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Heterogeneous noise enhances spatial reciprocity  [PDF]
Y. Yao,S. -S. Chen
Quantitative Biology , 2014, DOI: 10.1016/j.physa.2014.06.041
Abstract: Recent research has identified the heterogeneity as crucial for the evolution of cooperation in spatial population. However, the influence of heterogeneous noise is still lack. Inspired by this interesting question, in this work, we try to incorporate heterogeneous noise into the evaluation of utility, where only a proportion of population possesses noise, whose range can also be tuned. We find that increasing heterogeneous noise monotonously promotes cooperation and even translates the full defection phase (of the homogeneous version) into the complete cooperation phase. Moreover, the promotion effect of this mechanism can be attributed to the leading role of cooperators who have the heterogeneous noise. These type of cooperators can attract more agents penetrating into the robust cooperator clusters, which is beyond the text of traditional spatial reciprocity. We hope that our work may shed light on the understanding of the cooperative behavior in the society.
Host genotype by parasite genotype interactions underlying the resistance of anopheline mosquitoes to Plasmodium falciparum
Louis Lambrechts, Jean Halbert, Patrick Durand, Louis C Gouagna, Jacob C Koella
Malaria Journal , 2005, DOI: 10.1186/1475-2875-4-3
Abstract: To test for genotype by genotype interactions between malaria parasites and their anopheline vectors, different genetic backgrounds (families consisting of the F1 offspring of individual females) of the major African vector Anopheles gambiae were challenged with several isolates of the human malaria parasite Plasmodium falciparum (obtained from naturally infected children in Kenya).Averaged across all parasites, the proportion of infected mosquitoes and the number of oocysts found in their midguts were similar in all mosquito families. Both indices of resistance, however, differed considerably among isolates of the parasite. In particular, no mosquito family was most resistant to all parasites, and no parasite isolate was most infectious to all mosquitoes.These results suggest that the level of mosquito resistance depends on the interaction between its own and the parasite's genotype. This finding thus emphasizes the need to take into account the range of genetic diversity exhibited by mosquito and malaria field populations in ideas and studies concerning the control of malaria.In the last few years, exciting advances in the biology and molecular genetics of the development of Plasmodium parasites in their mosquito vectors [1,2] have led to the creation of transgenic mosquitoes that are partially resistant to malaria infection [3], bringing the efforts to control malaria with the techniques of transgenesis a major step forward [4,5]. A crucial aspect of these advances is, of course, the fact that the mosquito's genetic make-up determines, at least partly, its resistance to malaria infection [6,7], giving hope for the possibility that key genes controlling resistance may be identified. This hope has been reinforced by the recent identification, in a rodent model of malaria, of several mosquito immune genes that affect parasite development [8,9]. Unfortunately, several aspects of the current knowledge make it difficult to estimate the relevance of such laboratory-base
Spreading of Persistent Infections in Heterogeneous Populations  [PDF]
J. Sanz,L. M. Floria,Y. Moreno
Quantitative Biology , 2010, DOI: 10.1103/PhysRevE.81.056108
Abstract: Up to now, the effects of having heterogeneous networks of contacts have been studied mostly for diseases which are not persistent in time, i.e., for diseases where the infectious period can be considered very small compared to the lifetime of an individual. Moreover, all these previous results have been obtained for closed populations, where the number of individuals does not change during the whole duration of the epidemics. Here, we go one step further and analyze, both analytically and numerically, a radically different kind of diseases: those that are persistent and can last for an individual's lifetime. To be more specific, we particularize to the case of Tuberculosis' (TB) infection dynamics, where the infection remains latent for a period of time before showing up and spreading to other individuals. We introduce an epidemiological model for TB-like persistent infections taking into account the heterogeneity inherent to the population structure. This sort of dynamics introduces new analytical and numerical challenges that we are able to sort out. Our results show that also for persistent diseases the epidemic threshold depends on the ratio of the first two moments of the degree distribution so that it goes to zero in a class of scale-free networks when the system approaches the thermodynamic limit.
