Anti-bacterial glycosyl triazoles - Identification of an N-acetylglucosamine derivative with bacteriostatic activity against Bacillus.

N-acetylglucosaminidases (GlcNAcases) play an important role in the remodeling and recycling of bacterial peptidoglycan. Inhibitors of bacterial GlcNAcases can serve as antibacterial agents and provide an opportunity for the development of new antibiotics. We report the synthesis of triazole derivatives of -acetylglucosamine using a copper promoted azide-alkyne coupling reaction between 1-azido--acetylglucosamine and a small library of terminal alkynes prepared via the Ugi reaction.

Functional analysis of SleC from Clostridium difficile: an essential lytic transglycosylase involved in spore germination.

Clostridium difficile is the most common cause of enteric disease and presents a major burden on healthcare systems globally due in part to the observed rapid rise in antibiotic resistance. The ability of C. difficile to form endospores is a key feature in the organism's pathogenesis and transmission, and contributes greatly to its resilient nature.

Characterization of the pleiotropic effects of the genotype G-specific 36-nucleotide insertion in the context of other hepatitis B virus genotypes.

The pregenomic RNA (pgRNA) of hepatitis B virus (HBV) serves as the messenger for both core and P proteins, with the downstream P gene translated by ribosomal leaky scanning. HBV replication begins with packaging of the pgRNA and P protein into core protein particles, followed by conversion of RNA into DNA. Genotype G has a low replication capacity due to a low pgRNA level.

Improved method for rapid and efficient determination of genome replication and protein expression of clinical hepatitis B virus isolates.

Different hepatitis B virus (HBV) genotypes and variants are associated with different clinical outcomes and/or response to antiviral therapy, yet the comparison of the in vitro replication capacity of a large number of clinical isolates remains technically challenging and time-consuming. Although the full-length HBV genome can be amplified from high-titer blood samples by PCR using High Fidelity(plus) DNA polymerase and primers targeting the conserved precore region, the HBV clones thus generated are replication deficient due to the inability to generate the terminally redundant pregenomic RNA essential for genome replication. The transfection experiment is further complicated by PCR errors and the presence of viral quasispecies.