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Weaver wages war on microscopic enemy
By Marty Schladen
The Daily News
Published March 17, 2008
Most children don’t grow up dreaming of studying mosquitoes. Neither did Scott Weaver of the University of Texas Medical Branch.
But his work on the insects, the diseases they carry and the ecological systems in which they thrive promises to better the lives of millions. But that was never his primary goal, either.
“I think a lot of it’s chance,” Weaver, 50, said recently when asked how he happened onto his career.
After growing up in the Maryland suburbs of Washington, D.C., Weaver went off to college and majored in marine biology. But home for the summer his freshman year, he got a job with the Maryland Department of Agriculture helping with mosquito surveillance.
That sparked an interest in the blood-sucking insects. When Weaver returned to the College of William and Mary, it offered only one class in entomology, the study of insects. But a professor there took an interest and guided him toward graduate pursuit of his interests.
Killing Power
It wasn’t just an interest in mosquitoes themselves that compelled Weaver to study them. It was also that they’ve always been among the deadliest spreaders of disease.
This is because females suck the blood of other animals. They don’t need it to survive, but they need the protein and iron in blood to develop and lay their eggs.
When a female mosquito hops from host to host, she exposes each new animal to whatever virus or parasite might be left on her proboscis from the earlier animals she exploited.
That’s a very effective way to spread disease. Malaria, which kills somebody every 30 seconds, encephalitis, yellow fever, West Nile virus, Rift Valley fever and a host of other diseases are all communicated that way.
“I always thought it would be of medical relevance,” Weaver said of his work with mosquitoes.
Specifically, he works with mosquito-borne arboviruses. That’s a family of viruses that get passed around by arthropods, the group of animals that includes insects, crabs, spiders and a lot of other animals.
And Weaver doesn’t just study how the mosquitoes pass the viruses from one host to the next. He looks at how ecological systems get set up for mosquito-facilitated disease outbreaks.
Horse Disease
One disease he’s studied is Venezuelan equine encephalitis.
As the name implies, it infects horses, asses, zebras and other equines and it makes their brains swell. Infected equines can either die suddenly or they can suffer worse and worse disorders of the central nervous system.
The disease also afflicts humans.
In healthy adults, it produces fevers and headaches. But for the young, the sick and the old, VEE, as the scientists call it, can be much more severe, even deadly.
But outbreaks of the disease occur only occasionally. A 1969 outbreak began in Central America, then spread to Mexico and South Texas, killing an estimated 100,000 horses and sickening thousands of humans as it did, according to medical branch science writer Jim Kelly.
Another outbreak, in 1995, led to more than 14,000 suspected human infections, 1,200 hospitalizations and 26 deaths in Colombia alone, according to Pan American Health Organization.
A Breakthrough
Weaver has worked to piece together the circumstances needed for a VEE outbreak.
“I like to look at the big picture,” he said.
The virus usually exists in the forests of tropical America, with mosquitoes passing it between rodents. But, as environmentalists are keenly aware, ranchers have cut down great swaths of that forest in recent decades, bringing their livestock and horses close to the mosquitoes and rodents that carry the viruses.
When horses are infected with the VEE virus, they act as “amplifiers.” Virus reproduction grows rapidly in their large bodies, other mosquitoes swarm onto the infected animals, carry off the virus, land on healthy horses and start the process again.
It isn’t enough for horses to live close-in with forest critters to start an outbreak, however. Weaver said outbreaks start in the rainy season, when mosquito populations boom.
But VEE outbreaks don’t happen every time there’s a rainy season and horses are close to the animals that normally carry the virus.
A few years ago, Weaver led the team that found the final piece of the puzzle.
The virus must mutate to a form that easily infects horses. Weaver and his colleagues discovered that a single genetic mutation in the rapidly evolving organisms was all that was necessary.
That means that if you move horses into areas that naturally harbor VEE, a disease outbreak is bound to start sooner or later. And as more horses come into those areas, the chances of an outbreak increase.
“I think one could happen any year now,” Weaver said.
Governments in areas where outbreaks sometimes start could prevent them by vaccinating horses. But Weaver explained that it can be hard to get a cash-strapped government to put money into a problem that hasn’t reared its head recently.
Weaver said he understands the governments’ limitations, but “it’s still frustrating to know a lot of this could be prevented.”
Emerging Threat
You probably haven’t heard of chikungunya fever yet, but you might soon, Weaver says.
An alphavirus like the one that causes VEE, the chikungunya virus was isolated in Tanzania in 1953.
It is thought to have originated in Africa centuries ago, but the disease has been little noticed until recently. One reason is that doctors frequently confuse it with dengue or “breakbone” fever, another disease caused by a mosquito-borne virus.
Initial symptoms of chikungunya include fever, rashes and vomiting. But its worst symptom — and the one from which it gets its African name — is the incapacitating joint pain that it can cause. It can last for months.
The name is thought to be derived from a Makonde word that means “to dry up or become contorted,” according to the U.S. Centers for Disease Control.
Just as horses are amplifiers for VEE, humans are amplifiers for chikungunya. And humans are amplifying the virus right now in India.
By October 2006, more than 1 million cases had been reported in that country, according to the World Health Organization. By September 2007, it had spread to Italy, with 254 cases detected there, the health organization reported.
The virus is carried by a few species of mosquito, including aedes aegypti, which thrives in this region. Add to that the great frequency with which people travel between India, Africa, Italy and, say, Houston, and a local outbreak of chikungunya could occur.
“There are places where all the ingredients to set up the cycle exist,” Weaver said.
Possible Solution
The World Health Organization says a chikungunya vaccine doesn’t yet exist, but they’re working on one at the medical branch.
Weaver said he and a colleague, microbiologist Ilya Frolov, are developing an “attenuated” strain of chikungunya. That means they’ve weakened the virus’s ability to cause disease but maintained its ability to stimulate an immune response in humans. If you take it, you don’t get sick, but your body prepares itself to fight off the virus’s nasty relative.
If successful, the vaccine will do more than just keep people from getting sick.
In parts of world where plagues like chikungunya, VEE and malaria thrive, they keep countries from developing their economies, stabilizing and living in peace. Sick people can’t work and shaky governments are forced to expend their very limited resources in an often futile effort to fight diseases once they’ve already broken out.
The governments become increasingly unstable and wars often ensue.
Vaccines such as the one Weaver’s working on might offer a way out of that vicious cycle.
So is that what gets him out of bed in the morning? Not really, he says.
“It’s in the back of your mind,” he said. “But it’s really the scientific curiosity that motivates you. If you don’t have that, you can’t do this.”
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