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Infected Hosts (infected + hosts)
Selected AbstractsCTL quality and the control of human retroviral infectionsEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 7 2009Charles R. M. Bangham Abstract The CTL response plays a central part in deciding the outcome of viral infections. Evidence from host and viral genetics, gene expression microarrays and assays of T-cell phenotype and function indicate that individual differences in the efficiency of the virus-specific CTL response strongly determine the outcome of infection with the human retroviruses HTLV-1 and HIV-1. It is now believed that differences in anti-viral CTL efficiency or "quality" at the single-cell level are critical in determining the efficacy of the host response to viruses. However, it is difficult to identify and quantify the reasons for this apparent individual variation in CTL efficiency, because of the chronic course of infection and the dynamical complexity of the equilibrium that is established between the virus and the host immune response. Specifically, it is unclear whether the observed variations among infected hosts, i.e. in the frequency, phenotype and function or quality of T cells, are the causes or effects , or both , of the variation in the efficiency of virus control. [source] Regulation of whole bacterial pathogen transcription within infected hostsFEMS MICROBIOLOGY REVIEWS, Issue 3 2008My-Van La Abstract DNA microarrays are a powerful and promising approach to gain a detailed understanding of the bacterial response and the molecular cross-talk that can occur as a consequence of host,pathogen interactions. However, published studies mainly describe the host response to infection. Analysis of bacterial gene regulation in the course of infection has confronted many challenges. This review summarizes the different strategies used over the last few years to investigate, at the genomic scale, and using microarrays, the alterations in the bacterial transcriptome in response to interactions with host cells. Thirty-seven studies involving 19 different bacterial pathogens were compiled and analyzed. Our in silico comparison of the transcription profiles of bacteria grown in broth or in contact with eukaryotic cells revealed some features commonly observed when bacteria interact with host cells, including stringent response and cell surface remodeling. [source] Immune Response to a 26-kDa Protein, Alkyl Hydroperoxide Reductase, in Helicobacter pylori-Infected Mongolian Gerbil ModelHELICOBACTER, Issue 4 2001Jing Yan ABSTRACT Background. The host immune response is thought to play an important role in the outcome of Helico-bacter pylori infection. The successful development of the H. pylori -infected Mongolian gerbil model that mimics human disease has enabled study of the antibody response against H. pylori antigens. Materials and Methods. Serum samples from ulcer and carcinogenesis models of H. pylori -infected gerbils were used to screen for H. pylori antigens that cause a humoral immune response in the infected hosts. H. pylori alkyl hydroperoxide reductase (AhpC) is one such antigen on which we report here. The tsaA gene encoding AhpC was amplified by PCR from H. pylori ATCC 43504 strain, cloned into pMALTM -c2 expression vector and expressed in Escherichia coli. Maltose-binding protein fusion protein (MBP-AhpC) was purified by a MBP affinity column. Using purified recombinant AhpC protein as an antigen, the antibody response and changes of antibody levels against AhpC in the gerbil models were studied by Western blotting and ELISA. Results. Antibody against AhpC was negative in the early stages of infection, and became positive in the gerbils with the emergence of gastric diseases such as chronic active gastritis, gastric ulcer and gastric cancer. The antibody levels (ELISA) increased gradually over time and were higher in gerbils with gastric ulcer than that in gerbils without ulcers. Conclusions. Use of the gerbil model that mimics human H. pylori infection is likely to provide insights into the role of H. pylori -specific antigens possibly related to the subsequent development of gastric diseases. [source] Modelling hantavirus in fluctuating populations of bank voles: the role of indirect transmission on virus persistenceJOURNAL OF ANIMAL ECOLOGY, Issue 1 2003Frank Sauvage Summary 1Using field data published in the literature, we investigated pathogen dynamics and conditions of persistence in a mathematical model of the bank vole (Clethrionomys glareolus),Puumala hantavirus system. The host population is assumed to have a 3-year periodic cycle. The duration of very low host density is critical for virus transmission and survival. 2Field epidemiological data strongly suggested a transmission of the hantavirus by the contaminated environment. We thus studied whether this ,indirect' transmission affected the virus persistence in the host population. 3The model assumptions were derived from the following conditions found in the literature: (1) there is no additional mortality nor fecundity loss due to the virus in infected hosts, thus the cyclic demographical pattern is not due to the virus; (2) no remission has been observed, thus we did not consider the existence of recovered individuals; (3) adult females are territorial and juveniles disperse to find a new territory and reach sexual maturity. A fragmented landscape was assumed to occur: individuals can live in favourable or unfavourable patches. 4The model was a compartmental model; the population was structured into susceptible or infectious individuals. We considered two age classes, juveniles and adults, and two sites (populations) connected by juvenile dispersal. 5Model dynamics accurately predicted the cyclic trend in disease prevalence as observed in epidemiological studies. They also showed that indirect transmission significantly increased the probability for the virus to persist during the low-density period of the host population. More precisely, even a low survival rate of the virus outside the host was sufficient to decrease extinction risk of the infection by stochastic events. 