KREH2 helicase represses ND7 mRNA editing in procyclic-stage Trypanosoma brucei by opposite modulation of canonical and 'moonlighting' gRNA utilization creating a proposed mRNA structure.

Unknown factors regulate mitochondrial U-insertion/deletion (U-indel) RNA editing in procyclic-form (PCF) and bloodstream-form (BSF) T. brucei. This editing, directed by anti-sense gRNAs, creates canonical protein-encoding mRNAs and may developmentally control respiration.

Maternal transmission of Small Ruminant Lentivirus has no epidemiological importance.

The relative importance of maternal and horizontal transmission of small ruminant lentivirus (SRLV), the causative organism in maedi-visna, is poorly understood. Review of the literature shows that maternal transmission is inefficient, infecting only about 10-25 % of the lambs of infected ewes. Theory proves that maternal transmission alone cannot achieve the rates of transmission that would be required to start or maintain an outbreak.

Trypanosome RNA helicase KREH2 differentially controls non-canonical editing and putative repressive structure via a novel proposed 'bifunctional' gRNA in mRNA A6.

U-insertion/deletion (U-indel) RNA editing in trypanosome mitochondria is directed by guide RNAs (gRNAs). This editing may developmentally control respiration in bloodstream forms (BSF) and insect procyclic forms (PCF). Holo-editosomes include the accessory RNA Editing Substrate Binding Complex (RESC) and RNA Editing Helicase 2 Complex (REH2C), but the specific proteins controlling differential editing remain unknown.

Deep kinetoplast genome analyses result in a novel molecular assay for detecting -specific minicircles.

The World Health Organization targeted () human African trypanosomiasis for elimination of transmission by 2030. Sensitive molecular markers that specifically detect type 1 () parasites will be important tools to assist in reaching this goal. We aim at improving molecular diagnosis of 1 infections by targeting the abundant mitochondrial minicircles within the kinetoplast of these parasites.

Organization of minicircle cassettes and guide RNA genes in .

Mitochondrial DNA of protists of order comprises thousands of interlinked circular molecules arranged in a network. There are two types of molecules called minicircles and maxicircles. Minicircles encode guide RNA (gRNA) genes whose transcripts mediate post-transcriptional editing of maxicircle encoded genes.

Ecological divergence and hybridization of Neotropical parasites.

The tropical Andes are an important natural laboratory to understand speciation in many taxa. Here we examined the evolutionary history of parasites of the species complex based on whole-genome sequencing of 67 isolates from 47 localities in Peru. We first show the origin of Andean as a clade of near-clonal lineages that diverged from admixed Amazonian ancestors, accompanied by a significant reduction in genome diversity and large structural variations implicated in host-parasite interactions.

Epidemiology and control of maedi-visna virus: Curing the flock.

Maedi-visna (MV) is a complex lentiviral disease syndrome characterised by long immunological and clinical latencies and chronic progressive inflammatory pathology. Incurable at the individual level, it is widespread in most sheep-keeping countries, and is a cause of lost production and poor animal welfare. Culling seropositive animals is the main means of control, but it might be possible to manage virus transmission effectively if its epidemiology was better quantified.

A receptor for the complement regulator factor H increases transmission of trypanosomes to tsetse flies.

Persistent pathogens have evolved to avoid elimination by the mammalian immune system including mechanisms to evade complement. Infections with African trypanosomes can persist for years and cause human and animal disease throughout sub-Saharan Africa. It is not known how trypanosomes limit the action of the alternative complement pathway.

Assembly and annotation of the mitochondrial minicircle genome of a differentiation-competent strain of Trypanosoma brucei.

Kinetoplastids are protists defined by one of the most complex mitochondrial genomes in nature, the kinetoplast. In the sleeping sickness parasite Trypanosoma brucei, the kinetoplast is a chain mail-like network of two types of interlocked DNA molecules: a few dozen ∼23-kb maxicircles (homologs of the mitochondrial genome of other eukaryotes) and thousands of ∼1-kb minicircles. Maxicircles encode components of respiratory chain complexes and the mitoribosome.

Host circadian rhythms are disrupted during malaria infection in parasite genotype-specific manners.

Infection can dramatically alter behavioural and physiological traits as hosts become sick and subsequently return to health. Such "sickness behaviours" include disrupted circadian rhythms in both locomotor activity and body temperature. Host sickness behaviours vary in pathogen species-specific manners but the influence of pathogen intraspecific variation is rarely studied.

Plasticity and genetic variation in traits underpinning asexual replication of the rodent malaria parasite, Plasmodium chabaudi.

Background: The ability of malaria (Plasmodium) parasites to adjust investment into sexual transmission stages versus asexually replicating stages is well known, but plasticity in other traits underpinning the replication rate of asexual stages in the blood has received less attention. Such traits include burst size (the number of merozoites produced per schizont), the duration of the asexual cycle, and invasion preference for different ages of red blood cell (RBC).

Methods: Here, plasticity [environment (E) effects] and genetic variation [genotype (G) effects] in traits relating to asexual replication rate are examined for 4 genotypes of the rodent malaria parasite Plasmodium chabaudi.