Do Antenatal Parasite Infections Devalue Childhood Vaccination?  [PDF]
A. Desiree LaBeaud equal contributor ,Indu Malhotra equal contributor,Maria J. King,Christopher L. King,Charles H. King
PLOS Neglected Tropical Diseases , 2009, DOI: 10.1371/journal.pntd.0000442
Abstract: On a global basis, both potent vaccine efficacy and high vaccine coverage are necessary to control and eliminate vaccine-preventable diseases. Emerging evidence from animal and human studies suggest that neglected tropical diseases (NTDs) significantly impair response to standard childhood immunizations. A review of efficacy and effectiveness studies of vaccination among individuals with chronic parasitic infections was conducted, using PUBMED database searches and analysis of data from the authors' published and unpublished studies. Both animal models and human studies suggest that chronic trematode, nematode, and protozoan infections can result in decreased vaccine efficacy. Among pregnant women, who in developing countries are often infected with multiple parasites, soluble parasite antigens have been shown to cross the placenta and prime or tolerize fetal immune responses. As a result, antenatal infections can have a significant impact on later vaccine responses. Acquired childhood parasitic infections, most commonly malaria, can also affect subsequent immune response to vaccination. Additional data suggest that antiparasite therapy can improve the effectiveness of several human vaccines. Emerging evidence demonstrates that both antenatal and childhood parasitic infections alter levels of protective immune response to routine vaccinations. Successful antiparasite treatment may prevent immunomodulation caused by parasitic antigens during pregnancy and early childhood and may improve vaccine efficacy. Future research should highlight the varied effects that different parasites (alone and in combination) can have on human vaccine-related immunity. To optimize vaccine effectiveness in developing countries, better control of chronic NTDs may prove imperative.
Genotype-specific interactions and the trade-off between host and parasite fitness
Lucie Salvaudon, Virginie Héraudet, Jacqui A Shykoff
BMC Evolutionary Biology , 2007, DOI: 10.1186/1471-2148-7-189
Abstract: We performed a controlled cross inoculation experiment confronting six lines of the host plant with seven strains of the parasite in order to evaluate genetic variation for phenotypic traits of infection among hosts, parasites, and distinct combinations. Parasite infection intensity and transmission were highly variable among parasite strains and host lines but depended also on the interaction between particular genotypes of the protagonists, and genetic variation for the infection phenotype of parasites from natural populations was found even at a small spatial scale within population. Furthermore, increased parasite fitness led to a significant decrease in host fitness only on a single host line (Gb), although a trade-off between these two traits was expected because host and parasite share the same resource pool for their respective reproduction. We propose that different levels of compatibility dependent on genotype by genotype interactions might lead to different amounts of resources available for host and parasite reproduction. This variation in compatibility could thus mask the expected negative relationship between host and parasite fitness, as the total resource pool would not be constant.These results highlight the importance of host variation in the determination of parasite fitness traits. This kind of interaction may in turn decouple the relationship between parasite transmission and its negative effect on host fitness, altering theoretical predictions of parasite evolution.Understanding the selective forces driving parasite evolution is crucial in the fight against infectious diseases, both in agriculture and human health. Darwinian medicine aims at controlling the evolution of human pathogens in order to drive them toward "milder" forms or, ideally, to extinction [1]. Such control requires knowledge of which traits of infections are adaptive for the host or the parasite as well as the associated trade-offs between traits and constraints on their evolu
