Building a Sentiment Corpus of Tweets in Brazilian Portuguese

The large amount of data available in social media, forums and websites motivates researches in several areas of Natural Language Processing, such as sentiment analysis. The popularity of the area due to its subjective and semantic characteristics motivates research on novel methods and approaches for classification. Hence, there is a high demand for datasets on different domains and different languages. This paper introduces TweetSentBR, a sentiment corpora for Brazilian Portuguese manually annotated with 15.000 sentences on TV show domain. The sentences were labeled in three classes (positive, neutral and negative) by seven annotators, following literature guidelines for ensuring reliability on the annotation. We also ran baseline experiments on polarity classification using three machine learning methods, reaching 80.99% on F-Measure and 82.06% on accuracy in binary classification, and 59.85% F-Measure and 64.62% on accuracy on three point classification.Comment: Accepted for publication in 11th International Conference on Language Resources and Evaluation (LREC 2018

InDel variants at the canonical GP editing site.

<p>Huh7 and Mpg cells were infected with EBOV, SUDV, BDBV, or RESTV at moi = 0.1. Total RNA was harvested 3 dpi, and purified mRNAs were used to make NGS libraries. Variant detection was done using a minimum cut-off of 1%.</p

Transcriptional analysis of viral mRNAs reveals common transcription patterns in cells infected by five different filoviruses

<div><p>Filoviruses are notorious viral pathogens responsible for high-consequence diseases in humans and non-human primates. Transcription of filovirus mRNA shares several common features with transcription in other non-segmented negative-strand viruses, including differential expression of genes located across the viral genome. Transcriptional patterns of Ebola virus (EBOV) and Marburg virus (MARV) have been previously described using traditional, laborious methods, such as northern blots and in vivo labeling of viral mRNAs. More recently, however, the availability of the next generation sequencing (NGS) technology has offered a more straightforward approach to assess transcriptional patterns. In this report, we analyzed the transcription patterns of four ebolaviruses—EBOV, Sudan (SUDV), Bundibugyo (BDBV), and Reston (RESTV) viruses—in two different cell lines using standard NGS library preparation and sequencing protocols. In agreement with previous reports mainly focused on EBOV and MARV, the remaining filoviruses used in this study also showed a consistent transcription pattern, with only minor variations between the different viruses. We have also analyzed the proportions of the three mRNAs transcribed from the GP gene, which are characteristic of the genus <i>Ebolavirus</i> and encode the glycoprotein (GP), the soluble GP (sGP), and the small soluble GP (ssGP). In addition, we used NGS methodology to analyze the transcription pattern of two previously described recombinant MARV. This analysis allowed us to correct our construction design, and to make an improved version of the original MARV expressing reporter genes.</p></div

Etudes des mécanismes cellulaires et moléculaires de Plasmodium falciparum impliqués dans les résistances aux combinaisons à bases de dérivés de l’artémisinine

