Chemo-enzymatic synthesis of Lacto-N-biose I catalyzed by β-1,3-galactosidase from Bacillus circulans using 4,6-dimethoxy-1,3,5-triazin-2-yl β-galactopyranoside as a glycosyl donor.

Chemo-enzymatic synthesis of lacto-N-biose I (LNB) catalyzed by β-1,3-galactosidase from Bacillus circulans (BgaC) has been developed using 4,6-dimethoxy-1,3,5-triazin-2-yl β-galactopyranoside (DMT-β-Gal) and GlcNAc as the donor and acceptor substrates, respectively. BgaC transferred the Gal moiety to the acceptor, giving rise to LNB. The maximum yield of LNB was obtained at the acceptor : donor substrate ratio of 1:30.

Crystal structure and biochemical characterization of CJP38, a β-1,3-glucanase and allergen of Cryptomeria japonica pollen.

A 38 kDa β-1,3-glucanase allergen from Cryptomeria japonica pollen (CJP38) was recombinantly produced in E. coli and purified to homogeneity with the use of Ni-affinity resin. CJP38 hydrolyzed β-1,3-glucans such as CM-curdlan and laminarioligosaccharides in an endo-splitting manner.

Hepatitis C Continuum of Care in a Treatment Center in Sub-Saharan Africa.

Background: Hepatitis C virus (HCV) infection is a major public health challenge in Cameroon with over three million people infected. Government efforts to improve care and treatment are unsatisfactory and need to be assessed. We aimed at studying the several steps along the HCV continuum of care in one of two hepatitis treatment centers in Cameroon.

Inhibition of Influenza Virus Infection by Mycelia Extract Through Its Direct Action and Immunopotentiating Activity.

mycelia (LEM) solid culture extracts contain many bioactive compounds with diverse pharmacological activities such as antitumor, antiviral, and immunopotentiating effects. In this study, we examined the anti-influenza virus activity of LEM and . LEM directly inhibited influenza virus growth at early phases of infection, possibly at the entry process of viral particles to host cells.

RLR-mediated antiviral innate immunity requires oxidative phosphorylation activity.

Mitochondria act as a platform for antiviral innate immunity, and the immune system depends on activation of the retinoic acid-inducible gene I (RIG-I)-like receptors (RLR) signaling pathway via an adaptor molecule, mitochondrial antiviral signaling. We report that RLR-mediated antiviral innate immunity requires oxidative phosphorylation (OXPHOS) activity, a prominent physiologic function of mitochondria. Cells lacking mitochondrial DNA or mutant cells with respiratory defects exhibited severely impaired virus-induced induction of interferons and proinflammatory cytokines.