Trypanosoma congolense Infections: Induced Nitric Oxide Inhibits Parasite Growth In Vivo  [PDF]
Wenfa Lu,Guojian Wei,Wanling Pan,Henry Tabel
Journal of Parasitology Research , 2011, DOI: 10.1155/2011/316067
Abstract: Wild-type (WT) C57BL/6 mice infected intraperitoneally with Trypanosoma congolense survive for more than 30 days. C57BL/6 mice deficient in inducible nitric oxide synthase (iNOS?/?) and infected with 103 or parasites do not control the parasitemia and survive for only or days, respectively. Bloodstream trypanosomes of iNOS?/? mice infected with ??T. congolense had a significantly higher ratio of organisms in the S+G2+M phases of the cell cycle than trypanosomes in WT mice. We have reported that IgM anti-VSG-mediated phagocytosis of T. congolense by macrophages inhibits nitric oxide (NO) synthesis via CR3 (CD11b/CD18). Here, we show that during the first parasitemia, but not at later stages of infection, T. congolense-infected CD11b?/? mice produce more NO and have a significantly lower parasitemia than infected WT mice. We conclude that induced NO contributes to the control of parasitemia by inhibiting the growth of the trypanosomes. 1. Introduction Trypanosoma congolense is a protozoan pathogen of cattle and other livestock. The parasite causes N’gana in livestock, one form of the disease complex collectively known as African trypanosomiases [1]. In the mammalian host, the whole parasite is covered with a glycoprotein coat of a single molecular species, called variant surface glycoprotein (VSG) [2]. In host defense against infection, macrophages play an important role through their ability to remove specific substances from the blood stream via various receptors, such as complement receptors, Fc-receptors, scavenger receptors, and mannose receptors [3, 4]. The control of parasitemia in African trypanosomiasis is mediated by at least two known mechanisms: (1) antibody-mediated phagocytosis [5–9] and (2) to a lesser degree, by antibody/complement-mediated lysis [10–13]. A third mechanism, that is, release of trypanotoxic NO by macrophages has been demonstrated in vitro for T. brucei and T. congolense [14–18]. The role of NO in vivo has been controversial. We had speculated that NO might be involved in the control of T. congolense infections [9]. There is evidence that NO does not contribute to control of T. brucei in vivo [19, 20] but does contribute to control of T. congolense infections [21, 22]. We found that IgG2a anti-VSG antibody-mediated phagocytosis of T. congolense enhances the synthesis of NO by macrophages, whereas IgM anti-VSG antibody-mediated phagocytosis inhibited synthesis of NO [7, 14]. The inhibition of NO synthesis apparently increased with increasing amounts of IgM anti-VSG [14]. We further observed that macrophages of CD11b?/? mice
Probing Mixed-Genotype Infections II: High Multiplicity in Natural Infections of the Trypanosomatid, Crithidia bombi, in Its Host, Bombus spp  [PDF]
Martina Tognazzo, Regula Schmid-Hempel, Paul Schmid-Hempel
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0049137
Abstract: Mixed-genotype infections have major consequences for many essential elements of host-parasite interactions. With genetic exchange between co-infecting parasite genotypes increased diversity among parasite offspring and the emergence of novel genotypes from infected hosts is possible. We here investigated mixed- genotype infections using the host, Bombus spp. and its trypanosome parasite Crithidia bombi as our study case. The natural infections of C. bombi were genotyped with a novel method for a representative sample of workers and spring queens in Switzerland. We found that around 60% of all infected hosts showed mixed-genotype infections with an average of 2.47±0.22 (S.E.) and 3.65±1.02 genotypes per worker or queen, respectively. Queens, however, harboured up to 29 different genotypes. Based on the genotypes of co-infecting strains, these could be putatively assigned to either ‘primary’ and ‘derived’ genotypes - the latter resulting from genetic exchange among the primary genotypes. High genetic relatedness among co-infecting derived but not primary genotypes supported this scenario. Co-infection in queens seems to be a major driver for the diversity of genotypes circulating in host populations.
