The Hα Luminosity Function of Galaxies at z ∼ 4.5

We present the Hα luminosity function (LF) derived from a large sample of Lyman break galaxies at z ∼ 4.5 over the GOODS-South and North fields. This study makes use of the new, full-depth Spitzer/IRAC [3.6] and [4.5] imaging from the GOODS Re-ionization Era wide-Area Treasury from the Spitzer program. The Hα flux is derived from the offset between the continuum flux estimated from the best-fit spectral energy distribution, and the observed photometry in IRAC [3.6]. From these measurements, we build the Hα LF and study its evolution providing the best constraints of this property at high redshift, where spectroscopy of Hα is not yet available. Schechter parameterizations of the Hα LF show a decreasing evolution of Φ∗ with redshift, increasing evolution in L ∗, and no significant evolution in the faint-end slope at high z. We find that star formation rates (SFRs) derived from Hα are higher than those derived from the rest-frame UV for low SFR galaxies but the opposite happens for the highest SFRs. This can be explained by lower mass galaxies (also lower SFR) having, on average, rising star formation histories (SFHs), while at the highest masses the SFHs may be declining. The SFR function is steeper, and because of the excess SFR(Hα) compared to SFR(UV) at low SFRs, the SFR density estimated from Hα is higher than the previous estimates based on UV luminosities

Canine distemper virus persistence in demyelinating encephalitis by swift intracellular cell-to-cell spread in astrocytes is controlled by the viral attachment protein

The mechanism of viral persistence, the driving force behind the chronic progression of inflammatory demyelination in canine distemper virus (CDV) infection, is associated with non-cytolytic viral cell-to-cell spread. Here, we studied the molecular mechanisms of viral spread of a recombinant fluorescent protein-expressing virulent CDV in primary canine astrocyte cultures. Time-lapse video microscopy documented that CDV spread was very efficient using cell processes contacting remote target cells. Strikingly, CDV transmission to remote cells could occur in less than 6 h, suggesting that a complete viral cycle with production of extracellular free particles was not essential in enabling CDV to spread in glial cells. Titration experiments and electron microscopy confirmed a very low CDV particle production despite higher titers of membrane-associated viruses. Interestingly, confocal laser microscopy and lentivirus transduction indicated expression and functionality of the viral fusion machinery, consisting of the viral fusion (F) and attachment (H) glycoproteins, at the cell surface. Importantly, using a single-cycle infectious recombinant H-knockout, H-complemented virus, we demonstrated that H, and thus potentially the viral fusion complex, was necessary to enable CDV spread. Furthermore, since we could not detect CD150/SLAM expression in brain cells, the presence of a yet non-identified glial receptor for CDV was suggested. Altogether, our findings indicate that persistence in CDV infection results from intracellular cell-to-cell transmission requiring the CDV-H protein. Viral transfer, happening selectively at the tip of astrocytic processes, may help the virus to cover long distances in the astroglial network, “outrunning” the host’s immune response in demyelinating plaques, thus continuously eliciting new lesions