The ASAS-SN bright supernova catalogue - III. 2016

This catalogue summarizes information for all supernovae discovered by the All-Sky Automated Survey for SuperNovae (ASAS-SN) and all other bright (mpeak ≤ 17), spectroscopically confirmed supernovae discovered in 2016. We then gather the near-infrared through ultraviolet magnitudes of all host galaxies and the offsets of the supernovae from the centres of their hosts from public data bases. We illustrate the results using a sample that now totals 668 supernovae discovered since 2014 May 1, including the supernovae from our previous catalogues, with type distributions closely matching those of the ideal magnitude limited sample from Li et al. This is the third of a series of yearly papers on bright supernovae and their hosts from the ASAS-SN team

The ASAS-SN Bright Supernova Catalog - II. 2015

This manuscript presents information for all supernovae discovered by the All-Sky Automated Survey for SuperNovae (ASAS-SN) during 2015, its second full year of operations. The same information is presented for bright ($m_V\leq17$), spectroscopically confirmed supernovae discovered by other sources in 2015. As with the first ASAS-SN bright supernova catalog, we also present redshifts and near-UV through IR magnitudes for all supernova host galaxies in both samples. Combined with our previous catalog, this work comprises a complete catalog of 455 supernovae from multiple professional and amateur sources, allowing for population studies that were previously impossible. This is the second of a series of yearly papers on bright supernovae and their hosts from the ASAS-SN team

The ASAS-SN bright supernova catalogue - III. 2016

This catalogue summarizes information for all supernovae discovered by the All-Sky Automated Survey for SuperNovae (ASAS-SN) and all other bright (mpeak ≤ 17), spectroscopically confirmed supernovae discovered in 2016. We then gather the near-infrared through ultraviolet magnitudes of all host galaxies and the offsets of the supernovae from the centres of their hosts from public data bases. We illustrate the results using a sample that now totals 668 supernovae discovered since 2014 May 1, including the supernovae from our previous catalogues, with type distributions closely matching those of the ideal magnitude limited sample from Li et al. This is the third of a series of yearly papers on bright supernovae and their hosts from the ASAS-SN team

Massive stars exploding in a He-rich circumstellar medium - VII. The metamorphosis of ASASSN-15ed from a narrow line Type Ibn to a normal Type Ib Supernova

We present the results of the spectroscopic and photometric monitoring campaign of ASASSN-15ed. The transient was discovered quite young by the All Sky Automated Survey for SuperNovae (ASAS-SN) survey. Amateur astronomers allowed us to sample the photometric SN evolution around maximum light, which we estimate to have occurred on JD = 2457087.4 ± 0.6 in the r band. Its apparent r-band magnitude at maximum was r = 16.91 ± 0.10, providing an absolute magnitude Mr ≈ −20.04 ± 0.20, which is slightly more luminous than the typical magnitudes estimated for Type Ibn SNe. The post-peak evolution was well monitored, and the decline rate (being in most bands around 0.1 mag d−1 during the first 25 d after maximum) is marginally slower than the average decline rates of SNe Ibn during the same time interval. The object was initially classified as a Type Ibn SN because early-time spectra were characterized by a blue continuum with superimposed narrow P-Cygni lines of He I, suggesting the presence of a slowly moving (1200–1500 km s−1), He-rich circumstellar medium. Later on, broad P-Cygni He I lines became prominent. The inferred velocities, as measured from the minimum of the broad absorption components, were between 6000 and 7000 km s−1. As we attribute these broad features to the SN ejecta, this is the first time we have observed the transition of a Type Ibn SN to a Type Ib SN

Lung macrophage scavenger receptor SR-A6 (MARCO) is an adenovirus type-specific virus entry receptor

<div><p>Macrophages are a diverse group of phagocytic cells acting in host protection against stress, injury, and pathogens. Here, we show that the scavenger receptor SR-A6 is an entry receptor for human adenoviruses in murine alveolar macrophage-like MPI cells, and important for production of type I interferon. Scavenger receptors contribute to the clearance of endogenous proteins, lipoproteins and pathogens. Knockout of SR-A6 in MPI cells, anti-SR-A6 antibody or the soluble extracellular SR-A6 domain reduced adenovirus type-C5 (HAdV-C5) binding and transduction. Expression of murine SR-A6, and to a lower extent human SR-A6 boosted virion binding to human cells and transduction. Virion clustering by soluble SR-A6 and proximity localization with SR-A6 on MPI cells suggested direct adenovirus interaction with SR-A6. Deletion of the negatively charged hypervariable region 1 (HVR1) of hexon reduced HAdV-C5 binding and transduction, implying that the viral ligand for SR-A6 is hexon. SR-A6 facilitated macrophage entry of HAdV-B35 and HAdV-D26, two important vectors for transduction of hematopoietic cells and human vaccination. The study highlights the importance of scavenger receptors in innate immunity against human viruses.</p></div

Insight into the Mechanisms of Adenovirus Capsid Disassembly from Studies of Defensin Neutralization

Defensins are effectors of the innate immune response with potent antibacterial activity. Their role in antiviral immunity, particularly for non-enveloped viruses, is poorly understood. We recently found that human alpha-defensins inhibit human adenovirus (HAdV) by preventing virus uncoating and release of the endosomalytic protein VI during cell entry. Consequently, AdV remains trapped in the endosomal/lysosomal pathway rather than trafficking to the nucleus. To gain insight into the mechanism of defensin-mediated neutralization, we analyzed the specificity of the AdV-defensin interaction. Sensitivity to alpha-defensin neutralization is a common feature of HAdV species A, B1, B2, C, and E, whereas species D and F are resistant. Thousands of defensin molecules bind with low micromolar affinity to a sensitive serotype, but only a low level of binding is observed to resistant serotypes. Neutralization is dependent upon a correctly folded defensin molecule, suggesting that specific molecular interactions occur with the virion. CryoEM structural studies and protein sequence analysis led to a hypothesis that neutralization determinants are located in a region spanning the fiber and penton base proteins. This model was supported by infectivity studies using virus chimeras comprised of capsid proteins from sensitive and resistant serotypes. These findings suggest a mechanism in which defensin binding to critical sites on the AdV capsid prevents vertex removal and thereby blocks subsequent steps in uncoating that are required for release of protein VI and endosomalysis during infection. In addition to informing the mechanism of defensin-mediated neutralization of a non-enveloped virus, these studies provide insight into the mechanism of AdV uncoating and suggest new strategies to disrupt this process and inhibit infection