The separate and combined effects of MHC genotype, parasite clone, and host gender on the course of malaria in mice
Claus Wedekind, Mirjam Walker, Tom J Little
BMC Genetics , 2006, DOI: 10.1186/1471-2156-7-55
Abstract: We found that MHC haplotype and parasite clone each have a significant influence on the course of the disease, but there was no significant host genotype by parasite genotype interaction. We found no evidence for overdominance nor any other sort of heterozygote advantage or disadvantage.When tested under experimental conditions, variation in the MHC can significantly influence the course of malaria. However, MHC heterozygote advantage through overdominance or dominance of resistance cannot be assumed in the case of single-strain infections. Future studies might focus on the interaction between MHC heterozygosity and multiple-clone infections.The link between the MHC (major histocompatibility complex) and malaria [1,2] is a widely cited example of a link between host genes and the course of a disease. However, for humans, such links cannot be studied under controlled experimental conditions. Therefore, the significance of the MHC for disease severity is still not fully understood [3-12].The mouse model offers the possibility of studying potential MHC effects both under experimental conditions and in congenic strains, i.e. in strains that differ only in the MHC region but are identical on the rest of the genome [13-16]. However, even when working with MHC congenic strains, potential confounding effects remain. This include, firstly, host age which may influence pathogen susceptibility and should therefore not vary with MHC genotype. Secondly, maternal environmental effects are known to affect offspring size, number, and general vigour [17,18]. Such maternal effects could explain why some congenic strains produce different olfactory signals only in parental strains but not in F2 segregants [19], or why congenic strains sometimes differ in behavior [20]. Lastly, MHC-congenic lines may differ with respect to the mutation load on their background genes, as there is at least one example of different mortalities during the first days of development before blastocyst formati
Probing Mixed-Genotype Infections I: Extraction and Cloning of Infections from Hosts of the Trypanosomatid Crithidia bombi  [PDF]
Rahel Salathé, Martina Tognazzo, Regula Schmid-Hempel, Paul Schmid-Hempel
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0049046
Abstract: We here present an efficient, precise and reliable method to isolate and cultivate healthy and viable single Crithidia bombi cells from bumblebee faeces using flow cytometry. We report a precision of >99% in obtaining single trypanosomatid cells for further culture and analysis (“cloning”). In the study, we have investigated the use of different liquid media to cultivate C. bombi and present an optimal medium for obtaining viable clones from all tested, infected host donors. We show that this method can be applied to genotype a collection of clones from natural infections. Furthermore, we show how to cryo-preserve C. bombi cells to be revived to become infective clones after at least 4 years of storage. Considering the high prevalence of infections in natural populations, our method provides a powerful tool in studying the level and diversity of these infections, and thus enriches the current methodology for the studies of complex host-parasite interactions.
B-Cell Response during Protozoan Parasite Infections  [PDF]
María C. Amezcua Vesely,Daniela A. Bermejo,Carolina L. Montes,Eva V. Acosta-Rodríguez,Adriana Gruppi
Journal of Parasitology Research , 2012, DOI: 10.1155/2012/362131
Abstract: In this review, we discuss how protozoan parasites alter immature and mature B cell compartment. B1 and marginal zone (MZ) B cells, considered innate like B cells, are activated during protozoan parasite infections, and they generate short lived plasma cells providing a prompt antibody source. In addition, protozoan infections induce massive B cell response with polyclonal activation that leads to hypergammaglobulnemia with serum antibodies specific for the parasites and self and/or non related antigens. To protect themselves, the parasites have evolved unique ways to evade B cell immune responses inducing apoptosis of MZ and conventional mature B cells. As a consequence of the parasite induced-apoptosis, the early IgM response and an already establish humoral immunity are affected during the protozoan parasite infection. Moreover, some trypanosomatides trigger bone marrow immature B cell apoptosis, influencing the generation of new mature B cells. Simultaneously with their ability to release antibodies, B cells produce cytokines/quemokines that influence the characteristic of cellular immune response and consequently the progression of parasite infections. 1. B Cells Can Play Protective and Pathogenic Roles in Protozoan Infections Host resistance in protozoan infections is dependent on both innate and acquired cell-mediated immune responses. In addition, several studies have implicated B cells and antibodies (Abs) in host survival and protozoan parasite clearance [1–3]. B cells can function as Ab-producing cells but they can also modulate immune responses through critical Ab-independent mechanisms that include secretion of cytokines and chemokines as well as antigen presentation [4–6]. Furthermore, B cells can directly modulate dendritic cells and T-cell subsets, and, consequently, they can influence adaptive immunity and the progression of the infection [7]. Accordingly, in protozoan infections B cells may play a protective and a pathological role. In malaria and trypanosome infections, Abs appear to play a famajor role in immunity. In Trypanosoma cruzi and T. brucei gambiense infections, Ab-dependent cytotoxic reactions against the parasite have been reported [8]. Several studies demonstrated that Abs are responsible for the survival of susceptible animals in the initial phase of T. cruzi infection and for the maintenance of low levels of parasitemia in the chronic phase [9, 10]. Although Abs were shown to be responsible for clearing the African trypanosomes from the blood of infected animals, recent evidence suggests that the survival time of
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