Surface composition and structure of Co\u3csub\u3e3\u3c/sub\u3eO\u3csub\u3e4\u3c/sub\u3e(110) and the effect of impurity segregation

The Co3O4 (110) single crystal surface has been characterized by low energy electron diffraction (LEED), Auger electron spectroscopy, and x-ray photoelectron spectroscopy (XPS). LEED analysis of the clean Co3O4 (110) spinel surface shows a well-ordered pattern with sharp diffraction features. The XPS spectra are consistent with stoichiometric Co3O4 as determined by the concentration ratio of oxygen to cobalt (CO /CCo) and spectral peak shape. In particular, the cobalt 2p XPS spectra are characteristic of the spinel structure with Co3+ occupying octahedral sites and Co2+ in tetrahedral sites within the lattice. During prolonged heating at 630 K, bulk impurities of K, Ca, Na, and Cu segregated to the surface. Sodium desorbed from the surface as NaOH at 825 K, potassium and calcium were only removed by sputtering since no desorption from the surface was detected for temperatures up to 1000 K. Copper also disappeared upon heating above 700 K, most likely by desorbing although the possibility of diffusion back into the bulk could not be eliminated. The appearance of copper impurities correlated with Co3O4 (110) surface reduction to CoO, and the surface could not be fully reoxidized even upon extended oxygen annealing as long as the copper impurity remained on the surface. Upon removal of the Cu from the near-surface region, the surface was easily reoxidized to Co3O4 by O2

TAM Receptors Are Not Required for Zika Virus Infection in Mice

Summary: Tyro3, Axl, and Mertk (TAM) receptors are candidate entry receptors for infection with the Zika virus (ZIKV), an emerging flavivirus of global public health concern. To investigate the requirement of TAM receptors for ZIKV infection, we used several routes of viral inoculation and compared viral replication in wild-type versus Axl−/−, Mertk−/−, Axl−/−Mertk−/−, and Axl−/−Tyro3−/− mice in various organs. Pregnant and non-pregnant mice treated with interferon-α-receptor (IFNAR)-blocking (MAR1-5A3) antibody and infected subcutaneously with ZIKV showed no reliance on TAMs for infection. In the absence of IFNAR-blocking antibody, adult female mice challenged intravaginally with ZIKV showed no difference in mucosal viral titers. Similarly, in young mice that were infected with ZIKV intracranially or intraperitoneally, ZIKV replication occurred in the absence of TAM receptors, and no differences in cell tropism were observed. These findings indicate that, in mice, TAM receptors are not required for ZIKV entry and infection. : TAM receptors have been implicated as entry receptors for the Zika virus. In this study, Hastings et al. used genetic knockout mouse models to demonstrate that they are not necessary for the infection of mice via multiple routes of viral challenge. These results suggest the existence of redundant entry receptors for ZIKV in mice. Keywords: viral entry, flavivirus, neurotropic virus, CNS, pregnancy, congenital infectio

Compromised SARS-CoV-2-specific placental antibody transfer

SARS-CoV-2 infection causes more severe disease in pregnant women compared to age-matched non-pregnant women. Whether maternal infection causes changes in the transfer of immunity to infants remains unclear. Maternal infections have previously been associated with compromised placental antibody transfer, but the mechanism underlying this compromised transfer is not established. Here, we used systems serology to characterize the Fc profile of influenza-, pertussis-, and SARS-CoV-2-specific antibodies transferred across the placenta. Influenza- and pertussis-specific antibodies were actively transferred. However, SARS-CoV-2-specific antibody transfer was significantly reduced compared to influenza- and pertussis-specific antibodies, and cord titers and functional activity were lower than in maternal plasma. This effect was only observed in third-trimester infection. SARS-CoV-2-specific transfer was linked to altered SARS-CoV-2-antibody glycosylation profiles and was partially rescued by infection-induced increases in IgG and increased FCGR3A placental expression. These results point to unexpected compensatory mechanisms to boost immunity in neonates, providing insights for maternal vaccine design.NIH (Grants 3R37AI080289-11S1, R01AI146785, U19AI42790-01, U19AI135995-02, U19AI42790-01, 1U01CA260476 – 01, CIVIC5N93019C00052)Bill and Melinda Gates Foundation (Awards OPP1146996 and INV- 001650