Reconstructing the Timing and Dispersion Routes of HIV-1 Subtype B Epidemics in The Caribbean and Central America: A Phylogenetic Story.

The Caribbean and Central America are among the regions with highest HIV-1B prevalence worldwide. Despite of this high virus burden, little is known about the timing and the migration patterns of HIV-1B in these regions. Migration is one of the major processes shaping the genetic structure of virus populations. Thus, reconstruction of epidemiological network may contribute to understand HIV-1B evolution and reduce virus prevalence. We have investigated the spatio-temporal dynamics of the HIV-1B epidemic in The Caribbean and Central America using 1,610 HIV-1B partial pol sequences from 13 Caribbean and 5 Central American countries. Timing of HIV-1B introduction and virus evolutionary rates, as well as the spatial genetic structure of the HIV-1B populations and the virus migration patterns were inferred. Results revealed that in The Caribbean and Central America most of the HIV-1B variability was generated since the 80 s. At odds with previous data suggesting that Haiti was the origin of the epidemic in The Caribbean, our reconstruction indicated that the virus could have been disseminated from Puerto Rico and Antigua. These two countries connected two distinguishable migration areas corresponding to the (mainly Spanish-colonized) Easter and (mainly British-colonized) Western islands, which indicates that virus migration patterns are determined by geographical barriers and by the movement of human populations among culturally related countries. Similar factors shaped the migration of HIV-1B in Central America. The HIV-1B population was significantly structured according to the country of origin, and the genetic diversity in each country was associated with the virus prevalence in both regions, which suggests that virus populations evolve mainly through genetic drift. Thus, our work contributes to the understanding of HIV-1B evolution and dispersion pattern in the Americas, and its relationship with the geography of the area and the movements of human populations

Tácticas extremas de transmisión de los virus de plantas

Seminario de investigaciónLos virus causan la mitad de las enfermedades emergentes en de los cultivos. Estos agentes patógenos se caracterizan por su gran capacidad de dispersión. Por tanto, entender los mecanismos por los cuales los virus de plantas se transmiten es esencial para poder controlar las enfermedades que causan. Las teorías sobre este aspecto central de las interacciones planta-virus predicen que los virus maximizarán su transmisión a niveles intermedios de virulencia. Sin embargo, un número significativo de virus de plantas desafían estas predicciones. Por un lado, un 25% de ellos se transmite por semilla. Estos virus necesitan que la planta produzca descendencia para transmitirse. Por tanto, cuanto menor sea su virulencia mayor será su transmisión. Por otro lado, ciertos virus castran a sus huéspedes (ausencia de producción de semillas viables) para maximizar su transmisión por vectores. Nuestro grupo está interesado en entender cómo los virus de plantas evolucionan hacia estos extremos y cuáles son las consecuencias de esta evolución tanto para el virus como para la planta, y para la emergencia de enfermedades.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech. Master y programa de doctorado en Biotecnología Avanzad

Host responses in life-history traits and tolerance to virus infection in Arabidopsis thaliana

Knowing how hosts respond to parasite infection is paramount in understanding the effects of parasites on host populations and hence host¿parasite co-evolution. Modification of life-history traits in response to parasitism has received less attention than other defence strategies. Life-history theory predicts that parasitised hosts will increase reproductive effort and accelerate reproduction. However, empirical analyses of these predictions are few and mostly limited to animalparasite systems. We have analysed life-history trait responses in 18 accessions of Arabidopsis thaliana infected at two different developmental stages with three strains of Cucumber mosaic virus (CMV). Accessions were divided into two groups according to allometric relationships; these groups differed also in their tolerance to CMV infection. Life-history trait modification upon virus infection depended on the host genotype and the stage at infection. While all accessions delayed flowering, only the more tolerant allometric group modified resource allocation to increase the production of reproductive structures and progeny, and reduced the length of reproductive period. Our results are in agreement with modifications of life-history traits reported for parasitised animals and with predictions from life-history theory. Thus, we provide empirical support for the general validity of theoretical predictions. In addition, this experimental approach allowed us to quantitatively estimate the genetic determinism of life-history trait plasticity and to evaluate the role of life-history trait modification in defence against parasites, two largely unexplored issues

Clinical Determinants of HIV-1B Between-Host Evolution and their Association with Drug Resistance in Pediatric Patients

