Turning foe friendly: Domestication of infectious disease

infectious diseases

Disease is the byproduct of an inefficient pathogen, according to a prominent theory of the evolutionary biology of infectious disease widely held for the last 100 years.

The ideal pathogen would avoid making hosts sick so they could propagate themselves into as many other organisms as possible. Being sick and isolated in bed is not a good way to pass on a viral or bacterial infection to more humans .

But that theory left out a major factor: Pathogens must compete among themselves:

“There is a competition among strains to exploit their own host,” says Giulio De Leo, a researcher in ecological theory at Stanford. The latest research suggests that many pathogens do not necessarily evolve towards harmonious relationships, but instead, take a more selfish approach. If a pathogen can gain an advantage by usurping more resources, replicating more voraciously, or destroying more host cells, it will evolve toward virulence, even at the cost of destroying the host. Pathogens aren’t altruistic; each strain is searching for a fine balance point, which maximizes how aggressively it can reproduce while still maintaining maximum transmission. “There’s a tradeoff,” says De Leo.

Changing the competitive environment can alter which strains of a disease are favored. David Shultz describes the example of cholera in Peru during the 1990s. A severe outbreak of the disease was caused by fecal contamination in a dirty water supply. Cholera bacteria produces a toxin that causes extreme diarrhea that is often fatal.

But after public infrastructure improvements eliminated contaminated water as a transmission possibility, strains that caused particularly violent diarrhea offered no benefit. Instead, strains that produced less toxin and caused less diarrhea began to take over the cholera population because those milder strains could be transmitted through person to person contact and spread on contaminated surfaces. In fact, bacteria that produced lots of toxin reduced its transmission ability because its victims were bed bound, not out and about exchanging germs with other people:

By cleaning up the water supply, humans influence the evolution of a bacterium toward lower virulence. They made cholera behave more like the common cold. “The history of public health interventions is replete with successes and failures,” says evolutionary biologist Paul Ewald who observed the outbreak. “The concept of pathogen domestication helps us understand why some of the most dramatic successes were so successful.”

Ewald and his colleagues have wondered about using a similar approach in fighting malaria, which is unique in its ability to resist vaccines and treatments because it reproduces sexually and consequently shuffles genes back and forth rather than making identical copies of itself like a virus or bacteria, Shultz writes:

The same evolutionary flexibility afforded by sexual reproduction should also make it possible to domesticate Plasmodium. Mosquito-proof housing would cut off the mosquito’s access to anybody infected with a strain of the disease virulent enough to confine its host to bed. If the mosquito’s food sources are restricted to people healthy enough to be outside, walking around, then the only relatively non-virulent strains of Plasmodium can circulate. The idea is to make virulence produce dead-end hosts.

In a world where antibiotic resistance is fast becoming a terrifying global problem and infections that sicken millions of people each year are spreading in growing habitats, perhaps its time to start thinking of other ways of controlling disease besides relying on a slowed drug development system.

We know, as in the case of the cholera example, that these effects are already happening in nature. There seems to be no harm in fostering a similar situation in the laboratory to see what benefit an evolutionary biologist’s approach to infectious disease might have on global public health.

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