Classification of Quantum Hall Universality Classes by $\ W_{1+\infty}\ $ symmetry

We show how two-dimensional incompressible quantum fluids and their excitations can be viewed as $\ W_{1+\infty}\$ edge conformal field theories, thereby providing an algebraic characterization of incompressibility. The Kac-Radul representation theory of the $\ W_{1+\infty}\$ algebra leads then to a purely algebraic complete classification of hierarchical quantum Hall states, which encompasses all measured fractions. Spin-polarized electrons in single-layer devices can only have Abelian anyon excitations.Comment: 11 pages, RevTeX 3.0, MPI-Ph/93-75 DFTT 65/9

Generalized KdV and Quantum Inverse Scattering Description of Conformal Minimal Models

We propose an alternative description of 2 dimensional Conformal Field Theory in terms of Quantum Inverse Scattering. It is based on the generalized KdV systems attached to $A_2^{(2)}$, yielding the classical limit of Virasoro as Poisson bracket structure. The corresponding T-system is shown to coincide with the one recently proposed by Kuniba and Suzuki. We classify the primary operators of the minimal models that commute with all the Integrals of Motion, and that are therefore candidates to perturb the model by keeping the conservation laws. For our $A_2^{(2)}$ structure these happen to be $\phi_{1,2},\phi_{2,1},\phi_{1,5}$, in contrast to the $A_1^{(1)}$ case, studied by Bazhanov, Lukyanov and Zamolodchikov~\cite{BLZ}, related to $\phi_{1,3}$.Comment: 12 pages, latex. 1 reference adde

A functional assay for serum detection of antibodies against SARS-CoV-2 nucleoprotein.

The humoral immune response to SARS-CoV-2 results in antibodies against spike (S) and nucleoprotein (N). However, whilst there are widely available neutralization assays for S antibodies, there is no assay for N-antibody activity. Here, we present a simple in vitro method called EDNA (electroporated-antibody-dependent neutralization assay) that provides a quantitative measure of N-antibody activity in unpurified serum from SARS-CoV-2 convalescents. We show that N antibodies neutralize SARS-CoV-2 intracellularly and cell-autonomously but require the cytosolic Fc receptor TRIM21. Using EDNA, we show that low N-antibody titres can be neutralizing, whilst some convalescents possess serum with high titres but weak activity. N-antibody and N-specific T-cell activity correlates within individuals, suggesting N antibodies may protect against SARS-CoV-2 by promoting antigen presentation. This work highlights the potential benefits of N-based vaccines and provides an in vitro assay to allow the antibodies they induce to be tested

Trivalent RING Assembly on Retroviral Capsids Activates TRIM5 Ubiquitination and Innate Immune Signaling

TRIM5 is a RING domain E3 ubiquitin ligase with potent antiretroviral function. TRIM5 assembles into a hexagonal lattice on retroviral capsids, causing envelopment of the infectious core. Concomitantly, TRIM5 initiates innate immune signaling and orchestrates disassembly of the viral particle, yet how these antiviral responses are regulated by capsid recognition is unclear. We show that hexagonal assembly triggers N-terminal polyubiquitination of TRIM5 that collectively drives antiviral responses. In uninfected cells, N-terminal monoubiquitination triggers non-productive TRIM5 turnover. Upon TRIM5 assembly on virus, a trivalent RING arrangement allows elongation of N-terminally anchored K63-linked ubiquitin chains (N-K63-Ub). N-K63-Ub drives TRIM5 innate immune stimulation and proteasomal degradation. Inducing ubiquitination before TRIM5 assembly triggers premature degradation and ablates antiviral restriction. Conversely, driving N-K63 ubiquitination after TRIM5 assembly enhances innate immune signaling. Thus, the hexagonal geometry of TRIM5's antiviral lattice converts a capsid-binding protein into a multifunctional antiviral platform

Concrete substrate moisture requirements for durable concrete repairs – a field study

peer reviewedIn concrete repair specifications, the required moisture condition of the substrate, which can play an important role for bond development, and, ultimately, on the long-term repair / overlay durability, is generally ill-defined and addressed without due consideration to the given substrate characteristics. The standard specification, if any, is to require saturated surface dry (SSD) condition of the substrate prior to application of cementitious repair materials, which is theoretically achieved after saturating the substrate and then letting the surface just start to dry out. This does provide an intuitive solution founded on rational considerations, but it has never really been precisely defined, measured, nor validated. The influence of substrate surface moisture on the bond between the existing concrete and the new repair material is an issue of significant importance. This paper revisits the question, in light of results from a project designed to develop guidelines for moisture conditioning of a concrete substrate prior to a cementitious repair, which was part of a larger effort to develop guidelines for surface preparation of concrete prior to repair. Over the course of the project, multiple series of test slabs were repaired after being subjected to different surface moisture conditioning and then tested for bond strength tests at different ages. The findings are discussed, together with those from previous studies, and recommendations are issued.9. Industry, innovation and infrastructur

TRIM21 mediates antibody inhibition of adenovirus-based gene delivery and vaccination

Adenovirus has enormous potential as a gene-therapy vector, but preexisting immunity limits its widespread application. What is responsible for this immune block is unclear because antibodies potently inhibit transgene expression without impeding gene transfer into target cells. Here we show that antibody prevention of adenoviral gene delivery in vivo is mediated by the cytosolic antibody receptor TRIM21. Genetic KO of TRIM21 or a single-antibody point mutation is sufficient to restore transgene expression to near-naïve immune levels. TRIM21 is also responsible for blocking cytotoxic T cell induction by vaccine vectors, preventing a protective response against subsequent influenza infection and an engrafted tumor. Furthermore, adenoviral preexisting immunity can lead to an augmented immune response upon i.v. administration of the vector. Transcriptomic analysis of vector-transduced tissue reveals that TRIM21 is responsible for the specific up-regulation of hundreds of immune genes, the majority of which are components of the intrinsic or innate response. Together, these data define a major mechanism underlying the preimmune block to adenovirus gene therapy and demonstrate that TRIM21 efficiently blocks gene delivery in vivo while simultaneously inducing a rapid program of immune transcription