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PubMed2005

Organization and evolution of resistance gene analogs in peanut.

The scarcity of genetic polymorphism in Arachis hypogaea (peanut), as in other monophyletic polyploid species, makes it especially vulnerable to nematode, bacterial, fungal, and viral pathogens. Although no disease resistance genes have been cloned from peanut itself, the conserved motifs in cloned resistance genes from other plant species provide a means to isolate and analyze similar genes from peanut. To survey the number, diversity, evolutionary history, and genomic organization of resistance gene-like sequences in peanut, we isolated 234 resistance gene analogs (RGAs) by using primers designed from conserved regions of different classes of resistance genes including NBS-LRR, and LRR-TM classes. Phylogenetic and sequence analyses were performed to explore evolutionary relationships both among peanut RGAs and with orthologous genes from other plant taxa. Fifty-six overgos designed from the RGA sequences on the basis of their phyletic association were applied to a peanut BAC library; 736 hybridizing BAC clones were fingerprinted and contigs were formed in order to gain insights into the genomic organization of these genes. All the fingerprinting gels were blotted and screened with the respective overgos in order to verify the authenticity of the hits from initial screens, and to explore the physical organization of these genes in terms of both copy number and distribution in the genome. As a result, we identified 250 putative resistance gene loci. A correlation was found between the phyletic positions of the sequences and their physical locations. The BACs isolated here will serve as a valuable resource for future applications, such as map-based cloning, and will help improve our understanding of the evolution and organization of these genes in the peanut genome.

Amino Acid Sequence↗
PubMed2002

Dynamics of evolution and resistance to starvation of Triatoma vitticeps (Stal 1859) (Reduviidae: Triatominae), submitted to two different regimens of food deprivation.

The resistance to starvation of Triatoma vitticeps has been analyzed comparatively, according to different regimens of food deprivation under laboratory conditions. One cohort, composed of 100 specimens of each evolutionary nymphal stage, was submitted to continuous fasting until death; the second group, arranged in the same way, was fed once on chicken. Through this work, it was possible not only to compare the results obtained from the first group with other authors' results but, also, to analyze the dynamics of evolution, molting, longevity and the increase in insect longevity, in the second group. The average values recorded for survival time revealed statistical differences between the two groups. Among the important results detected, there is one that deserves to be emphasized: the incredible increase in longevity among insects that received only one feed - an average increase in survival time that reached 2.95 to 3.30 times in nymphs of 3rd and 4th stages, respectively. One 5th stage nymph survived for up to 350 days and the females may triplicate their survival rate, what represents an important epidemiological factor. The knowledge about this type of biological characteristic of T. vitticeps may contribute to prevent the domiciliation of this species, what seems to be incipient in some municipal districts, in Brazil.

Animals↗
PubMed2003

Genome-level evolution of resistance genes in Arabidopsis thaliana.

Pathogen resistance genes represent some of the most abundant and diverse gene families found within plant genomes. However, evolutionary mechanisms generating resistance gene diversity at the genome level are not well understood. We used the complete Arabidopsis thaliana genome sequence to show that most duplication of individual NBS-LRR sequences occurs at close physical proximity to the parent sequence and generates clusters of closely related NBS-LRR sequences. Deploying the statistical strength of phylogeographic approaches and using chromosomal location as a proxy for spatial location, we show that apparent duplication of NBS-LRR genes to ectopic chromosomal locations is largely the consequence of segmental chromosome duplication and rearrangement, rather than the independent duplication of individual sequences. Although accounting for a smaller fraction of NBS-LRR gene duplications, segmental chromosome duplication and rearrangement events have a large impact on the evolution of this multigene family. Intergenic exchange is dramatically lower between NBS-LRR sequences located in different chromosome regions as compared to exchange between sequences within the same chromosome region. Consequently, once translocated to new chromosome locations, NBS-LRR gene copies have a greater likelihood of escaping intergenic exchange and adopting new functions than do gene copies located within the same chromosomal region. We propose an evolutionary model that relates processes of genome evolution to mechanisms of evolution for the large, diverse, NBS-LRR gene family.

Arabidopsis↗
PubMed2004

The evolution of resistance through costly acquired immunity.