6Elasticity analysis showed a high robustness of the model to changes in the parameters of indirect transmission but a high sensitivity to changes in adult density. [source] A HCMV pp65 polypeptide promotes the expansion of CD4+ and CD8+ T cells across a wide range of HLA specificitiesJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 8b 2009Maurizio Provenzano Abstract Human cytomegalovirus (HCMV) can cause life-threatening disease in infected hosts. Immunization with human leukocyte antigen (HLA)-restricted immunodominant synthetic peptides and adoptive transfer of epitope-specific T cells have been envisaged to generate or boost HCMV-specific cellular immunity, thereby preventing HCMV infection or reactivation. However, induction or expansion of T cells effective against HCMV are limited by the need of utilizing peptides with defined HLA restrictions. We took advantage of a combination of seven predictive algorithms to identify immunogenic peptides of potential use in the prevention or treatment of HCMV infection or reactivation. Here we describe a pp65-derived peptide (pp65340,355, RQYDPVAALFFFDIDL: RQY16-mer), characterized by peculiar features. First, RQY-16mer is able to stimulate HCMV pp65 specific responses in both CD4+ and CD8+ T cells, restricted by a wide range of HLA class I and II determinants. Second, RQY-16mer is able to induce an unusually wide range of effector functions in CD4+ T cells, including proliferation, killing of autologous HCMV-infected target cells and cytokine production. Third, and most importantly, the RQY-16mer is able to stimulate CD4+ and CD8+ T-cell responses in pharmacologically immunosuppressed patients. These data suggest that a single reagent might qualify as synthetic immunogen for potentially large populations exposed to HCMV infection or reactivation. [source] Identification of Candida albicans genes induced during thrush offers insight into pathogenesisMOLECULAR MICROBIOLOGY, Issue 5 2003Shaoji Cheng Summary Candida albicans causes a wide spectrum of diseases, ranging from mucocutaneous infections like oral thrush to disseminated candidiasis. Screening for C. albicans genes expressed within infected hosts might advance understanding of candidal pathogenesis, but is impractical using existing techniques. In this study, we used an antibody-based strategy to identify C. albicans genes expressed during thrush. We adsorbed sera from HIV-infected patients with thrush against candidal cells grown in vitro and screened a C. albicans genomic expression library. We identified 10 genes encoding immunogenic antigens and used reverse transcription-polymerase chain reaction to verify that they were induced within thrush pseudomembranes recovered from a patient. The in vivo induced genes are involved in diverse functions, including regulation of yeast-hyphal morphogenesis, adhesion to host cells, nutrient uptake, phospholipid biosynthesis and amino acid catabolism. Four genes encode known virulence determinants (HWP1, CST20, CPP1 and RBF1). Another gene, LPD1, for which a role in candidal pathogenesis is unknown, encodes a protein homologous to a bacterial virulence determinant. Most importantly, disruption of CaNOT5, a newly identified gene, conferred defects in morphogenesis, decreased adherence to human buccal epithelial cells and attenuated mortality during murine disseminated candidiasis, proving that our strategy can identify genes encoding novel virulence determinants. [source] Symbiont-mediated changes in Lolium arundinaceum inducible defenses: evidence from changes in gene expression and leaf compositionNEW PHYTOLOGIST, Issue 3 2007Terrence J. Sullivan Summary ,,Plants have multiple strategies to deal with herbivory, ranging from chemical or physical defenses to tolerating damage and allocating resources for regrowth. Grasses usually tolerate herbivory, but for some cool-season grasses, their strategy may depend upon their interactions with intracellular symbionts. Neotyphodium endophytes are common symbionts in pooid grasses, and, for some host species, they provide chemical defenses against both vertebrate and invertebrate herbivores. ,,Here, it was tested whether defenses provided by Neotyphodium coenophialum in Lolium arundinaceum (tall fescue) are inducible by both mechanical damage and herbivory from an invertebrate herbivore, Spodoptera frugiperda (fall armyworm), via a bioassay and by quantifying mRNA expression for lolC, a gene required for loline biosysnthesis. ,,Both mechanical and herbivore damage had a negative effect on the reproduction of a subsequent herbivore, Rhopalosiphum padi (bird cherry-oat aphid), and herbivore damage caused an up-regulation of lolC. Uninfected grass hosts also had significantly higher foliar N% and lower C : N ratio compared with infected hosts, suggesting greater allocation to growth rather than defense. ,,For L. arundinaceum, N. coenophialum appears to switch its host's defensive strategy from tolerance via compensation to resistance. [source] A meta-analysis of parasite virulence in nestling birdsBIOLOGICAL REVIEWS, Issue 4 2009A. P. Møller Abstract Parasitism is a common cause of host mortality, but little is known about the ecological factors affecting parasite virulence (the rate of mortality among infected hosts). We reviewed 117 field estimates of parasite-induced nestling mortality in birds, showing that there was significant consistency in mortality among host and parasite taxa. Virulence increased towards the tropics in analyses of both species-specific data and phylogenetic analyses. We found evidence of greater parasite prevalence being associated with reduced virulence. Furthermore, bird species breeding in open nest sites suffered from greater parasite-induced mortality than hole-nesting species. By contrast, parasite specialization and generation time of parasites relative to that of hosts explained little variation in virulence. Likewise, there were little or no significant effects of host genetic variability, host sociality, host migration, host insular distribution or host survival on parasite virulence. These findings suggest that parasite-induced nestling mortality in birds is mainly determined by geographical location and to a smaller extent nest site and prevalence. [source] | |||||||||||||