Browse our latest Microbiology and Infectious Disease articles

Intervention of CHI3L1 using anti-CHI3L1 monoclonal antibody or chitinase inhibitor kasugamycin blocks epithelial infection of various SARS-CoV2 variants, suggesting that CHI3L1 is a universal and effective therapeutic target of COVID-19 infection, including recent omicron variants.

A large-scale analysis of Staphylococcus aureus within-host evolution based on a comprehensive catalogue of bacterial genetic variation reveals an excess of genome degradation signatures in infecting strains and new genetic loci of clinically relevant adaptation.

Distinct surfaces of an interbacterial competition cell wall toxin mediate interactions with different cellular binding partners, resulting in an inherent evolutionary trade-off across the toxin superfamily.

Metabolic pathways found to date in giant virus raise the question if these viral enzymes provide some level of autonomy to viruses or if they are used to expand the host metabolism.

Models of malaria and treatment dynamics were combined with emulator-based global sensitivity analysis to elucidate the interplay between drug, biology, and epidemiological factors on the evolution of resistance to malaria treatments, including artemisinin.

In primary schools, where vaccination coverage can be low, a repetitive testing strategy reduces SARS-CoV-2 infections while keeping classes and schools open, as such limiting infection transmissions and absenteeism.

Glycans are remodeled by HIV and are determinants of CD4+ T cell susceptibility to HIV infection.

Labeling with ¹³C and ¹⁵N in the absence of metabolic engineering enabled the exploration of peptidoglycan metabolism at a very fine level of detail based on kinetic characterization of isotopologues predicted to occur according to known recycling and biosynthesis pathways.

A novel high-throughput method for Plasmodium falciparum genotyping will enable malaria control programs to make informed decisions about the best tool to use for the diagnosis of malaria.

SARS-CoV-2 host-shutoff inhibits innate NK surveillance by suppressing activating ligands, however ADCC provides a potent NK stimulus that is mediated by antibodies targeting Nucleocapsid, ORF3a, and Membrane, with those targeting Spike being significantly weaker.