We examine the evolutionary dynamics of resistance to parasites through acquired immunity. Resistance can be achieved through the innate mechanisms of avoidance of infection and reduced pathogenicity once infected, through recovery from infection and through remaining immune to infection: acquired immunity. We assume that each of these mechanisms is costly to the host and find that the evolutionary dynamics of innate immunity in hosts that also have acquired immunity are quantitatively the same as in hosts that possess only innate immunity. However, compared with resistance through avoidance or recovery, there is less likely to be polymorphism in the length of acquired immunity within populations. Long-lived organisms that can recover at intermediate rates faced with fast-transmitting pathogens that cause intermediate pathogenicity (mortality of infected individuals) are most likely to evolve long-lived acquired immunity. Our work emphasizes that because whether or not acquired immunity is beneficial depends on the characteristics of the disease, organisms may be selected to only develop acquired immunity to some of the diseases that they encounter.

Biological Evolution↗
PubMed2005

Antibiotic resistance and the evolution of group-beneficial traits. II: a metapopulation model.

Inspired by the evolution of antibiotic resistance in bacteria, we have developed a model that examines the evolution of "producers" (who secrete a substance that breaks down antibiotics) and non-producers. In a previous study, we found that frequency-dependent selection could favor an intermediate frequency of producers in a single, large population. Here we develop a metapopulation model that examines the evolution of producers and non-producers. Our results indicate that in a metapopulation with many groups, each of size N, the equilibrial frequency of producers decreases with group size. Even when N is high (e.g. 150 individuals/group), however, a significant frequency of producers is still predicted. We also found that the equilibrial frequency of producers increases as the minimum numbers of producers necessary to provide protection to non-producers increases. Lastly, increasing the benefit/cost ratio (b/c) for producers increases their equilibrial frequency.

Adaptation, Biological↗
PubMed1993

Modeling and simulating the evolution of resistance against antibiotics.

An epidemiological model is proposed for the spread of resistance against antibiotics in populations of bacterial pathogens. The host population, which is assumed to be constant, is divided into three compartments, viz. susceptible, hosts infected by an antibiotic-sensitive strain and hosts infected by a resistant strain. It is further assumed that susceptibles can be infected by either strain and that there is a possibility for cross-infection between hosts infected by the two strains. The rate of cross-infection can be enhanced by mutations or the transfer of plasmids conferring resistance. Equilibrium analysis was performed in order to determine which of the strain 'wins' the competition by the host. It is assumed that the eventual shift in the competition between the two strains is due to treatment by antibiotic (selective pressure).

Amikacin↗
PubMed1997

The evolution of resistance to cephalosporins.

The expression of resistance to cephalosporins is highly varied and due to various mechanisms. The greatest disadvantage of the cephalosporins is that they are inactivated by the array of beta-lactamases produced by bacteria. The high levels of chromosomal enzymes produced by these organisms are a major cause of cephalosporin resistance. Plasmid-mediated beta-lactamases (PMBLs) have also been implicated as causes of resistance, and other cephalosporinases have been described. Point mutations of specific amino acids of well-recognized PMBLs (e.g., TEM-1 and SHV-1) have also produced enzymes capable of attacking a wider spectrum of beta-lactam agents. The availability of newer beta-lactams may be conducive to the development of such beta-lactamases, in which chromosomal and newer plasmid derivatives that may or may not contain the AmpC gene are selected. The occurrence of such enzymes is likely to continue to increase.

Bacteria↗
PubMed2004

Evolution of resistance to drugs in HIV-1-infected patients failing antiretroviral therapy.

BACKGROUND AND OBJECTIVE: The optimal time for changing failing antiretroviral therapy (ART) is not known. It involves balancing the risk of exhausting future treatment options against the risk of developing increased drug resistance. The frequency with which new drug-resistance mutations (DRM) developed and their potential consequences in patients continuing unchanged treatment despite persistent viremia were assessed. DESIGN: A retrospective study of consecutive sequence samples from 106 patients at one institution with viral load (VL) of more than 400 copies/ml, with no change in ART for more than 2 months despite virologic failure. METHODS: Two consecutive pol sequences, CD4 cell counts and VL were analyzed to quantify the development of new DRM and to identify changes in immunologic and virologic parameters. Genotypic susceptibility scores (GSS) and viral drug susceptibilities were calculated by a computer program (HIVDB). Poisson log-linear regression models were used to predict the expected number of mutations at the second time point. RESULTS: : After a median of 14 months of continued ART, 75% (80 of 106) of patients acquired new DRM and were assigned a significantly lower GSS, potentially limiting the success of future ART. The development of new DRM was proportional to the time between the two sequences and inversely proportional to the number of DRM in the first sequence. However, the development of DRM was not associated with significant changes in CD4 or VL counts. CONCLUSIONS: Despite stable levels of CD4 and VL over time, maintaining a failing therapeutic regimen increases drug resistance and may limit future treatment options.

