions. Here, we address the problems in coupling evolutionary and population dynamics of host–parasitoid interactions.
We review previous theoretical and empirical studies and show that evolution can alter the ecological dynamics of a host–parasitoid
interaction. Whether evolution stabilizes or destabilizes the interaction depends on the direction of evolutionary changes,
which are affected by ecological, physiological, and genetic details of the insect biology. We examine the effect of life
history correlations on population persistence and stability, embedding two types, one of which is competitively inferior
but superior in encapsulation (for parasitoid, virulence), in a Nicholson–Bailey model with intraspecific resource competition
for host. If a trade-off exists between intraspecific competitive ability and encapsulation (or virulence, as a countermeasure)
in both the host and parasitoid, the trade-off or even positive correlation in the parasitoid is less influential to ecological
stability than the trade-off in the host. We comment on the bearing this work has on the broader issues of understanding host–parasitoid
interactions, including long-term biological control.
Received: November 10, 1998 / Accepted: January 18, 1999 相似文献
12.
Classical predator–prey and host–parasite systems have been extensively studied in a food web context. Less attention has
been paid to communities that include pathogens and their vectors. We present a coarse-grained, pan-African analysis of the
relationships between the abiotic environment (location, precipitation, temperature), the species richness and community composition
of ixodid ticks, and the species richness and community composition of pathogens that ticks transmit to humans. We found strong
correlations between the abiotic environment and tick species richness, and a weak but significant correlation between the
abiotic environment and pathogen species richness. A substantial amount of variation in community composition of parasites
and pathogens was not explained by the variables that we considered. A structural equation model that compensated for the
indirect effects of climate on the pathogen community via tick community composition suggested that while the environment
strongly regulates tick community composition and tick community composition strongly regulates pathogen community composition,
abiotic influences on pathogen species richness and community composition are weak. Our results support the view that changes
in the broader environment will influence tick-borne pathogens primarily via the influence of the environment on ticks. The
interactions that regulate host–vector–pathogen dynamics are of particular relevance in understanding the relationships between
environmental change and health concerns, such as the impact of climate change on the occurrence of vector-borne diseases. 相似文献
13.
牛基因组中一些重要基因的DNA突变通过改变基因的表达和蛋白质功能来影响机体对疾病的抗性或易感性。控制牛疾病的DNA变异主要分为单基因座及多基因座两类。导致疾病的单基因座类型亦称因果突变,其遗传基础较简单,突变一般位于基因编码区或非编码区,多为单碱基或少数几个碱基的突变,这些突变导致氨基酸的错义突变、翻译提前终止或部分外显子缺失等。相比而言,多基因相关疾病的遗传基础较为复杂,遗传-病原体-环境间的互作是导致这类复杂疾病的主要原因。文章综述了由单基因座和多基因座遗传变异所控制的牛主要疾病的研究和应用现状,以及在牛育种及生产中为降低这些疾病的发生所采用的遗传控制策略。 相似文献
14.
C.-G. Chu J. D. Faris S. S. Xu Timothy L. Friesen 《TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik》2010,120(7):1451-1459
Stagonospora nodorum is a foliar pathogen of wheat that produces several host-selective toxins (HSTs) and causes the disease Stagonospora nodorum
blotch (SNB). The wheat genes Snn1 and Tsn1 confer sensitivity to the HSTs SnTox1 and SnToxA, respectively. The objectives of this study were to dissect, quantify, and
compare the effects of compatible Snn1–SnTox1 and Tsn1–SnToxA interactions on susceptibility in the wheat-S. nodorum pathosystem. Inoculation of a wheat doubled haploid population that segregates for both Snn1 and Tsn1 with an S. nodorum isolate that produces both SnTox1 and SnToxA indicated that both interactions were strongly associated with SNB susceptibility.
