Extended Black Box Theorem for Lepton Number and Flavor Violating processes

We revisit the well known "Black Box" theorem establishing a fundamental relation between the amplitude of neutrinoless double beta decay and the effective Majorana neutrino mass. We extend this theorem to the general case of arbitrary lepton number and lepton flavor violating (LFNV) processes and to the three generation Majorana neutrino mass matrix. We demonstrate the existence of a general set of one-to-one correspondence relations between the effective operators generating these processes, and elements of the neutrino mass matrix, such that if one of these two quantities vanishes the other is guaranteed to vanish as well, and moreover, if one of these quantities is non-zero the other is guaranteed to be non-zero. We stress that this statement remains valid even in the presence of arbitrary new physics contributions. As a particularly important example, we then show that neutrino oscillation data imply that neutrinoless double beta decay must occur at a certain non-zero rate.Comment: 11 pages, 1 fi

Virus Restriction and Adaptation during Latent and Chronic Infection

Přírodovědecká fakult

Proton Stability in Leptoquark Models

We show that in generic leptoquark (LQ) extensions of the standard model lepton and baryon numbers are broken at the level of renormalizable operators. In particular, this may cause fast proton decay unless the leptoquarks are heavy enough. We derive stringent bounds for the 1st generation LQ masses and couplings from the proton stability constraints.Comment: 7 pages, 1 tabl

Heavy Sterile Neutrinos in Tau Decays and the MiniBooNE Anomaly

Current results of the MiniBooNE experiment show excess events that indicate neutrino oscillations, but only if one goes beyond the standard 3 family scenario. Recently a different explanation of the events has been given, not in terms of oscillations but by the production and decay of a massive sterile neutrino with large transition magnetic moment. We study the effect of such a sterile neutrino in the rare decays $\tau^- \rightarrow \mu^- \mu^+ \pi^- \nu$ and $\tau^{-}\rightarrow \mu^{-} \mu^{+} e^{-} \nu \nu$. We find that searches for these decays featuring displaced vertices between the $\mu^-$ and the other charged particles, constitute good tests for the existence of the sterile neutrino proposed to explain the MiniBooNE anomaly. These searches could be done with already existing experimental data.Comment: 4 pages, 1 figur

Hepatitis C Virus Is a Weak Inducer of Interferon Alpha in Plasmacytoid Dendritic Cells in Comparison with Influenza and Human Herpesvirus Type-1

Plasmacytoid dendritic cells (pDCs) are responsible for the production of type I IFN during viral infection. Viral elimination by IFN-α-based therapy in more than 50% of patients chronically infected with hepatitis C virus (HCV) suggests a possible impairment of production of endogenous IFN-α by pDCs in infected individuals. In this study, we investigated the impact of HCV on pDC function. We show that exposure of pDCs to patient serum- and cell culture-derived HCV resulted in production of IFN-α by pDCs isolated from some donors, although this production was significantly lower than that induced by influenza and human herpesvirus type 1 (HHV-1). Using specific inhibitors we demonstrate that endocytosis and endosomal acidification were required for IFN-α production by pDCs in response to cell culture-derived HCV. HCV and noninfectious HCV-like particles inhibited pDC-associated production of IFN-α stimulated with Toll-like receptor 9 (TLR9) agonists (CpG-A or HHV-1) but not that of IFN-α stimulated with TLR7 agonists (resiquimod or influenza virus). The blockade of TLR9-mediated production of IFN-α, effective only when pDCs were exposed to virus prior to or shortly after CpG-A stimulation, was already detectable at the IFN-α transcription level 2 h after stimulation with CpG-A and correlated with down-regulation of the transcription factor IRF7 expression and of TLR9 expression. In conclusion, rapidly and early occurring particle–host cell protein interaction during particle internalization and endocytosis followed by blockade of TLR9 function could result in less efficient sensing of HCV RNA by TLR7, with impaired production of IFN-α. This finding is important for our understanding of HCV-DC interaction and immunopathogenesis of HCV infection

Truncated forms of human and simian immunodeficiency virus in infected individuals and rhesus macaques are unique or rare quasispecies

AbstractTruncated proviruses of variable sizes are present in peripheral blood mononuclear cells (PBMC) of human immunodeficiency virus type 1 (HIV-1)-infected persons and simian immunodeficiency virus (SIV)-infected rhesus macaques. Here, we investigated whether the highly deleted HIV and SIV proviruses are present in infected organisms as multiple copies or whether each truncated provirus is unique. Using end-point dilution, multiple long-distance (LD) DNA PCR assays were run in parallel using DNA extracted from PBMC of seropositive, treatment-naive persons and from lymph nodes of a rhesus monkey inoculated with cloned, full-length SIVmac239 DNA. The PCR products were titrated and mapped. Most truncated proviruses were present in the DNA samples tested as single, nonintegrated molecules that differed from one another in size and/or nucleotide sequence. These results indicate that truncated primate lentiviral sequences found in infected tissues are unique or rare quasispecies that do not replicate significantly