Theory of collective opinion shifts: from smooth trends to abrupt swings

We unveil collective effects induced by imitation and social pressure by analyzing data from three different sources: birth rates, sales of cell phones and the drop of applause in concert halls. We interpret our results within the framework of the Random Field Ising Model, which is a threshold model for collective decisions accounting both for agent heterogeneity and social imitation. Changes of opinion can occur either abruptly or continuously, depending on the importance of herding effects. The main prediction of the model is a scaling relation between the height h of the speed of variation peak and its width $w$ of the form h ~ w^{-kappa}, with kappa = 2/3 for well connected populations. Our three sets of data are compatible with such a prediction, with kappa ~ 0.62 for birth rates, kappa ~ 0.71 for cell phones and kappa ~ 0.64 for clapping. In this last case, we in fact observe that some clapping samples end discontinuously (w=0), as predicted by the model for strong enough imitation.Comment: 11 pages, 8 figure

Branching random walk with infinite progeny mean: a tale of two tails

Analysis and Stochastic

Differential regulation of the attachment of KSHV infected human B cells to ECM by KSHV encoded gB and cellular alpha-V integrins

Kaposi’s sarcoma-associated herpesvirus (KSHV) has two modes replication: latent and lytic replication. Reactivation from latency is dictated, in part, by the cell cycle. Herein, we have attempted to delineate the importance of cell cycle in KSHV pathogenesis by exploring the expression pattern of cell surface receptors during different phases of the cell cycle. αV integrin expression is augmented during S phase in fibroblasts, epithelial, and KSHV infected cells. Using a Matrigel system, we pioneer the concept that KSHV infected primary effusion lymphoma (PEL) cells can attach to extracellular matrix proteins. This attachment is mediated primarily via αV integrins or virally encoded gB, and occurs preferentially in cells from S phase or cells from S phase actively supporting a lytic infection, respectively. Such an ability of infected B cells to attach to endothelial cells may also aid in the dissemination of infection. The keystone of this work is that for the first time, we describe the ability of KSHV infected B cells to preferentially use cellular (αV) or viral (gB) receptors to specifically bind cells, depending upon the stage of the cell cycle and infection. Originally published Cellular Microbiology, Vol. 10, No. 7, July 200

Kaposi's sarcoma-associated herpesvirus oncoprotein K13 protects against B cell receptor induced growth arrest and apoptosis through NF-κB activation

Kaposi's sarcoma-associated herpesvirus (KSHV) has been linked to the development of Kaposi's sarcoma, primary effusion lymphoma and multicentric Castleman's disease (MCD). We have characterized the role of KSHV-encoded viral FLICE inhibitory protein K13 in the modulation of anti-IgM induced growth arrest and apoptosis in B cells. We demonstrate that K13 protects WEHI 231, an immature B cell line, against anti-IgM induced growth arrest and apoptosis. The protective effect of K13 was associated with the activation of the NF-κB pathway and was deficient in its mutant, K13-58AAA, and a structural homolog, vFLIP E8, which lack NF-κB activity. K13 upregulated the expression of NF-κB subunit RelB and blocked the anti-IgM induced decline in c-Myc and rise in p27(Kip1) that have been associated with growth arrest and apoptosis. K13 also upregulated the expression of Mcl-1, an anti-apoptotic member of the Bcl2 family. Finally, K13 protected the mature B cell line Ramos against anti-IgM induced apoptosis through NF-κB activation. Inhibition of anti-IgM induced apoptosis by K13 may contribute to the development of KSHV-associated lymphoproliferative disorders

Granular superconductivity and charge/orbital order in YBa 2 Cu 3 O 7 /manganite trilayers

We studied how the electronic, superconducting, and magnetic properties of YBa2Cu3O7/Nd1−x(Ca1−ySry )xMnO3 multilayers depend on the tolerance factor and the hole doping of the manganite. In particular, we investigated the granular superconducting state and the related magnetic-field-driven insulator-to- superconductor transition that was previously discovered in corresponding multilayers with Pr0.5La0.2Ca0.3MnO3 [B. P. P. Mallett et al., Phys. Rev. B 94, 180503(R) (2016)]. We found that this granular uperconducting state occurs only when the manganite layer is in a charge/orbital ordered and CE-type antiferromagnetic state (Mn-CO/OO). The coupling mechanism underlying this intriguing proximity effect seems to involve the domain boundaries of the Mn-CO/OO and/or the charge disordered regions of the manganite layer that become more numerous as the hole doping is reduced below x = 0.5

Hepatitis C virus cell-cell transmission and resistance to direct-acting antiviral agents

Hepatitis C virus (HCV) is transmitted between hepatocytes via classical cell entry but also uses direct cell-cell transfer to infect neighboring hepatocytes. Viral cell-cell transmission has been shown to play an important role in viral persistence allowing evasion from neutralizing antibodies. In contrast, the role of HCV cell-cell transmission for antiviral resistance is unknown. Aiming to address this question we investigated the phenotype of HCV strains exhibiting resistance to direct-acting antivirals (DAAs) in state-of-the-art model systems for cell-cell transmission and spread. Using HCV genotype 2 as a model virus, we show that cell-cell transmission is the main route of viral spread of DAA-resistant HCV. Cell-cell transmission of DAA-resistant viruses results in viral persistence and thus hampers viral eradication. We also show that blocking cell-cell transmission using host-targeting entry inhibitors (HTEIs) was highly effective in inhibiting viral dissemination of resistant genotype 2 viruses. Combining HTEIs with DAAs prevented antiviral resistance and led to rapid elimination of the virus in cell culture model. In conclusion, our work provides evidence that cell-cell transmission plays an important role in dissemination and maintenance of resistant variants in cell culture models. Blocking virus cell-cell transmission prevents emergence of drug resistance in persistent viral infection including resistance to HCV DAAs

The 5′HS4 insulator element is an efficient tool to analyse the transient expression of an Eμ-GFP vector in a transgenic mouse model

Letter to the Edito

Cancers associated with Kaposi's sarcoma (KS) in AIDS: a link between KS herpesvirus and immunoblastic lymphoma

Kaposi's sarcoma (KS), common among persons with acquired immunodeficiency syndrome (AIDS), is caused by KS herpesvirus (KSHV) but whether KSHV causes other malignancies is uncertain. Using linked United States AIDS and cancer registries, we measured the incidence of specific malignancies in persons with AIDS (4–27 months after AIDS onset). We identified associations with KSHV by calculating a relative risk: cancer incidence in persons with KS (all were KSHV-infected) divided by incidence in persons without KS. Using Poisson regression, relative risks were adjusted for human immunodeficiency virus risk group, gender, age, race, and calendar year. We included 189 159 subjects (26 972 with KS). Immunoblastic lymphoma was significantly associated with KS (506 cases; relative risks: unadjusted 2.44, 95%CI 2.00–2.96, adjusted 1.58, 95%CI 1.29–1.93). Only one immunoblastic lymphoma had pleura as primary site. None of 37 other specified malignancies (other non-Hodgkin lymphomas, haematological malignancies, solid tumours) was significantly associated with KS. In summary, the association of immunoblastic lymphoma with KS was specific among examined malignancies and remained significant after statistical adjustment. Our findings, and the previously demonstrated presence of KSHV in the histologically related primary effusion lymphoma, suggest that KSHV is involved in the pathogenesis of some immunoblastic lymphomas. © 2001 Cancer Research Campaig