An Exploratory Study of COVID-19 Information on Twitter in the Greater Region

The outbreak of the COVID-19 leads to a burst of information in major online social networks (OSNs). Facing this constantly changing situation, OSNs have become an essential platform for people expressing opinions and seeking up-to-the-minute information. Thus, discussions on OSNs may become a reflection of reality. This paper aims to figure out the distinctive characteristics of the Greater Region (GR) through conducting a data-driven exploratory study of Twitter COVID-19 information in the GR and related countries using machine learning and representation learning methods. We find that tweets volume and COVID-19 cases in GR and related countries are correlated, but this correlation only exists in a particular period of the pandemic. Moreover, we plot the changing of topics in each country and region from 2020-01-22 to 2020-06-05, figuring out the main differences between GR and related countries

A multilingual dataset of COVID-19 vaccination attitudes on Twitter

Vaccine hesitancy is considered as one main cause of the stagnant uptake ratio of COVID-19 vaccines in Europe and the US where vaccines are sufficiently supplied. A fast and accurate grasp of public attitudes toward vaccination is critical to addressing vaccine hesitancy, and social media platforms have proved to be an effective source of public opinions. In this paper, we describe the collection and release of a dataset of tweets related to COVID-19 vaccines. This dataset consists of the IDs of 2,198,090 tweets collected from Western Europe, 17,934 of which are annotated with the originators’ vaccination stances. Our annotation will facilitate using and developing data-driven models to extract vaccination attitudes from social media posts and thus further confirm the power of social media in public health surveillance. To lay the groundwork for future research, we not only perform statistical analysis and visualization of our dataset, but also evaluate and compare the performance of established text-based benchmarks in vaccination stance extraction. We demonstrate one potential use of our data in practice in tracking the temporal changes in public COVID-19 vaccination attitudes

The Burden of Being a Bridge: Analysing Subjective Well-Being of Twitter Users During the COVID-19 Pandemic

The outbreak of the COVID-19 pandemic triggers infodemic over online social media, which significantly impacts public health around the world, both physically and psychologically. In this paper, we study the impact of the pandemic on the mental health of influential social media users, whose sharing behaviours significantly promote the diffusion of COVID-19 related information. Specifically, we focus on subjective well-being (SWB), and analyse whether SWB changes have a relationship with their bridging performance in information diffusion, which measures the speed and wideness gain of information transmission due to their sharing. We accurately capture users' bridging performance by proposing a new measurement. Benefiting from deep-learning natural language processing models, we quantify social media users' SWB from their textual posts. With the data collected from Twitter for almost two years, we reveal the greater mental suffering of influential users during the COVID-19 pandemic. Through comprehensive hierarchical multiple regression analysis, we are the first to discover the strong {relationship} between social users' SWB and their bridging performance

Exploring Spillover Effects for COVID-19 Cascade Prediction

An information outbreak occurs on social media along with the COVID-19 pandemic and leads to an infodemic. Predicting the popularity of online content, known as cascade prediction, allows for not only catching in advance information that deserves attention, but also identifying false information that will widely spread and require quick response to mitigate its negative impact. Among the various information diffusion patterns leveraged in previous works, the spillover effect of the information exposed to users on their decisions to participate in diffusing certain information has not been studied. In this paper, we focus on the diffusion of information related to COVID-19 preventive measures due to its special role in consolidating public efforts to slow down the spread of the virus. Through our collected Twitter dataset, we validate the existence of the spillover effects. Building on this finding, we propose extensions to three cascade prediction methods based on Graph Neural Networks (GNNs). Experiments conducted on our dataset demonstrated that the use of the identified spillover effects significantly improves the state-of-the-art GNN methods in predicting the popularity of not only preventive measure messages, but also other COVID-19 messages

HIV-1 Tat Promotes Kaposi's Sarcoma-Associated Herpesvirus (KSHV) vIL-6-Induced Angiogenesis and Tumorigenesis by Regulating PI3K/PTEN/AKT/GSK-3β Signaling Pathway

Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is etiologically associated with KS, the most common AIDS-related malignancy. KS is characterized by vast angiogenesis and hyperproliferative spindle cells. We have previously reported that HIV-1 Tat can trigger KSHV reactivation and accelerate Kaposin A-induced tumorigenesis. Here, we explored Tat promotion of KSHV vIL-6-induced angiogenesis and tumorigenesis. Tat promotes vIL-6-induced cell proliferation, cellular transformation, vascular tube formation and VEGF production in culture. Tat enhances vIL-6-induced angiogenesis and tumorigenesis of fibroblasts and human endothelial cells in a chicken chorioallantoic membrane (CAM) model. In an allograft model, Tat promotes vIL-6-induced tumorigenesis and expression of CD31, CD34, SMA, VEGF, b-FGF, and cyclin D1. Mechanistic studies indicated Tat activates PI3K and AKT, and inactivates PTEN and GSK-3β in vIL-6 expressing cells. LY294002, a specific inhibitor of PI3K, effectively impaired Tat's promotion of vIL-6-induced tumorigenesis. Together, these results provide the first evidence that Tat might contribute to KS pathogenesis by synergizing with vIL-6, and identify PI3K/AKT pathway as a potential therapeutic target in AIDS-related KS patients. © 2013 Zhou et al

