Temperature and ionic conditions control the mechanical properties of virally encapsidated DNA and act as a switch between synchronized and desynchronized genome ejection dynamics in a phage population.
The rapid killing of macrophages by Mycobacterium tuberculosis aggregates, and the subsequent proliferation of the bacteria inside the dead cell, leads to a cell death cascade and explains the coupling of necrosis and pathogen growth observed in active disease.
The helical rod structure and dynamic spring-like properties of the type 1 pilus are evolutionarily fine-tuned for functioning in host-pathogen interactions during urinary tract infection and gut colonization.
A mathematical model that combines stochasticity and spatial structure describes the dynamics of the viral population during an infection cycle, and fitting the model to RNA and virus abundances over time shows that poliovirus follows a geometric replication mode.
Macrophage dynamics are fundamentally different between two commonly used inbred mouse strains and differences in local resident cell expansion versus monocyte recruitment determine the outcome of tissue nematode infection.
Publication bias, in which positive results are preferentially reported by authors and published by journals, can restrict the visibility of evidence against false claims and allow such claims to be canonized inappropriately as facts.