Is the interpretation of rapid antigen testing for respiratory syncytial virus as simple as positive or negative?

Objective: To measure the performance characteristics of an immunochromatographic rapid antigen test for respiratory syncytial virus (RSV) and determine how its interpretation should be contextualised in patients presenting to the emergency department (ED) with bronchiolitis.

Design: Diagnostic accuracy study of a rapid RSV test.

Setting: County hospital ED.

Comparison of respiratory virus detection rates for infants and toddlers by use of flocked swabs, saline aspirates, and saline aspirates mixed in universal transport medium for room temperature storage and shipping.

A nylon flocked swab/universal transport medium collection method developed for bacterial sexually transmitted infections was adapted to detect respiratory viruses in infants and toddlers. This method significantly outperformed the traditional use of nasal aspirates in terms of PCR-based virus detection (P = 0.016), and the samples were easier for clinicians to evaluate, store, and transport.

CD147 immunoglobulin superfamily receptor function and role in pathology.

The immunoglobulin superfamily member CD147 plays an important role in fetal, neuronal, lymphocyte and extracellular matrix development. Here we review the current understanding of CD147 expression and protein interactions with regard to CD147 function and its role in pathologic conditions including heart disease, Alzheimer's disease, stroke and cancer. A model linking hypoxic conditions found within the tumor microenvironment to upregulation of CD147 expression and tumor progression is introduced.

FOXP3 is a homo-oligomer and a component of a supramolecular regulatory complex disabled in the human XLAAD/IPEX autoimmune disease.

We have found that FOXP3 is an oligomeric component of a large supramolecular complex. Certain FOXP3 mutants with single amino acid deletions in the leucine zipper domain of FOXP3 are associated with the X-linked autoimmunity-allergic dysregulation (XLAAD) and immunodysregulation, polyendocrinopathy and enteropathy, X-linked (IPEX) syndrome in humans. We report that the single amino acid deletion found in human XLAAD/IPEX patients within the leucine zipper domain of FOXP3 does not disrupt its ability to join the larger protein complex, but eliminates FOXP3 homo-oligomerization as well as heteromerization with FOXP1.

FOXP3 interactions with histone acetyltransferase and class II histone deacetylases are required for repression.

The forkhead family protein FOXP3 acts as a repressor of transcription and is both an essential and sufficient regulator of the development and function of regulatory T cells. The molecular mechanism by which FOXP3-mediated transcriptional repression occurs remains unclear. Here, we report that transcriptional repression by FOXP3 involves a histone acetyltransferase-deacetylase complex that includes histone acetyltransferase TIP60 (Tat-interactive protein, 60 kDa) and class II histone deacetylases HDAC7 and HDAC9.

FOXP3 ensembles in T-cell regulation.

Our recent studies have identified dynamic protein ensembles containing forkhead box protein 3 (FOXP3) that provide insight into the molecular complexity of suppressor T-cell activities, and it is our goal to determine how these ensembles regulate FOXP3's transcriptional activity in vivo. In this review, we summarize our current understanding of how FOXP3 expression is induced and how FOXP3 functions in vivo as a transcriptional regulator by assembling a multisubunit complex involved in histone modification as well as chromatin remodeling.

Both spike and background genes contribute to murine coronavirus neurovirulence.

Various strains of mouse hepatitis virus (MHV) exhibit different pathogenic phenotypes. Infection with the A59 strain of MHV induces both encephalitis and hepatitis, while the highly neurovirulent JHM strain induces a fatal encephalitis with little, if any, hepatitis. The pathogenic phenotype for each strain is determined by the genetic composition of the viral genome, as well as the host immune response.

Amino acid substitutions within the heptad repeat domain 1 of murine coronavirus spike protein restrict viral antigen spread in the central nervous system.

Targeted recombination was carried out to select mouse hepatitis viruses (MHVs) in a defined genetic background, containing an MHV-JHM spike gene encoding either three heptad repeat 1 (HR1) substitutions (Q1067H, Q1094H, and L1114R) or L1114R alone. The recombinant virus, which expresses spike with the three substitutions, was nonfusogenic at neutral pH. Its replication was significantly inhibited by lysosomotropic agents, and it was highly neuroattenuated in vivo.