A novel mathematical modeling framework for antibiotic-resistant bacteria combining within-host microbiome-pathogen interactions with population-level pathogen epidemiology, demonstrating how antibiotic consumption and ecological competition come together to drive the spread of resistance.

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

With a data-driven mathematical modelling approach, within-host ecological information alone can provide clues on the mechanistic basis of diverse malaria infection outcomes.

An individual-based model estimates exogenous boosting of immunity following re-exposure to chickenpox is limited to 2 years after re-exposure, but an increase in herpes zoster incidence is still expected to occur following universal varicella vaccination.

Despite the virus' error prone polymerase, influenza virus antigenic evolution is rare, even in previously immune hosts, virus replication occurs before producing new antibodies.

The mathematical modeling approach disentangles the impacts of the COVID-19 pandemic on antibiotic resistance in Streptococcus pneumoniae in the community setting and identifies the three most plausible driving mechanisms responsible for the observed trends in invasive isolates and pneumococcal carriage.

A new mathematical method has been developed, implemented and validated for the analysis of time-lapse confocal laser scanning microscopy images to characterize the swimming behavior of bacterial swimmers moving in the exogenous matrix of pathogenic biofilms.

Both within and between hosts, the key factor guiding whether increasing treatment strength will increase or decrease antibiotic resistance is whether inter-strain competition is effective, not whether it is present.

Bats' uniquely robust innate antiviral immune defenses select for faster transmitting viruses likely to generate extreme virulence upon spillover to secondary hosts with immune systems divergent from those of bat.

In baboon gut microbiota, most pairwise correlations in bacterial abundances are weak and negative, and bacterial correlation patterns are largely shared across hosts, rather than personalized to each hosts.