virulence

Researchers use genetic clues to track the spread of antibiotic resistant bacteria from the environment to patients.

By combining experimental data with computer models, researchers were able to predict a pathogen’s evolution toward more virulence.

Meet some of the people featured in the October 2017 issue of The Scientist.

Tracking the myxoma virus in the wild rabbit populations of Australia has yielded insight into how pathogens and their hosts evolve.

Researchers characterize a protein that could be key to the virus’s virulence—and to developing a vaccine against the mosquito-borne disease.

In some pathogenic bacteria, certain antibiotic resistance–associated mutations may also confer an unexpected growth advantage.

The strain of Ebola that has circulated in West Africa for the last year takes longer to kill macaques than the virus that caused an outbreak in Central Africa in 1976.

A better knowledge of the pathogenesis of emerging zoonotic diseases is crucial if we want to prepare for “the next Ebola.”

A new technique could soon spur unprecedented insight into the role of bacterial epigenetics in the evolution of pathogen virulence.

Weakened viruses used in vaccines can swap genes and produce disease-causing strains.

Field studies reveal non-virulent bacteria take advantage of their virulent counterparts to get a free pass into their host.

To protect themselves during malaria infections, mice can kill their own healthy red blood cells, cutting off the parasite’s primary resource.

As much as rainforests or deep-sea vents, the human gut holds rich stores of microbial chemicals that should be mined for their pharmacological potential.

Microbes, both good and bad, can exert direct effects on host cells and vice versa.