Prices and the Real Exchange Rate in Hong Kong: 1985-2006

This paper has been presented at the XIII Encuentros de Economía Aplicada, Sevilla, Spain, 2010.Real Exchange Rate (RER), Balassa-Samuelson hypothesis, inflation

Business cycles in a small open economy: The case of Hong Kong

This paper was presented at the All China Economics (ACE) International Conference, Hong Kong, 2006, XXXIII Symposium of Economic Analysis, Spain, 2007, DEGIT XVI Dynamics, Economic Growth and International Trade, Los Angeles, USA, 2009.small open economy, business cycles, financial frictions, total factor productiviy, country risk spread, neoclassical model

Mutation analysis of a recombinant NS replicon shows that influenza virus NS1 protein blocks the splicing and nucleo-cytoplasmic transport of its own viral mRNA

The genome of influenza A virus consists of eight single-stranded RNA molecules of negative polarity. Their replication and transcription take place in the nucleus of infected cells using ribonucleoprotein complexes (RNPs) as templates. Two of the viral transcripts, those generated by RNPs 7 and 8, can be spliced and lead to two alternative protein products (M1 and M2, NS1 and NEP/NS2, respectively). Previous studies have shown that when expressed from cDNA, NS1 protein alters the splicing and transport of RNA polymerase II-driven transcripts. Here we used a transient replication/transcription system, in which RNP 8 is replicated and transcribed by recombinant RNA and proteins, to study the splicing and nucleo-cytoplasmic transport of true viral transcripts. Our results show that the encoded NS1 protein inhibits the splicing of the collinear transcript. This regulation is mediated by the N-terminal region of the protein but does not involve its RNA-binding activity. We also show that NS1 protein preferentially blocks the nucleo-cytoplasmic transport of the collinear RNP 8 transcript in an RNA-binding dependent manner. These results rule out previous models to explain the regulation of mRNA processing and transport by NS1 and underlines the relevance of NS1 protein in the control of virus gene expression

Hepatitis C Virus Blocks Interferon Effector Function by Inducing Protein Kinase R Phosphorylation

SummaryHepatitis C virus (HCV) is a single-stranded RNA virus encoding a single polyprotein whose translation is driven by an internal ribosome entry site (IRES). HCV infection strongly induces antiviral interferon-stimulated gene (ISG) expression in the liver, yet it persists, suggesting that HCV can block ISG effector function. We now show that HCV infection triggers phosphorylation and activation of the RNA-dependent protein kinase PKR, which inhibits eukaryotic translation initiation factor eIF2α and attenuates ISG protein expression despite normal ISG mRNA induction. ISG protein induction is restored and the antiviral effects of interferon are enhanced when PKR expression is suppressed in interferon-treated infected cells. Whereas host protein translation, including antiviral ISGs, is suppressed by activated PKR, HCV IRES-dependent translation is not. These results suggest that the ability of HCV to activate PKR may, paradoxically, be advantageous for the virus during an IFN response by preferentially suppressing the translation of ISGs

Business cycles in a small open economy: The case of Hong Kong

This paper was presented at the All China Economics (ACE) International Conference, Hong Kong, 2006, XXXIII Symposium of Economic Analysis, Spain, 2007, DEGIT XVI Dynamics, Economic Growth and International Trade, Los Angeles, USA, 2009.This paper analyzes the business cycle properties of the Hong Kong economy during the 1982-2004 period, which includes the financial crisis experienced in 1997-98. We show that output, output growth rate and real interest rates volatilities in Hong Kong are higher than their respective average volatilities among developed economies. In this paper, we build a stochastic neoclassical small open economy model that seeks to replicate the main business cycle characteristics of Hong Kong, and through which we try to quantify the role played by exogenous Total Factor Productivity (transitory and permanent), real interest rates shocks and financial frictions. The main findings are that the trend volatility has to be higher than the volatility of the transitory fluctuations around the trend; that the volatility of real interest rates are mainly due to country risk spread, and that financial frictions matter to explain real interest rates countercyclicality.Financial support from Universidad del País Vasco MACLAB, project IT-241-07, and Ministerio de Ciencia e Innovación, project ECO2009-09732 are gratefully acknowledged

Implicación de la proteína NS1 del virus de la gripe en la regulación de la expresión génica y en la morfogénesis viral

Tesis Doctoral inédita leida en la Universidad Autónoma de Madrid, Facultad de Ciencias, Departamento de Biología Molecular. Fecha de lectura: 25-05-200

Fear who said fear

Fear who said fear is an educational project of the Department of Education and Cultural Action of ARTIUM encolaboración with the Day hospital of Addictions of Alava, which consists of the creation of a series of notebooks - diaries and a video that they work as loudspeaker of the thoughts, the emotions, the worries and the fears of his seven participants. The artistic creation appears as a way of sharing and debating questions that they have to see with the own vital experiences, in a mixture of humor and critical in that the group forms a part it activates

Identification of Niemann-Pick C1 protein as a potential novel SARS-CoV-2 intracellular target

Niemann-Pick type C1 (NPC1) receptor is an endosomal membrane protein that regulates intracellular cholesterol traffic. This protein has been shown to play an important role for several viruses. It has been reported that SARS-CoV-2 enters the cell through plasma membrane fusion and/or endosomal entry upon availability of proteases. However, the whole process is not fully understood yet and additional viral/host factors might be required for viral fusion and subsequent viral replication. Here, we report a novel interaction between the SARS-CoV-2 nucleoprotein (N) and the cholesterol transporter NPC1. Furthermore, we have found that some compounds reported to interact with NPC1, carbazole SC816 and sulfides SC198 and SC073, were able to reduce SARS-CoV-2 viral infection with a good selectivity index in human cell infection models. These findings suggest the importance of NPC1 for SARS-CoV-2 viral infection and a new possible potential therapeutic target to fight against COVID-19

Codon conservation in the influenza A virus genome defines RNA packaging signals

Genome segmentation facilitates reassortment and rapid evolution of influenza A virus. However, segmentation complicates particle assembly as virions must contain all eight vRNA species to be infectious. Specific packaging signals exist that extend into the coding regions of most if not all segments, but these RNA motifs are poorly defined. We measured codon variability in a large dataset of sequences to identify areas of low nucleotide sequence variation independent of amino acid conservation in each segment. Most clusters of codons showing very little synonymous variation were located at segment termini, consistent with previous experimental data mapping packaging signals. Certain internal regions of conservation, most notably in the PA gene, may however signify previously unidentified functions in the virus genome. To experimentally test the bioinformatics analysis, we introduced synonymous mutations into conserved codons within known packaging signals and measured incorporation of the mutant segment into virus particles. Surprisingly, in most cases, single nucleotide changes dramatically reduced segment packaging. Thus our analysis identifies cis-acting sequences in the influenza virus genome at the nucleotide level. Furthermore, we propose that strain-specific differences exist in certain packaging signals, most notably the haemagglutinin gene; this finding has major implications for the evolution of pandemic viruses