Persistence pays: how viruses promote host group survival.

Recently, we have realized that viruses numerically dominate all life. Although viruses are known to affect host survival in populations, this has not been previously evaluated in the context of host group selection. Group selection per se is not a currently accepted idea and its apparent occurrence is explained by statistical gene frequency models of kin selection. Viruses were not considered in such models. Prevalent views associate viruses and disease. Yet many viruses establish species-specific persistent, inapparent infections that are stable on an evolutionary time scale. Such persistent infections can have large effects on relative reproductive fitness of competing host populations. In this essay, I present arguments on how persistent infections can promote population survival. Mouse hepatitis virus is used as well studied examplar to re-evaluate the theoretical basis of the mouse haystack model of M Smith. This virus-centric re-examination concludes that viruses can indeed affect and promote relative group selection

Force for ancient and recent life: viral and stem-loop RNA consortia promote life.

Lytic viruses were thought to kill the most numerous host (i.e., kill the winner). But persisting viruses/defectives can also protect against viruses, especially in a ubiquitous virosphere. In 1991, Yarmolinsky et al. discovered the addiction modules of P1 phage, in which opposing toxic and protective functions stabilize persistence. Subsequently, I proposed that lytic and persisting cryptic virus also provide addiction modules that promote group identity. In eukaryotes (and the RNA world), a distinct RNA virus-host relationship exists. Retrovirurses/retroposons are major contributors to eukaryotic genomes. Eukaryotic complexity appears to be mostly mediated by regulatory complexity involving noncoding retroposon-derived RNA. RNA viruses evolve via quasispecies, which contain cooperating, minority, and even opposing RNA types. Quasispecies can also demonstrate group preclusion (e.g., hepatitis C). Stem-loop RNA domains are found in long terminal repeats (and viral RNA) and mediate viral regulation/identity. Thus, stem-loop RNAs may be ancestral regulators. I consider the RNA (ribozyme) world scenario from the perspective of addiction modules and cooperating quasispecies (i.e., subfunctional agents that establish group identity). Such an RNA collective resembles a "gang" but requires the simultaneous emergence of endonuclease, ligase, cooperative catalysis, group identity, and history markers (RNA). I call such a collective a gangen (pathway to gang) needed for life to emerge

Viral Ancestors of Antiviral Systems

All life must survive their corresponding viruses. Thus antiviral systems are essential in all living organisms. Remnants of virus derived information are also found in all life forms but have historically been considered mostly as junk DNA. However, such virus derived information can strongly affect host susceptibility to viruses. In this review, I evaluate the role viruses have had in the origin and evolution of host antiviral systems. From Archaea through bacteria and from simple to complex eukaryotes I trace the viral components that became essential elements of antiviral immunity. I conclude with a reexamination of the ‘Big Bang’ theory for the emergence of the adaptive immune system in vertebrates by horizontal transfer and note how viruses could have and did provide crucial and coordinated features

Metabolomic Changes in Naturally MAP-Infected Holstein–Friesian Heifers Indicate Immunologically Related Biochemical Reprogramming

Johne's disease, caused by Mycobacterium avium subsp. paratuberculosis (MAP), causes weight loss, diarrhoea, and reduced milk yields in clinically infected cattle. Asymptomatic, subclinically infected cattle shed MAP bacteria but are frequently not detected by diagnostic tests. Herein, we compare the metabolite profiles of sera from subclinically infected Holstein-Friesian heifers and antibody binding to selected MAP antigens. The study used biobanked serum samples from 10 naturally MAP-infected and 10 control heifers, sampled monthly from ~1 to 19 months of age. Sera were assessed using flow infusion electrospray-high-resolution mass spectrometry (FIE-HRMS) on a Q Exactive hybrid quadrupole-Orbitrap mass spectrometer for high-throughput, sensitive, non-targeted metabolite fingerprinting. Partial least-squares discriminant analyses (PLS-DA) and hierarchical cluster analysis (HCA) of the data discriminated between naturally MAP-infected and control heifers. In total, 33 metabolites that differentially accumulated in naturally MAP-infected heifers compared to controls were identified. Five were significantly elevated within MAP-infected heifers throughout the study, i.e., leukotriene B4, bicyclo prostaglandin E2 (bicyclo PGE2), itaconic acid, 2-hydroxyglutaric acid and N6-acetyl-L-lysine. These findings highlight the potential of metabolomics in the identification of novel MAP diagnostic markers and particular biochemical pathways, which may provide insights into the bovine immune response to MAP