Artemisinin-based combination therapies (ACTs) are one of the pillars of the current strategies implemented for fighting malaria. Over the last decade, ACTs have played a major role in decreasing malaria burden. However, this progress is being jeopardized by the emergence of artemisinin-resistant Plasmodium falciparum parasites. Artemisinin (ART) resistance was first detected in western Cambodia in 2008 and has since been observed in neighboring countries in Southeast Asia. The problem of antimalarial drug resistance has recently worsened in Cambodia, with reports of parasites resistant to piperaquine (PPQ), the latest generation of partner drug used in combination with dihydroartemisinin, leading to worrying rates of clinical treatment failure. The monitoring and the comprehension of both types of resistance are crucial to prevent the spread of multi-drug resistant parasites outside Southeast Asia, and particularly to Africa, where the public health consequences would be catastrophic. To this end, new tools are required for studies of the biological and molecular mechanisms underlying resistance to antimalarial drugs and for monitoring the geographic distribution of the resistant parasites.In the first section of this thesis, centered on artemisinin resistance, we first present the discovery of mutations within the K13 gene as a molecular marker for ART resistance. Then we confirm their role as a major determinant of such a resistance. Finally, we analyze the extent of ART resistance through a global mapping of K13 polymorphisms. In the second section, we present our work on the emergence of piperaquine resistance in Cambodia, by initially confirming that multiresistant parasites now circulate in the country. Then we detail the development of a new phenotypical test for the detection of PPQ-resistant parasites, the Piperaquine Survival Assay or PSA. Lastly, we report the discovery of the PfPM2 gene amplification as a candidate molecular marker for PPQ-resistance.Les combinaisons thérapeutiques à base d’artémisinine (ou CTAs) sont une des clés de voûte des stratégies actuelles de lutte contre le paludisme : ces thérapies ont en effet joué un rôle important dans la réduction de l’impact du paludisme au cours de la dernière décennie. Cependant, ces progrès sont aujourd’hui compromis par l’émergence de parasites Plasmodium falciparum résistants aux dérivés de l’artémisinine (ART). Les premiers parasites résistants ont été détectés pour la première fois en 2008 dans l’ouest du Cambodge, puis dans plusieurs pays avoisinants d’Asie du Sud-Est. Le problème de la multirésistance aux antipaludiques s’est récemment aggravé au Cambodge : plusieurs études ont rapporté l’émergence de parasites résistants à la pipéraquine (PPQ), la dernière génération de molécule partenaire utilisée en combinaison avec la dihydroartémisinine, entraînant des taux alarmants d’échecs cliniques. Pour préserver l’efficacité de ces combinaisons, la surveillance et la compréhension de ces deux types de résistance sont cruciales afin d’éviter la dissémination de parasites multirésistants en dehors d’Asie du Sud-Est, et particulièrement en Afrique où les conséquences sanitaires seraient désastreuses. À cette fin, le développement de nouveaux outils est nécessaire pour étudier les mécanismes biologiques et moléculaires impliqués dans la résistance aux CTAs et pour surveiller la distribution géographique des parasites multirésistants. Dans la première partie de cette thèse, axée sur la résistance à l’artémisinine, nous présentons tout d’abord la découverte de mutations au sein du gène K13, marqueur moléculaire pour la résistance à l'ART. Puis nous confirmons leur rôle comme déterminant majeur de cette résistance. Enfin, nous analysons l’étendue de cette résistance au travers d'une cartographie mondiale des polymorphismes de K13. Dans la seconde partie de cette thèse, nous présentons nos travaux portant sur l’émergence de la résistance à la pipéraquine au Cambodge, en confirmant dans un premier temps que des parasites multirésistants à l’ART et à la PPQ circulent désormais dans le pays. Puis en détaillant la mise en point d’un nouveau test phénotypique pour la détection des parasites PPQ-résistants, le Piperaquine Survival Assay ou PSA. Pour finir, nous exposons la découverte de l’amplification du gène PfPM2 comme marqueur moléculaire pour la résistance à la PPQ

Sequences analyzed in this study.

<p>Sequences analyzed in this study.</p

Sequence comparison of full-length viral genomes of representative RESTV isolates.

<p>Sequence identity (%) is indicated in the lower diagonal half, while the number of differing residues is indicated in the upper diagonal half. Asterisks indicate the 9 sequences determined in this study.</p

Phylogenetic analysis of available full-length RESTV genomes.

<p>Phylogenetic analysis was done with a Bayesian algorithm using Geneious 6.1.5. Clades I to V are indicated with brackets, Asterisks indicate the 9 sequences determined in this study. Posterior probabilities are listed next to each nodes. Scale bar indicates nucleotide substitutions per site.</p

Development of a reverse genetics system for Sosuga virus allows rapid screening of antiviral compounds

