Effects of Active Labor Market Programs on the Transition Rate from Unemployment into Regular Jobs in the Slovak Republic

The system of active labor market policies (ALMP) in the Slovak Republic consists to a large extent of the creation of socially purposeful and publicly useful jobs and of retraining of unemployed workers. So far, the effects of these types of active labor market policies have hardly been analyzed. This paper uses a unique administrative data from 20 Slovak districts to analyze to what extent it is beneficial for unemployed workers who want a regular job to accept a temporary ALMP-job or enter a retraining program. We find that indeed it is beneficial for workers to do so.models;unemployment;labour policy

Unemployment Durations of Job Losers in a Labor Market in Transition

Slovakia is one of the Central European countries in transformation from a centralised command system to a decentralised market economy. Along with the transition of the economy came unemployment. Other than before workers who lost their job did not find a new job immediately. This paper studies the labour market position of Slovak job losers. Using data from labour force surveys we analyse exit rates out of unemployment. We find that male, young, higher educated job losers in districts with low unemployment rates have substantially shorter unemployment durations than their counterparts. There is evidence that for some job losers it is very hard to find a new job.unemployment durations;job losers;transition economy

Unemployment Durations of Job Losers in a Labor Market in Transition

Slovakia is one of the Central European countries in transformation from a centralised command system to a decentralised market economy. Along with the transition of the economy came unemployment. Other than before workers who lost their job did not find a new job immediately. This paper studies the labour market position of Slovak job losers. Using data from labour force surveys we analyse exit rates out of unemployment. We find that male, young, higher educated job losers in districts with low unemployment rates have substantially shorter unemployment durations than their counterparts. There is evidence that for some job losers it is very hard to find a new job.

A Calculation of the Full Neutrino Phase Space in Cold+Hot Dark Matter Models

This paper presents a general-relativistic N-body technique for evolving the phase space distribution of massive neutrinos in linear perturbation theory. The method provides a much more accurate sampling of the neutrino phase space for the HDM initial conditions of N-body simulations in a cold+hot dark matter universe than previous work. Instead of directly sampling the phase space at the end of the linear era, we first compute the evolution of the metric perturbations by numerically integrating the coupled, linearized Einstein, Boltzmann, and fluid equations for all particle species. We then sample the phase space shortly after neutrino decoupling at redshift z=10^9 when the distribution is Fermi-Dirac. To follow the trajectory of each neutrino, we subsequently integrate the geodesic equations for each neutrino in the perturbed background spacetime from z=10^9 to z=13.55, using the linearized metric found in the previous calculation to eliminate discreteness noise. The positions and momenta resulting from this integration represent a fair sample of the full neutrino phase space and can be used as HDM initial conditions for N-body simulations of nonlinear structure evolution in this model. A total of 21 million neutrino particles are used in a 100 Mpc box, with Omega_cdm=0.65, Omega_hdm=0.30, Omega_baryon=0.05, and Hubble constant H_0=50. We find that correlations develop in the neutrino densities and momenta which are absent when only the zeroth-order Fermi-Dirac distribution is considered.Comment: 20 pages, AAS LaTeX v3.0, figures and/or postscript available by anonymous ftp to arcturus.mit.edu, MIT CSR-93-1

Antagonism of Host Antiviral Responses by Kaposi's Sarcoma-Associated Herpesvirus Tegument Protein ORF45

Virus infection of a cell generally evokes an immune response by the host to defeat the intruder in its effort. Many viruses have developed an array of strategies to evade or antagonize host antiviral responses. Kaposi's sarcoma-associated herpesvirus (KSHV) is demonstrated in this report to be able to prevent activation of host antiviral defense mechanisms upon infection. Cells infected with wild-type KSHV were permissive for superinfection with vesicular stomatitis virus (VSV), suggesting that KSHV virions fail to induce host antiviral responses. We previously showed that ORF45, a KSHV immediate-early protein as well as a tegument protein of virions, interacts with IRF-7 and inhibits virus-mediated type I interferon induction by blocking IRF-7 phosphorylation and nuclear translocation (Zhu et al., Proc. Natl. Acad. Sci. USA. 99:5573-5578, 2002). Here, using an ORF45-null recombinant virus, we demonstrate a profound role of ORF45 in inhibiting host antiviral responses. Infection of cells with an ORF45-null mutant recombinant KSHV (BAC-stop45) triggered an immune response that resisted VSV super-infection, concomitantly associated with appreciable increases in transcription of type I IFN and downstream anti-viral effector genes. Gain-of-function analysis showed that ectopic expression of ORF45 in human fibroblast cells by a lentivirus vector decreased the antiviral responses of the cells. shRNA-mediated silencing of IRF-7, that predominantly regulates both the early and late phase induction of type I IFNs, clearly indicated its critical contribution to the innate antiviral responses generated against incoming KSHV particles. Thus ORF45 through its targeting of the crucial IRF-7 regulated type I IFN antiviral responses significantly contributes to the KSHV survival immediately following a primary infection allowing for progression onto subsequent stages in its life-cycle

A Gammaherpesvirus Cooperates with Interferon-alpha/beta-Induced IRF2 to Halt Viral Replication, Control Reactivation, and Minimize Host Lethality

The gammaherpesviruses, including Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), establish latency in memory B lymphocytes and promote lymphoproliferative disease in immunocompromised individuals. The precise immune mechanisms that prevent gammaherpesvirus reactivation and tumorigenesis are poorly defined. Murine gammaherpesvirus 68 (MHV68) is closely related to EBV and KSHV, and type I (alpha/beta) interferons (IFNαβ) regulate MHV68 reactivation from both B cells and macrophages by unknown mechanisms. Here we demonstrate that IFNβ is highly upregulated during latent infection, in the absence of detectable MHV68 replication. We identify an interferon-stimulated response element (ISRE) in the MHV68 M2 gene promoter that is bound by the IFNαβ-induced transcriptional repressor IRF2 during latency in vivo. The M2 protein regulates B cell signaling to promote establishment of latency and reactivation. Virus lacking the M2 ISRE (ISREΔ) overexpresses M2 mRNA and displays uncontrolled acute replication in vivo, higher latent viral load, and aberrantly high reactivation from latency. These phenotypes of the ISREΔ mutant are B-cell-specific, require IRF2, and correlate with a significant increase in virulence in a model of acute viral pneumonia. We therefore identify a mechanism by which a gammaherpesvirus subverts host IFNαβ signaling in a surprisingly cooperative manner, to directly repress viral replication and reactivation and enforce latency, thereby minimizing acute host disease. Since we find ISREs 5′ to the major lymphocyte latency genes of multiple rodent, primate, and human gammaherpesviruses, we propose that cooperative subversion of IFNαβ-induced IRFs to promote latent infection is an ancient strategy that ensures a stable, minimally-pathogenic virus-host relationship