A genetic study and meta-analysis of the genetic predisposition of prostate cancer in a Chinese population.

Prostate cancer predisposition has been extensively investigated in European populations, but there have been few studies of other ethnic groups. To investigate prostate cancer susceptibility in the under-investigated Chinese population, we performed single-nucleotide polymorphism (SNP) array analysis on a cohort of Chinese cases and controls and then meta-analysis with data from the existing Chinese prostate cancer genome-wide association study (GWAS). Genotyping 211,155 SNPs in 495 cases and 640 controls of Chinese ancestry identified several new suggestive Chinese prostate cancer predisposition loci. However, none of them reached genome-wide significance level either by meta-analysis or replication study. The meta-analysis with the Chinese GWAS data revealed that four 8q24 loci are the main contributors to Chinese prostate cancer risk and the risk alleles from three of them exist at much higher frequencies in Chinese than European populations. We also found that several predisposition loci reported in Western populations have different effect on Chinese men. Therefore, this first extensive single-nucleotide polymorphism study of Chinese prostate cancer in comparison with European population indicates that four loci on 8q24 contribute to a great risk of prostate cancer in a considerable large proportion of Chinese men. Based on those four loci, the top 10% of the population have six- or two-fold prostate cancer risk compared with men of the bottom 10% or median risk respectively, which may facilitate the design of prostate cancer genetic risk screening and prevention in Chinese men. These findings also provide additional insights into the etiology and pathogenesis of prostate cancer.This work was conducted on behalf of the CHIPGECS and The PRACTICAL consortia (see Supplementary Consortia). We acknowledge the contribution of doctors, nurses and postgraduate research students at the CHIPGENCS sample collecting centers. We thank Orchid and Rosetrees for funding support. This work was also supported by National Natural Science foundation of China for funding support to H Zhang (Grant No: 30671793 and 81072377), N Feng (Grant No: 81272831), X Zhang (Grant No: 30572139, 30872924 and 81072095), S Zhao (Grant No: 81072092 and 81328017), Y Yu (Grant No: 81172448) and Program for New Century Excellent Talents in University from Department of Education of China (NCET-08-0223) and the National High Technology Research and Development Program of China (863 Program 2012AA021101) to X Zhang.This is the final version of the article. It first appeared from Impact Journals via http://dx.doi.org/10.18632/oncotarget.725

Herpes Simplex Virus Type 2 Triggers Reactivation of Kaposi's Sarcoma-Associated Herpesvirus from Latency and Collaborates with HIV-1 Tat

Kaposi's sarcoma-associated herpesvirus (KSHV) infection was necessary but not sufficient for Kaposi's sarcoma (KS) development without other cofactors. Previously, we identified that both human immunodeficiency type 1 (HIV-1) Tat and herpes simplex virus 1 (HSV-1) were important cofactors reactivating KSHV from latency. Here, we further investigated the potential of herpes simplex virus 2 (HSV-2) to influence KSHV replication and examined the role of Tat in this procedure. We demonstrated that HSV-2 was a potentially important factor in the pathogenesis of KS, as determined by production of lytic phase mRNA transcripts, viral proteins and infectious viral particles in BCBL-1 cells. These results were further confirmed by an RNA interference experiment using small interfering RNA targeting KSHV Rta and a luciferase reporter assay testing Rta promoter-driven luciferase activity. Mechanistic studies showed that HSV-2 infection activated nuclear factor-kappa B (NF-κB) signaling pathway. Inhibition of NF-κB pathway enhanced HSV-2-mediated KSHV activation, whereas activation of NF-κB pathway suppressed KSHV replication in HSV-2-infected BCBL-1 cells. Additionally, ectopic expression of Tat enhanced HSV-2-induced KSHV replication. These novel findings suggest a role of HSV-2 in the pathogenesis of KS and provide the first laboratory evidence that Tat may participate HSV-2-mediated KSHV activation, implying the complicated pathogenesis of acquired immunodeficiency syndrome (AIDS)-related KS (AIDS-KS) patients