RSV's unique ability to co-opt host cell mitochondria to facilitate viral infection reveals the RSV-mitochondrial interface as a viable target for therapeutic intervention.

HIV co-infection does not affect Mycobacterium tuberculosis mutation rates and does not drive the emergence of antimicrobial resistance within patients in the largest outbreak of multidrug-resistant tuberculosis in Latin America to date.

Helminth infected hosts are an important cause of variation in the level, frequency and duration of Bordetella bronchiseptica shedding and dynamics of infection.

The expression of DECTIN-2 family C-type lectin receptors on macrophages and monocytes is inhibited by the Th2 cytokine IL-4, which suggests a mechanism for inhibition of Th17 responses to MINCLE-dependent vaccination responses by underlying helminth infection.

Type-I interferon enriched microenvironment generated by Mycobacterium tuberculosis induces the Siglec-1 receptor expression in human macrophages, including on tunneling nanotubes, and contributes to the exacerbation of cell-to-cell transfer of HIV-1.

Neither the presence nor the intensity of Hematodinium sp. parasitisation drives co-infection occurrence, severity, or diversity in the ecologically ubiquitous shore crab, Carcinus maenas.

An experimental animal model provides further insights into the host and viral mechanisms underlying airborne transmission of SARS-CoV-2.

The co-stimulatory molecule CD28 is required after T cell priming for helper T cell polarization in response to an infection.

Redundancy in the costimulatory signals that drive CD8⁺ T cell expansion is dictated by pathogen-specific cues.

Updated estimates of the generation time of SARS-CoV-2 infections indicate that the generation time has become shorter.