Full-depth Coadds of the WISE and First-year NEOWISE-Reactivation Images

The Near Earth Object Wide-field Infrared Survey Explorer (NEOWISE) Reactivation mission released data from its first full year of observations in 2015. This data set includes ~2.5 million exposures in each of W1 and W2, effectively doubling the amount of WISE imaging available at 3.4 and 4.6 microns relative to the AllWISE release. We have created the first ever full-sky set of coadds combining all publicly available W1 and W2 exposures from both the AllWISE and NEOWISE-Reactivation (NEOWISER) mission phases. We employ an adaptation of the unWISE image coaddition framework (Lang 2014), which preserves the native WISE angular resolution and is optimized for forced photometry. By incorporating two additional scans of the entire sky, we not only improve the W1/W2 depths, but also largely eliminate time-dependent artifacts such as off-axis scattered moonlight. We anticipate that our new coadds will have a broad range of applications, including target selection for upcoming spectroscopic cosmology surveys, identification of distant/massive galaxy clusters, and discovery of high-redshift quasars. In particular, our full-depth AllWISE+NEOWISER coadds will be an important input for the Dark Energy Spectroscopic Instrument (DESI) selection of luminous red galaxy and quasar targets. Our full-depth W1/W2 coadds are already in use within the DECam Legacy Survey (DECaLS) and Mayall z-band Legacy Survey (MzLS) reduction pipelines. Much more work still remains in order to fully leverage NEOWISER imaging for astrophysical applications beyond the solar system.Comment: coadds available at http://unwise.me, zoomable full-sky rendering at http://legacysurvey.org/viewe

Differential regulation of innate and adaptive immune responses in viral encephalitis.

Viral encephalitis is a global health concern. The ability of a virus to modulate the immune response can have a pivotal effect on the course of disease and the fate of the infected host. In this study, we sought to understand the immunological basis for the fatal encephalitis following infection with the murine coronavirus, mouse hepatitis virus (MHV)-JHM, in contrast with the more attenuated MHV-A59. Distinct glial cell cytokine and chemokine response patterns were observed within 3 days after infection, became progressively more polarized during the course of infection and with the infiltration of leukocytes. In the brain, MHV-JHM infection induced strong accumulation of IFNbeta mRNA relative to IFNgamma mRNA. This trend was reversed in MHV-A59 infection and was accompanied by increased CD8 T cell infiltration into brain compared to MHV-JHM infection. Increased apoptosis appeared to contribute to the diminished presence of CD8 T cells in MHV-JHM-infected brain with the consequence of a lower potential for IFNgamma production and antiviral activity. MHV-JHM infection also induced sustained mRNA accumulation of the innate immune response products interleukin (IL)-6 and IL-1. Furthermore, high levels of macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta, and MIP-2 mRNA were observed at the onset of MHV-JHM infection and correlated with a marked elevation in the number of macrophages in the brain on day 7 compared to MHV-A59 infection. These observations indicate that differences in the severity of viral encephalitis may reflect the differential ability of viruses to stimulate innate immune responses within the CNS and subsequently the character of infiltrating leukocyte populations