Adult↗
PubMed2005

Evolution of resistance mutations pattern in HIV-1-infected patients during intensification therapy with a boosted protease inhibitor.

Intensification therapy adding a boosted protease inhibitor (PI) to a failing regimen has the potential to worsen the resistance profile. Sixty-six patients included in four different boosted PI intensification studies were assessed and resistance mutations in the reverse transcriptase and protease genes were evaluated at baseline and 4 weeks after the initiation of the intensification strategy. Only one of the 66 patients developed changes in their pattern of mutations able to generate or increase resistance to new drugs.

Antiretroviral Therapy, Highly Active↗
PubMed2004

Evolution of resistance to sulfadoxine-pyrimethamine in Plasmodium falciparum.

The development of resistance to sulfadoxine-pyrimethamine by Plasmodium parasites is a major problem for the effective treatment of malaria, especially P. falciparum malaria. Although the molecular basis for parasite resistance is known, the factors promoting the development and transmission of these resistant parasites are less clear. This paper reports the results of a quantitative comparison of factors previously hypothesized as important for the development of drug resistance, drug dosage, time of treatment, and drug elimination half-life, with an in-host dynamics model of P. falciparum malaria in a malaria-naïve host. The results indicate that the development of drug resistance can be categorized into three stages. The first is the selection of existing parasites with genetic mutations in the dihydrofolate reductase or dihydropteroate synthetase gene. This selection is driven by the long half-life of the sulfadoxine-pyrimethamine combination. The second stage involves the selection of parasites with allelic types of higher resistance within the host during an infection. The timing of treatment relative to initiation of a specific anti-P. falciparum EMP1 immune response is an important factor during this stage, as is the treatment dosage. During the third stage, clinical treatment failure becomes prevalent as the parasites develop sufficient resistance mutations to survive therapeutic doses of the drug combination. Therefore, the model output reaffirms the importance of correct treatment of confirmed malaria cases in slowing the development of parasite resistance to sulfadoxine-pyrimethamine.

Animals↗
PubMed2004

Evolution of resistance under insecticide selection pressure in Culex pipiens quinquefasciatus (Diptera, Culicidae) from Martinique.

Population surveys of Culex pipiens quinquefasciatus carried out in 1991 and 1999 were compared with data collected in 1990 before the beginning of the control program against this mosquito. Larval samples collected in 1999 displayed resistance to the four tested insecticides: permethrin, propoxur, temephos, and chlorpyrifos. Temephos resistance ratio at LC50 (RR50) ranged between 8.1- and 42-fold compared with 2.9- and 4.6-fold in 1990, and chlorpyrifos RR50 ranged between 8.6- and 123-fold compared with 6.4- and 19-fold in 1990. This increased resistance to organophosphorus insecticides was associated with a sharp decrease of susceptible genotypes at two loci (Ester and ace-1), as well as to an allele replacement at the Ester locus.

Animals↗
PubMed2003

Fitness variations and their impact on the evolution of antiretroviral drug resistance.

The human immunodeficiency virus (HIV) exhibits extensive heterogeneity due to its rapid turnover, high mutation rate, and high frequency of recombination. Its remarkable genetic diversity plays a key role in virus adaptation, including development of drug resistance. The increasing complexity of antiretroviral regimens has favored selection of HIV variants harboring multiple drug resistance mutations. Evolution of drug resistance is characterized by severe fitness losses, which can be partially overcome by compensatory mutations or other adaptive changes that restore virus replication capacity. Recent reports have addressed the impact of drug-resistance mutations on viral fitness. Methods include in vitro estimates based on the determination of viral replication kinetics, viral infectivity in single-cycle assays and growth competition experiments; as well as estimates of the relative fitness of viral populations in vivo calculated from standard population genetics theory. This review focuses on the effects in viral fitness of mutations arising during treatment with reverse transcriptase and protease inhibitors, and the molecular mechanisms (including compensatory mutations) that improve the viral fitness of drug-resistant variants.

Anti-HIV Agents↗