Understanding the factors that modulate the evolution of virus populations is essential to design efficient control strategies. Mathematical models predict that factors affecting viral within-host evolution may also determine that at the between-host level. Although HIV-1 within-host evolution has been associated with clinical factors used to monitor AIDS progression, such as patient age, CD4 cells count, viral load, and antiretroviral experience, little is known about the role of these clinical factors in determining between-host HIV-1 evolution. Moreover, whether the relative importance of such factors in HIV-1 evolution vary in adult and children patients, in which the course of infection is different, has seldom been analysed. To address these questions, HIV-1 subtype B (HIV-1B) pol sequences of 163 infected children and 450 adults of Madrid, Spain, were used to estimate genetic diversity, rates of synonymous and non-synonymous mutations, selection pressures and frequency of drug-resistance mutations (DRMs). The role and relative importance of patient age, %CD4, CD4/mm3, viral load, and antiretroviral experience in HIV-1B evolution was analysed. In the pediatric HIV-1B population, three clinical factors were primary predictors of virus evolution: Higher HIV-1B genetic diversity was observed with increasing children age, decreasing CD4/mm3 and upon antiretroviral experience. This was mostly due to higher rates of non-synonymous mutations, which were associated with higher frequency of DRMs. Using this data, we have also constructed a simple multivariate model explaining between 55% and 66% of the variance in HIV-1B evolutionary parameters in pediatric populations. On the other hand, the analysed clinical factors had little effect in adult-infecting HIV-1B evolution. These findings highlight the different evolutionary dynamics of HIV-1B in children and adults, and contribute to understand the factors shaping HIV-1B evolution and the appearance of drug-resistance mutation in pediatric patients

Cucumber mosaic virus Is Unable to Self-Assemble in Tobacco Plants When Transmitted by Seed

Cucumber mosaic virus (CMV), which has great impact on agronomic production worldwide, is both aphid and seed transmitted. Although the mechanisms of aphid transmission have been widely studied, those underlying the ability of CMV to survive and remain infectious during the passage from one generation to the next through the seeds are still to be clarified. Moreover, the viral determinants of seed transmission rate are poorly understood. Three viral genotypes produced from same RNA 1 and 2 components of CMV-Fny but differing in RNA 3 (the wild type CMV-Fny, a pseudorecombinant CMV-Fny/CMV-S and a chimeric CMV previously obtained by our group, named F, FS and CS, respectively) were propagated in Nicotiana tabacum cv Xanthi plants in order to assess differences in tobacco seed transmission rate and persistence through plant generations in the absence of aphid transmission. Seed-growth tests revealed CMV infection in the embryos, but not in the integuments. Seedlings from seed-growth tests showed the presence of all considered viruses but at different rates: from 4% (F, FS) to 16% (CS). Electron microscopy revealed absence (CS) of viral particles or virions without the typical central hole (F and FS). In agreement, structural characteristics of purified CMV particles, assessed by circular dichroism spectroscopy, showed anomalous spectra of nucleic acids rather than the expected nucleoproteins. These alterations resulted in no seed transmission beyond the first plant generation. Altogether, the results show for the first time that correct virion assembly is needed for seed infection from the mother plant but not to seedling invasion from the seed. We propose that incorrect virion formation, self-assembly and architecture stability might be explained if during the first stages of germination and seedling development some tobacco seed factors target viral regions responsible for protein-RNA interactions

Effect of Biodiversity Changes in Disease Risk: Exploring Disease Emergence in a Plant-Virus System

The effect of biodiversity on the ability of parasites to infect their host and cause disease (i.e. disease risk) is a major question in pathology, which is central to understand the emergence of infectious diseases, and to develop strategies for their management. Two hypotheses, which can be considered as extremes of a continuum, relate biodiversity to disease risk: One states that biodiversity is positively correlated with disease risk (Amplification Effect), and the second predicts a negative correlation between biodiversity and disease risk (Dilution Effect). Which of them applies better to different host-parasite systems is still a source of debate, due to limited experimental or empirical data. This is especially the case for viral diseases of plants. To address this subject, we have monitored for three years the prevalence of several viruses, and virus-associated symptoms, in populations of wild pepper (chiltepin) under different levels of human management. For each population, we also measured the habitat species diversity, host plant genetic diversity and host plant density. Results indicate that disease and infection risk increased with the level of human management, which was associated with decreased species diversity and host genetic diversity, and with increased host plant density. Importantly, species diversity of the habitat was the primary predictor of disease risk for wild chiltepin populations. This changed in managed populations where host genetic diversity was the primary predictor. Host density was generally a poorer predictor of disease and infection risk. These results support the dilution effect hypothesis, and underline the relevance of different ecological factors in determining disease/infection risk in host plant populations under different levels of anthropic influence. These results are relevant for managing plant diseases and for establishing conservation policies for endangered plant species

Host Responses in Life-History Traits and Tolerance to Virus Infection in Arabidopsis thaliana

Knowing how hosts respond to parasite infection is paramount in understanding the effects of parasites on host populations and hence host–parasite co-evolution. Modification of life-history traits in response to parasitism has received less attention than other defence strategies. Life-history theory predicts that parasitised hosts will increase reproductive effort and accelerate reproduction. However, empirical analyses of these predictions are few and mostly limited to animal-parasite systems. We have analysed life-history trait responses in 18 accessions of Arabidopsis thaliana infected at two different developmental stages with three strains of Cucumber mosaic virus (CMV). Accessions were divided into two groups according to allometric relationships; these groups differed also in their tolerance to CMV infection. Life-history trait modification upon virus infection depended on the host genotype and the stage at infection. While all accessions delayed flowering, only the more tolerant allometric group modified resource allocation to increase the production of reproductive structures and progeny, and reduced the length of reproductive period. Our results are in agreement with modifications of life-history traits reported for parasitised animals and with predictions from life-history theory. Thus, we provide empirical support for the general validity of theoretical predictions. In addition, this experimental approach allowed us to quantitatively estimate the genetic determinism of life-history trait plasticity and to evaluate the role of life-history trait modification in defence against parasites, two largely unexplored issues

Genomic and biological characterization of chiltepin yellow mosaic virus, a new tymovirus infecting Capsicum annuum var. aviculare in Mexico.

