When people think about infectious diseases — as many have, these last three years — they think mainly about the immune system. The severity of an individual’s illness, it’s assumed, is down to how well the immune system detects, attacks and eliminates the pathogenic invader.
The immune system is said to resist disease. Resistance reduces the amount of pathogen residing inside a host, thereby curtailing disease progression, driving recovery or preventing infections altogether. People who are immunocompromised fear infections because they cannot effectively resist pathogens.
And vaccines work because they teach immune systems to recognize — and so more effectively resist — pathogens before the actual bug is encountered.
But there have always been nagging issues with so straightforwardly relating illness to the abundance of pathogen in a host. And when Janelle Ayres, a physiologist now working at the Salk Institute in San Diego, entered grad school 20 years ago, these anomalies bothered her. “I was very interested in the conventional thought or assumption that all that’s necessary to survive an infection is that you have to kill the pathogen,” she says. “I was interested in this because there are clearly examples in humans and animal models where this is just too simplistic.”
Most obviously, there are asymptomatic infections. Long before we knew that certain individuals infected with SARS-CoV-2 develop no symptoms, there was the famous case of New York cook Mary Mallon. Christened “Typhoid Mary,” Mallon unknowingly lived with a Salmonella Typhi infection in the early 1900s and, in good health, transmitted the bacteria to dozens of people, some of whom died.
