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

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

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

Recovery of Recombinant Crimean Congo Hemorrhagic Fever Virus Reveals a Function for Non-structural Glycoproteins Cleavage by Furin

<div><p>Crimean Congo hemorrhagic fever virus (CCHFV) is a negative-strand RNA virus of the family <i>Bunyaviridae</i> (genus: <i>Nairovirus</i>). In humans, CCHFV causes fever, hemorrhage, severe thrombocytopenia, and high fatality. A major impediment in precisely determining the basis of CCHFV’s high pathogenicity has been the lack of methodology to produce recombinant CCHFV. We developed a reverse genetics system based on transfecting plasmids into BSR-T7/5 and Huh7 cells. In our system, bacteriophage T7 RNA polymerase produced complementary RNA copies of the viral S, M, and L segments that were encapsidated with the support, in <i>trans</i>, of CCHFV nucleoprotein and L polymerase. The system was optimized to systematically recover high yields of infectious CCHFV. Additionally, we tested the ability of the system to produce specifically designed CCHFV mutants. The M segment encodes a polyprotein that is processed by host proprotein convertases (PCs), including the site-1 protease (S1P) and furin-like PCs. S1P and furin cleavages are necessary for producing the non-structural glycoprotein GP38, while S1P cleavage yields structural Gn. We studied the role of furin cleavage by rescuing a recombinant CCHFV encoding a virus glycoprotein precursor lacking a functional furin cleavage motif (RSKR mutated to ASKA). The ASKA mutation blocked glycoprotein precursor’s maturation to GP38, and Gn precursor’s maturation to Gn was slightly diminished. Furin cleavage was not essential for replication, as blocking furin cleavage resulted only in transient reduction of CCHFV titers, suggesting that either GP38 and/or decreased Gn maturation accounted for the reduced virion production. Our data demonstrate that nairoviruses can be produced by reverse genetics, and the utility of our system uncovered a function for furin cleavage. This viral rescue system could be further used to study the CCHFV replication cycle and facilitate the development of efficacious vaccines to counter this biological and public health threat.</p></div

KFDV and AHFV-infected mice developed significant lymphopenia relative to control mice.

<p>Complete blood counts were run on KFDV-, AHFV- and mock-infected mice on 1, 4, 6, and 7 dpi. (A) Leukocyte, (B) lymphocyte, (C) monocyte and (D) granulocyte counts are displayed. Asterisks indicate significant differences between KFDV-infected mice (blue) or AHFV-infected mice (green) relative to mock-infected animals (p<0.05). On each day, data was collected from a minimum of 3 and a maximum of 5 mice per group.</p

Survival data for C57BL/6 mice following infection with KFDV or AHFV sc.

<p>Values indicate the number of mice (out of 5) that survived infection with KFDV or AHFV as of 30 dpi.</p

KFDV-infected mice have higher viral RNA loads than AHFV-infected mice early in infection.

<p>Viral RNA loads in the (A) blood, (B) spleen, (C) gastrointestinal tract and (D) brain were compared between KFDV- and AHFV-infected mice on 1, 4, 6 and 7 dpi. Asterisks indicate significant differences between KFDV- and AHFV-infected mice (n = 5; p<0.05). The gray dotted line denotes limit of detection of the assay.</p

More severe histopathologic lesions were apparent in the brains and gastrointestinal tracts of KFDV-infected mice than AHFV-infected mice.

<p>(A) Brain, hippocampus, KFDV-infected mouse, 6 dpi; acute necrosis and loss of hippocampal neurons (segment delineated by arrowheads), with adjacent, relatively unaffected neurons (arrow). (B) Brainstem, KFDV-infected mouse, 6 dpi; severe meningoencephalitis with perivascular cuffing (arrow) and widespread gliosis in the adjacent neuropil (asterisk). (C) Brainstem, AHFV-infected mouse, 7 dpi; mild meningoencephalitis characterized by perivascular cuffing (arrows). (D) Small intestine, mock-inoculated mouse; normal tissue section demonstrating anatomic location of submucosal (arrow) and myenteric (arrowhead) nerve plexi and normal intestinal villi; inset shows higher magnification of neuron cell bodies in plexus. (E) Small intestine, KFDV-infected mouse, 7 dpi; moderate, predominantly histiocytic, inflammatory infiltrate in submucosa and muscularis, involving and disrupting myenteric plexi (arrowheads). Inset shows higher magnification of infiltrate and cell debris in plexus. (F) Small intestine, KFDV-infected mouse, 7 dpi; intestinal crypts are dilated and filled with necrotic cells (asterisks), intestinal lumen contains abundant cellular debris (top of image), and villi are blunted and fused. All H&E images, original magnification 200x.</p

KFDV- and AHFV-infected mice mount an early innate response to infection in the CNS.

<p>In the brains of mice infected with KFDV or AHFV, there was significant upregulation of (A) interferon-stimulated genes and (B) pathogen recognition receptors (PRRs). There were not significant differences in gene expression between mice infected with AHFV and those infected with KFDV (n = 5; p>0.05).</p

KFDV is more virulent than AHFV in 3 immunocompetent mouse strains.

<p>C3H, A/J and C57BL/6J mice were inoculated subcutaneously with either 1×10⁵ TCID₅₀ AHFV or 1×10⁵ TCID₅₀ KFDV (n = 10/group) and monitored for 28 days. Regardless of strain, KFDV infection resulted in higher mortality and more severe disease than AHFV.</p