The characterization of viruses infecting wild plants is a key step towards understanding the ecology of plant viruses. In this work, the complete genomic nucleotide sequence of a new tymovirus species infecting chiltepin, the wild ancestor of Capsicum annuum pepper crops, in Mexico was determined, and its host range has been explored. The genome of 6,517 nucleotides has the three open reading frames described for tymoviruses, putatively encoding an RNA-dependent RNA polymerase, a movement protein and a coat protein. The 5′ and 3′ untranslated regions have structures with typical signatures of the tymoviruses. Phylogenetic analyses revealed that this new virus is closely related to the other tymoviruses isolated from solanaceous plants. Its host range is mainly limited to solanaceous species, which notably include cultivated Capsicum species. In the latter, infection resulted in a severe reduction of growth, indicating the potential of this virus to be a significant crop pathogen. The name of chiltepin yellow mosaic virus (ChiYMV) is proposed for this new tymovirus

The Relationship of Within-Host Multiplication and Virulence in a Plant-Virus System

Background. Virulence does not represent any obvious advantage to parasites. Most models of virulence evolution assume that virulence is an unavoidable consequence of within-host multiplication of parasites, resulting in trade-offs between within-host multiplication and between-host transmission fitness components. Experimental support for the central assumption of this hypothesis, i.e., for a positive correlation between within-host multiplication rates and virulence, is limited for plant-parasite systems. Methodology/Principal Findings. We have addressed this issue in the system Arabidopsis thaliana-Cucumber mosaic virus (CMV). Virus multiplication and the effect of infection on plant growth and on viable seed production were quantified for 21 Arabidopsis wild genotypes infected by 3 CMV isolates. The effect of infection on plant growth and seed production depended of plant architecture and length of postembryonic life cycle, two genetically-determined traits, as well as on the time of infection in the plant's life cycle. A relationship between virus multiplication and virulence was not a general feature of this host-parasite system. This could be explained by tolerance mechanisms determined by the host genotype and operating differently on two components of plant fitness, biomass production and resource allocation to seeds. However, a positive relationship between virus multiplication and virulence was detected for some accessions with short life cycle and high seed weight to biomass ratio, which show lower levels of tolerance to infection. Conclusions/Significance. These results show that genotype-specific tolerance mechanisms may lead to the absence of a clear relationship between parasite multiplication and virulence. Furthermore, a positive correlation between parasite multiplication and virulence may occur only in some genotypes and/or environmental conditions for a given host-parasite system. Thus, our results challenge the general validity of the trade-off hypothesis for virulence evolution, and stress the need of considering the effect of both the host and parasite genotypes in analyses of host-parasite interactions. © 2007 Pagán et al.Ministerio de Educación y Ciencia, Spain.Peer Reviewe

Differential tolerance to direct and indirect density-dependent costs of viral infection in Arabidopsis thaliana.

Population density and costs of parasite infection may condition the capacity of organisms to grow, survive and reproduce, i.e. their competitive ability. In host-parasite systems there are different competitive interactions: among uninfected hosts, among infected hosts, and between uninfected and infected hosts. Consequently, parasite infection results in a direct cost, due to parasitism itself, and in an indirect cost, due to modification of the competitive ability of the infected host. Theory predicts that host fitness reduction will be higher under the combined effects of costs of parasitism and competition than under each factor separately. However, experimental support for this prediction is scarce, and derives mostly from animal-parasite systems. We have analysed the interaction between parasite infection and plant density using the plant-parasite system of Arabidopsis thaliana and the generalist virus Cucumber mosaic virus (CMV). Plants of three wild genotypes grown at different densities were infected by CMV at various prevalences, and the effects of infection on plant growth and reproduction were quantified. Results demonstrate that the combined effects of host density and parasite infection may result either in a reduction or in an increase of the competitive ability of the host. The two genotypes investing a higher proportion of resources to reproduction showed tolerance to the direct cost of infection, while the genotype investing a higher proportion of resources to growth showed tolerance to the indirect cost of infection. Our findings show that the outcome of the interaction between host density and parasitism depends on the host genotype, which determines the plasticity of life-history traits and consequently, the host capacity to develop different tolerance mechanisms to the direct or indirect costs of parasitism. These results indicate the high relevance of host density and parasitism in determining the competitive ability of a plant, and stress the need to simultaneously consider both factors to understand the selective pressures that drive host-parasite co-evolution. © 2009 Pagán et al.Ministerio de Ciencia y Tecnología, Spain.Peer Reviewe