<div><p>Sosuga virus (SOSV) is a recently discovered zoonotic paramyxovirus isolated from a single human case in 2012; it has been ecologically and epidemiologically associated with transmission by the Egyptian rousette bat (<i>Rousettus aegyptiacus</i>). Bats have long been recognized as sources of novel zoonotic pathogens, including highly lethal paramyxoviruses like Nipah virus (NiV) and Hendra virus (HeV). The ability of SOSV to cause severe human disease supports the need for studies on SOSV pathogenesis to better understand the potential impact of this virus and to identify effective treatments. Here we describe a reverse genetics system for SOSV comprising a minigenome-based assay and a replication-competent infectious recombinant reporter SOSV that expresses the fluorescent protein ZsGreen1 in infected cells. First, we used the minigenome assay to rapidly screen for compounds inhibiting SOSV replication at biosafety level 2 (BSL-2). The antiviral activity of candidate compounds was then tested against authentic viral replication using the reporter SOSV at BSL-3. We identified several compounds with anti-SOSV activity, several of which also inhibit NiV and HeV. Alongside its utility in screening for potential SOSV therapeutics, the reverse genetics system described here is a powerful tool for analyzing mechanisms of SOSV pathogenesis, which will facilitate our understanding of how to combat the potential public health threats posed by emerging bat-borne paramyxoviruses.</p></div

Optimization of an antiviral screening assay using a recombinant SOSV expressing ZsG.

<p><b>a.</b> Schematic representation of the wild-type recombinant SOSV (rSOSV), and the reporter SOSV expressing ZsG (rSOSV/ZsG). The ZsG coding sequence was inserted immediately 5′ of the M coding sequence (antigenomic sense), separated from the viral protein by the P2A sequence from porcine teschovirus 1. This self-cleaving amino acid motif allows expression of both ZsG and M from a single mRNA generated by the parental SOSV M promoter and terminator sequences. <b>b.</b> Vero-E6 cells infected with either rSOSV or rSOSV/ZsG at 72 hpi showing formation of syncytia. In rSOSV/ZsG-infected cell monolayers, syncytia were associated with extensive ZsG expression (images taken at 4 × magnification). <b>c.</b> Growth curves for wild-type SOSV, rSOSV, and rSOSV/ZsG were performed in Vero-E6 cells infected at MOI 0.1. Titers (TCID₅₀) were determined at 24, 48, 72, 96, and 120 hpi. <b>d.</b> The optimized rSOSV/ZsG antiviral screening assay was validated using ribavirin. Huh7 cells were treated with a serial 2-fold dilution of ribavirin 1 h prior to infection at MOI 0.2. ZsG fluorescence (green) was measured at 72 hpi and normalized to levels in mock-treated cells (DMSO only). Cell viability (blue) was determined concurrently by measuring ATP content, with values normalized to mock-infected cells. Each point represents the mean of quadruplicate wells, with error bars showing standard deviation; graph representative of 3 independent experiments.</p

Using SOSV/ZsG as a tool to screen antiviral compounds.

<p><b>a.</b> Representative concentration-response curves of Huh7 cells treated with 2-fold serial dilutions of compound 1 h prior to infection with rSOSV/ZsG at MOI 0.2. ZsG fluorescence (green) was measured at 48 hpi and normalized to mock-treated cells. Cell viability was assessed concurrently by determining ATP content (blue), with values normalized to mock-infected cells. Each point represents the mean of quadruplicate wells, with error bars showing standard deviation; graph is representative of 3 independent experiments. <b>b.</b> Confirmatory counter-screening of each compound with wild-type rSOSV. Huh7 cells were treated with serial dilutions of compound 1 h prior to infection with rSOSV at MOI 0.2. At 2 days post infection cells were fixed, and SOSV proteins stained and quantified using immunofluorescence microscopy. Relative fluorescence (red; total fluorescence normalized to mock-treated cells) in each well was determined, with cell viability assessed concurrently by determining ATP content (blue). Each point represents the mean of quadruplicate wells, with error bars showing standard deviation. Values stated are the 50% effective concentration (EC₅₀), 50% cytotoxic concentration (CC₅₀), and selectivity index (SI).</p