IDENTIFICACIÓN DE HELICOBACTER PYLORI A PARTIR DE LESIÓN ATEROSCLERÓTICA CORONARIA HUMANA

Introduction: The main pathogenic mechanism underlying the genesis and development of diseases of the circulatory system is atherosclerosis. It is a complex and progressive pathological process of the arterial wall that affects especially the coronary, cerebral and peripheral arteries. Currently, there is talk about "The infectious hypothesis of atherosclerosis". Helicobacter pylori infection has been one of the most researched worldwide. Objective: To identify H. pylori from atherosclerotic lesions of patients who attend the cardiovascular and angiology services of the city of Barranquilla. Methods: A descriptive cross-sectional study was carried out. In a sample of 102 participants. The atheromas were taken by expert personnel in endarterectomy and dissection of blood vessels. The specimens were embedded in 4% formaldehyde solution. DNA extraction was performed from atheromas. The molecular diagnosis of H. pylori was performed by ANIDADA PCR, evidencing a 120 bp fragment after electrophoresis in a 3.5% agarose gel in 0.5X TBE. Results: 102 samples of atheromas were obtained. One sample was positive for H. pylori (Sample # 14, 1/102). The atherosclerotic tissue was obtained from the right coronary artery. Conclusion: The infectious hypothesis of atherosclerosis has been one of the main research topics worldwide in recent decades. H. pylori infection is a risk factor, however, several studies are necessary to be able to conclude more accurately.Introducción: El principal mecanismo patogénico que subyace la génesis y desarrollo de enfermedades del sistema circulatorio es la aterosclerosis. Es un proceso patológico complejo y progresivo de la pared arterial que afecta especialmente a las arterias coronarias, cerebrales y periféricas. Actualmente se habla sobre “La hipótesis infecciosa de la aterosclerosis”. La infección por Helicobacter pylori ha sido una de las más investigadas a nivel global. Objetivo: Identificar H. pylori a partir de lesiones ateroscleróticas de pacientes que acuden a los servicios de cirugía cardiovascular y angiología de la ciudad de Barranquilla. Métodos: Se realizó un estudio descriptivo de corte transversal. En una muestra de 102 participantes. Los ateromas fueron tomados por personal experto en endarterectomía y disección de vasos sanguíneos. Los especímenes fueron embebidos en solución formaldehído al 4%. Se realizó extracción de ADN a partir de ateromas. El diagnóstico molecular de H. Pylori se realizó por PCR ANIDADA, evidenciando un fragmento de 120 pb posterior a la electroforesis en gel de agarosa al 3,5% en TBE 0,5X. Resultados: Se obtuvieron 102 muestras de ateromas. Una muestra resultó positiva para H. pylori (Muestra #14; 1/102). El tejido aterosclerótico fue obtenido a partir de arteria coronaria derecha. Conclusión: La hipótesis infecciosa de la aterosclerosis ha sido uno de los principales temas de investigación a nivel mundial en las últimas décadas. La infección por H. pylori es un factor de riesgo, sin embargo, varios estudios son necesarios para poder concluir de manera más precisa

Nutrient supply does play a role on the structure of marine picophytoplankton communities

Conference communicationThe Margalef´s mandala (1978) is a simplified bottom-up control model that explains how mixing and nutrient concentration determine the composition of marine phytoplankton communities. Due to the difficulties of measuring turbulence in the field, previous attempts to verify this model have applied different proxies for nutrient supply, and very often used interchangeably the terms mixing and stratification. Moreover, because the mandala was conceived before the discovery of smaller phytoplankton groups (picoplankton <2 µm), it describes only the succession of vegetative phases of microplankton. In order to test the applicability of the classical mandala to picoplankton groups, we used a multidisciplinary approach including specifically designed field observations supported by remote sensing, database analyses, and modeling and laboratory chemostat experiments. Simultaneous estimates of nitrate diffusive fluxes, derived from microturbulence observations, and picoplankton abundance collected in more than 200 stations, spanning widely different hydrographic regimes, showed that the contribution of eukaryotes to picoautotrophic biomass increases with nutrient supply, whereas that of picocyanobacteria shows the opposite trend. These findings were supported by laboratory and modeling chemostat experiments that reproduced the competitive dynamics between picoeukaryote sand picocyanobacteria as a function of changing nutrient supply. Our results indicate that nutrient supply controls the distribution of picoplankton functional groups in the ocean, further supporting the model proposed by Margalef.Spanish Governmen

IEOOS, the Spanish Institute of Oceanography integrated ocean Observing System

Since its foundation, 100 years ago, the Spanish Institute of Oceanography (IEO) has been observing and measuring the ocean characteristics. Some systems like the tide gauges network has been working for more than 60 years. The IEO standard sections began at different moments depending on the local projects, and nowadays there are XXX coastal stations and XXX deep ones that are systematically sampled, taking physical as well as biochemical measurements. At this moment, the IEO Observing System (IEOOS) includes 4 permanent moorings equipped with currentmeters, an open-sea ocean-meteorological buoy offshore Santander and an SST satellital image reception station. It also supports the Spanish contribution to the ARGO international program with 47 deployed profilers, and continuous monitoring thermosalinometers, meteorological stations and ADCP installed on the IEO research vessels. All these networks are linked to international iniciatives like SeaDataNet, Emodnet, IbiROOS and MONGOOS. The system is completed with the IEO contribution to the RAIA and Gibraltar observatories, and the development of regional prediction models. All these systematic measurements allow IEO to give responses to ocean research activities, official agencies requirements and industrial and main society demands

IEOOS: the Spanish Institute of Oceanography Observing System

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Phycodnavirus Potassium Ion Channel Proteins Question the Virus Molecular Piracy Hypothesis

Phycodnaviruses are large dsDNA, algal-infecting viruses that encode many genes with homologs in prokaryotes and eukaryotes. Among the viral gene products are the smallest proteins known to form functional K+ channels. To determine if these viral K+ channels are the product of molecular piracy from their hosts, we compared the sequences of the K+ channel pore modules from seven phycodnaviruses to the K+ channels from Chlorella variabilis and Ectocarpus siliculosus, whose genomes have recently been sequenced. C. variabilis is the host for two of the viruses PBCV-1 and NY-2A and E. siliculosus is the host for the virus EsV-1. Systematic phylogenetic analyses consistently indicate that the viral K+ channels are not related to any lineage of the host channel homologs and that they are more closely related to each other than to their host homologs. A consensus sequence of the viral channels resembles a protein of unknown function from a proteobacterium. However, the bacterial protein lacks the consensus motif of all K+ channels and it does not form a functional channel in yeast, suggesting that the viral channels did not come from a proteobacterium. Collectively, our results indicate that the viruses did not acquire their K+ channel-encoding genes from their current algal hosts by gene transfer; thus alternative explanations are required. One possibility is that the viral genes arose from ancient organisms, which served as their hosts before the viruses developed their current host specificity. Alternatively the viral proteins could be the origin of K+ channels in algae and perhaps even all cellular organisms