The Snn1–SnTox1 and Tsn1–SnToxA interactions explained 22 and 28% of the variation in disease, respectively, and together they explained 48% indicating
that their effects are largely additive. The Snn1–SnTox1 interaction accounted for 50% of the variation when the population was inoculated with an S. nodorum strain where the SnToxA gene had been mutated, eliminating the Tsn1–SnToxA interaction. These results support the theory that the wheat-S. nodorum pathosystem is largely based on multiple host–toxin interactions that follow an inverse gene-for-gene scenario at the host–toxin
interface, but disease exhibits quantitative variation due to the mainly additive nature of compatible interactions. The elimination
of either Snn1 or Tsn1 toxin sensitivity alleles resulted in decreased susceptibility, but the elimination of both interactions was required to
obtain high levels of resistance. We propose the use of molecular markers to select against Snn1, Tsn1, and other toxin sensitivity alleles to develop wheat varieties with high levels of SNB resistance. 相似文献
15.
The amenability of Caenorhabditis elegans against pathogen provides a valuable tool for studying host–pathogen interactions. Physiological experiments revealed that
the P. aeruginosa was able to kill C. elegans efficiently. The effects of P. aeruginosa PA14, PAO1 and their isolated lipopolysaccharide (LPS) on the host system were analyzed. The LPS at higher concentrations
(≥2 mg/ml) was toxic to the host animals. Kinetic studies using qPCR revealed the regulation of host-specific candidate antimicrobial
genes during pathogen-mediated infections. In addition, the pathogen-specific virulent gene, exoT expression, was anlyzed and found to be varied during the interactions with the host system. Ability of the pathogens to
modify their internal machinery in the presence of the host was analyzed by XRD, FTIR and PCA. LPS isolated from pathogens
upon exposure to C. elegans showed modifications at their functional regions. LPS from PAO1 showed difference in d-spacing angle (Å) and °2Th position.
FTIR spectra revealed alterations in polysaccharide (1,200–900 cm−1) and fatty acid (3,000–2,800 cm−1) regions of LPS from P. aeruginosa PAO1 exposed to the host system. These data provide additional insights on how the pathogens subvert its own and host machinery
during interactions. 相似文献
16.
Masami Takagi 《Population Ecology》1999,41(1):121-126
We have not yet had sufficient theoretical explanation for successful biological control in which a key pest is controlled
after an introduction of natural enemies. I compare here real features of successful biological control and theoretical host–parasitoid
population models to reduce the gap between theory and practice. I first review the historical interaction between classical
biological control projects and theoretical population models. Second, I consider the importance of host refuges in host–parasitoid
population dynamics as concerns the mechanisms of low and stable host density. The importance of density–dependent parasitism
through parasitoid reproduction in multivoltine host–parasitoid systems and supplemental generalist natural enemies are also
discussed. Finally, I consider the difference in tactics for classical biological control and for augmentation of natural
enemies in annual crop systems.
Received: December 20, 1998 / Accepted: January 15, 1999 相似文献
17.
Sialic acid, a nine-carbon sugar acid usually is present in the non-reducing terminal position of free oligosaccharides and glycoconjugates. Sialylated conjugates in mammals perform important roles in cellular recognition, signaling, host–pathogen interaction and neuronal development. Metabolism of sialylated conjugates involves a complex pathway consisting of enzymes distributed among the different compartments in the cell. These enzymes are encoded by 32 genes diversely distributed throughout the mammalian genome. Genetic variants in some of these genes are associated with embryonic lethality and abnormal phenotypes in mice and neuromuscular diseases, carcinomas and immune-mediated diseases in humans. In humans, the CMP-NeuAc-hydroxylase (CMAH) enzyme is inactivated due to a deletion mutation in the encoded enzyme. This lack of Neu5Gc phenotype makes humans unique among mammals. This review focuses on genes encoding enzymes in sialic acid metabolism pathways in mammalian cells with special emphasis on the human, mouse and cow. 相似文献
18.