The Challenge of Quantifying Synchrony in Malaria Parasites.

Malaria infection is often accompanied by periodic fevers, triggered by synchronous cycles of parasite replication within the host. The degree of synchrony in parasite development influences the efficacy of drugs and immune defenses and is therefore relevant to host health and infectiousness. Synchrony is thought to vary over the course of infection and across different host-parasite genotype or species combinations, but the evolutionary significance - if any - of this diversity remains elusive.

Predicted impact of mass drug administration on the development of protective immunity against Schistosoma haematobium.

Previous studies suggest that protective immunity against Schistosoma haematobium is primarily stimulated by antigens from dying worms. Praziquantel treatment kills adult worms, boosting antigen exposure and protective antibody levels. Current schistosomiasis control efforts use repeated mass drug administration (MDA) of praziquantel to reduce morbidity, and may also reduce transmission.

Immune-mediated competition in rodent malaria is most likely caused by induced changes in innate immune clearance of merozoites.

Malarial infections are often genetically diverse, leading to competitive interactions between parasites. A quantitative understanding of the competition between strains is essential to understand a wide range of issues, including the evolution of virulence and drug resistance. In this study, we use dynamical-model based Bayesian inference to investigate the cause of competitive suppression of an avirulent clone of Plasmodium chabaudi (AS) by a virulent clone (AJ) in immuno-deficient and competent mice.

Quantitative analysis of porcine reproductive and respiratory syndrome (PRRS) viremia profiles from experimental infection: a statistical modelling approach.

Porcine reproductive and respiratory syndrome (PRRS) is one of the most economically significant viral diseases facing the global swine industry. Viremia profiles of PRRS virus challenged pigs reflect the severity and progression of infection within the host and provide crucial information for subsequent control measures. In this study we analyse the largest longitudinal PRRS viremia dataset from an in-vivo experiment.

The effectiveness of mass vaccination on Marek's disease virus (MDV) outbreaks and detection within a broiler barn: a modeling study.

Marek's disease virus (MDV), a poultry pathogen, has been increasing in virulence since the mid twentieth century. Since multiple vaccines have been developed and widely implemented, losses due to MDV have decreased. However, vaccine failure has occurred in the past and vaccine breakthroughs remain a problem.

Vaccination and reduced cohort duration can drive virulence evolution: Marek's disease virus and industrialized agriculture.

Marek's disease virus (MDV), a commercially important disease of poultry, has become substantially more virulent over the last 60 years. This evolution was presumably a consequence of changes in virus ecology associated with the intensification of the poultry industry. Here, we assess whether vaccination or reduced host life span could have generated natural selection, which favored more virulent strains.

Protective immunity to Schistosoma haematobium infection is primarily an anti-fecundity response stimulated by the death of adult worms.

Protective immunity against human schistosome infection develops slowly, for reasons that are not yet fully understood. For many decades, researchers have attempted to infer properties of the immune response from epidemiological studies, with mathematical models frequently being used to bridge the gap between immunological theory and population-level data on schistosome infection and immune responses. Here, building upon earlier model findings, stochastic individual-based models were used to identify model structures consistent with observed field patterns of Schistosoma haematobium infection and antibody responses, including their distributions in cross-sectional surveys, and the observed treatment-induced antibody switch.

Modelling the within-host dynamics of the foot-and-mouth disease virus in cattle.

In this paper we investigate the within-host dynamics of the foot-and-mouth disease virus (FMDV) in cattle using previously published data for 8 experimentally infected cows. An 8-compartment, 14-parameter differential equation model was fitted to data collected from each cow every 24 h over the course of an infection on: (i) the concentration of FMDV genomes in the blood, (ii) the concentration of infectious virus in the blood, (iii) antibody levels, and (iv) interferon levels. Model parameters were estimated using maximum-likelihood methods.

Trypanosomal immune evasion, chronicity and transmission: an elegant balancing act.

During their life cycle, trypanosomes must overcome conflicting demands to ensure their survival and transmission. First, they must evade immunity without overwhelming the host. Second, they must generate and maintain transmission stages at sufficient levels to allow passage into their tsetse vector.

Causes of variation in malaria infection dynamics: insights from theory and data.

Parasite strategies for exploiting host resources are key determinants of disease severity (i.e., virulence) and infectiousness (i.

Modelling Marek's disease virus (MDV) infection: parameter estimates for mortality rate and infectiousness.

Background: Marek's disease virus (MDV) is an economically important oncogenic herpesvirus of poultry. Since the 1960s, increasingly virulent strains have caused continued poultry industry production losses worldwide. To understand the mechanisms of this virulence evolution and to evaluate the epidemiological consequences of putative control strategies, it is imperative to understand how virulence is defined and how this correlates with host mortality and infectiousness during MDV infection.

Explaining observed infection and antibody age-profiles in populations with urogenital schistosomiasis.

Urogenital schistosomiasis is a tropical disease infecting more than 100 million people in sub-Saharan Africa. Individuals in endemic areas endure repeated infections with long-lived schistosome worms, and also encounter larval and egg stages of the life cycle. Protective immunity against infection develops slowly with age.