The Zika virus has probably existed for millennia, passing among animals in African forests with little fanfare. The first known diagnoses in humans occurred about 60 years ago, in Nigeria, but scientists think the pathogen has been infecting us for a couple of centuries or so. That nobody took note of Zika until relatively recently isn’t that surprising: The virus usually causes only a fever and a headache.
But as often happens with mutation-prone viruses, something has changed. Zika is currently making headlines as it jet-sets across the tropics, possibly causing birth defects in babies born to infected women. So what makes a virus that’s been hanging out in the background for thousands of years suddenly go on a pernicious tear through 20 countries? It’s Shannon Bennett’s job to find out.
Bennett is a microbiologist at the California Academy of Sciences who jokingly refers to her job as “CSI: Virus.” Viruses can rapidly evolve, jumping to new species and causing new symptoms, and Bennett and her team look for clues in the environment that might explain why viruses go, well, viral. Her hope is to catch the next pathogen before it becomes a global issue, so public health officials can be better prepared. The task isn’t easy.
To catch a virus, you’ve got to think like a virus. By doing so, Bennett hopes to see what circumstances keep the pathogens at bay, innocently flitting around the microorganism background, and what primes them for an outbreak. A good place to start this search is the favorite host of many a microbe: the mosquito. In 2008, Bennett and her team collected mosquitos in six habitat types in Thailand, ranging from cities to highly biodiverse forests.
The team had a hunch that more biodiverse ecosystems might create a kind of buffer zone between certain pathogens and humans. In a happy forest, for example, lots of different types of mosquito species fly around biting many different animals, and there are numerous microorganisms, including viruses, coursing through the blood of all these creatures. Maybe the pathogens exist there in quiet competition—until the ecological balance is thrown askew by, say, humans clearing said forest. Bennett thinks ecosystem changes might sometimes line up with the kind of mutation that helps the virus reproduce more quickly, creating the perfect storm for a pandemic.
In its research, Bennett’s team learned that two invasive mosquito species do particularly well in urban environments: Aedes aegypti and Culex quinquefasciatus. These two human-loving, invasive mosquitos are notorious disease vectors—the first for yellow fever and the second for West Nile virus. The researchers found that as the habitats they examined became more urbanized, those invasive mosquito species seemed to thrive as they feasted on (and infected) humans. If you’re a pathogen, you want to ride successful skeeters all the way to the top. That’s what Zika has done with Aedes aegypti.
This mosquito, originally from Africa, thrives in tropical cities, like Recife, Brazil, and Port au Prince, Haiti, because it reproduces in clean standing water—which people without indoor plumbing tend to have around the house for bathing, cooking, and drinking. These insects can also raise a brood of youngsters in the tiniest slivers of water pooling in used tires, tarps above construction sites, or even bottle caps. Even though they are weak fliers, holing up near a human dwelling keeps their meals are at close proximity. In such urban settings, any virus the mosquitos might harbor would only have to move among two hosts: mosquitos and humans. And viruses are good at getting good at things fast.
A virus isn’t trying to kill its host. Its goal is to survive and spread. But Bennett wonders whether the kinds of mutations that boost a virus’s ability to successfully reproduce happen to come with more serious side effects for its hosts. West Nile virus has been infecting people in Southeast Asia since the 1950s, but it started causing severe encephalitis only when it landed on the U.S. East Coast in 1999, from where it spread to every state in the union by 2002. To understand how it had moved so swiftly, researchers sequenced the strain of West Nile traveling across the country via birds and mosquitos and found that it had evolved to move through the bodies of Culex pipiens and Culex tarsalis mosquitos two days faster than it does in Culex quinquefasciatus, its Southeast Asian vector. The increased reproduction capabilities meant it could get into the birds and humans the mosquitos bit more quickly, and spread much more rapidly. Whatever mutation sped up this transmission rate might have also contributed to the virus’s newfound ability to cause encephalitis. And that sort of one-two punch might be operating right now in Zika.
There are still so many unknowns in the world of viruses that you could liken Bennett’s job to chasing viral dark matter. Her pathogenic quarry can be in constant flux, taking seemingly random twists and turns, sometimes before she even knows it exists.
Originally posted 2016-02-25 15:15:15.