Rodrigo Cogni Jonathan P. Day Calum Bridson Francis M. Jiggins 《Molecular ecology》2016,25(20):5228-5241
Variation in susceptibility to infection has a substantial genetic component in natural populations, and it has been argued that selection by pathogens may result in it having a simpler genetic architecture than many other quantitative traits. This is important as models of host–pathogen co‐evolution typically assume resistance is controlled by a small number of genes. Using the Drosophila melanogaster multiparent advanced intercross, we investigated the genetic architecture of resistance to two naturally occurring viruses, the sigma virus and DCV (Drosophila C virus). We found extensive genetic variation in resistance to both viruses. For DCV resistance, this variation is largely caused by two major‐effect loci. Sigma virus resistance involves more genes – we mapped five loci, and together these explained less than half the genetic variance. Nonetheless, several of these had a large effect on resistance. Models of co‐evolution typically assume strong epistatic interactions between polymorphisms controlling resistance, but we were only able to detect one locus that altered the effect of the main effect loci we had mapped. Most of the loci we mapped were probably at an intermediate frequency in natural populations. Overall, our results are consistent with major‐effect genes commonly affecting susceptibility to infectious diseases, with DCV resistance being a near‐Mendelian trait. 相似文献
19.
Scalzo AA Corbett AJ Rawlinson WD Scott GM Degli-Esposti MA 《Immunology and cell biology》2007,85(1):46-54
Cytomegalovirus (CMV) remains a major human pathogen causing significant morbidity and mortality in immunosuppressed or immunoimmature individuals. Although significant advances have been made in dissecting out certain features of the host response to human CMV (HCMV) infection, the strict species specificity of CMVs means that most aspects of antiviral immunity are best assessed in animal models. The mouse model of murine CMV (MCMV) infection is an important tool for analysis of in vivo features of host-virus interactions and responses to antiviral drugs that are difficult to assess in humans. Important studies of the contribution of host resistance genes to infection outcome, interplays between innate and adaptive host immune responses, the contribution of virus immune evasion genes and genetic variation in these genes to the establishment of persistence and in vivo studies of resistance to antiviral drugs have benefited from the well-developed MCMV model. In this review, we discuss recent advances in the immunobiology of host-CMV interactions that provide intriguing insights into the complex interplay between host and virus that ultimately facilitates viral persistence. We also discuss recent studies of genetic responses to antiviral therapy, particularly changes in DNA polymerase and protein kinase genes of MCMV and HCMV. 相似文献
20.
Yann Bourgeois Peter D Fields Gilberto Bento Dieter Ebert 《Molecular biology and evolution》2021,38(11):4918
The link between long-term host–parasite coevolution and genetic diversity is key to understanding genetic epidemiology and the evolution of resistance. The model of Red Queen host–parasite coevolution posits that high genetic diversity is maintained when rare host resistance variants have a selective advantage, which is believed to be the mechanistic basis for the extraordinarily high levels of diversity at disease-related genes such as the major histocompatibility complex in jawed vertebrates and R-genes in plants. The parasites that drive long-term coevolution are, however, often elusive. Here we present evidence for long-term balancing selection at the phenotypic (variation in resistance) and genomic (resistance locus) level in a particular host–parasite system: the planktonic crustacean Daphnia magna and the bacterium Pasteuria ramosa. The host shows widespread polymorphisms for pathogen resistance regardless of geographic distance, even though there is a clear genome-wide pattern of isolation by distance at other sites. In the genomic region of a previously identified resistance supergene, we observed consistent molecular signals of balancing selection, including higher genetic diversity, older coalescence times, and lower differentiation between populations, which set this region apart from the rest of the genome. We propose that specific long-term coevolution by negative-frequency-dependent selection drives this elevated diversity at the host''s resistance loci on an intercontinental scale and provide an example of a direct link between the host’s resistance to a virulent pathogen and the large-scale diversity of its underlying genes. 相似文献