In today’s New York Times, Manny Fernandez and Donald McNeil report that West Nile virus is wreaking havoc in Dallas. This summer, 200 people have become ill in Dallas County, and 10 people have died so far. Those are worryingly high numbers in a single Texas county of 2.4 million people, and so Dallas has declared a state of emergency. The city is now swept up in a debate about the safety of widespread pesticide spraying to kill off mosquitoes, which carry the virus. Fernandez and McNeil quote public health experts who warn that it’s probably a harbinger of things to come throughout the country this year.
For many young people in the United States, West Nile virus has been a fact of life for as long as they can remember. But before 1999, there was no West Nile virus in this country. None. Its arrival and its spread are a sobering lesson in how quickly diseases can establish themselves.
To offer some background to today’s news, I am reprinting an essay from my 2011 book, A Planet of Viruses, about how West Nile came to America.
In the summer of 1999, Tracey McNamara got worried. McNamara was the chief pathologist at the Bronx Zoo. When an animal at the zoo died, it was her job to figure out what killed it. She began to see dead crows on the ground near the zoo, and she wondered if they were being killed by some new virus spreading through the city. If the crows were dying, the zoo’s animals might start to die too.
Over Labor Day weekend, her worst fears were realized: three flamingoes died suddenly. So did a pheasant, a bald eagle, and a cormorant. McNamara examined the dead birds and found they had all suffered bleeding in their brains. Their symptoms suggested that they had been killed by the same pathogen. But McNamara could not figure out what pathogen was responsible, so she sent tissue samples to government laboratories. The government scientists ran test after test for the various pathogens that might be responsible. For weeks, the tests kept coming up negative.
Meanwhile, doctors in Queens were seeing a worrying number of cases of encephalitis—an inflammation of the brain. The entire city of New York normally only sees nine cases a year, but in August 1999, doctors in Queens found eight cases in one weekend. As the summer waned, more cases came to light. Some patients suffered fevers so dire that they became paralyzed, and by September nine had died. Initial tests pointed to a viral disease called Saint Louis encephalitis, but later tests failed to match the results.
As doctors struggled to make sense of the human outbreak, McNamara was finally getting the answer to her own mystery. The National Veterinary Services Laboratory in Iowa managed to grow viruses from the bird tissue samples she had sent them from the zoo. They bore a resemblance to the Saint Louis encephalitis virus. McNamara wondered now if both humans and birds were succumbing to the same pathogen. She convinced the Centers for Disease Control and Prevention to analyze the genetic material in the viruses. On September 22, the CDC researchers were stunned to find that the birds were not killed by Saint Louis encephalitis. Instead, the culprit was a pathogen called West Nile virus, which infects birds as well as people in parts of Asia, Europe, and Africa. No one had imagined that the Bronx Zoo birds were dying of West Nile virus, because it had never been seen in a bird in the Western Hemisphere before.
Public health workers puzzling over the human cases of encephalitis decided it was time to broaden their search as well. Two teams—one at the CDC and another led by Ian Lipkin, who was then at the University of California, Irvine—isolated the genetic material from the human viruses. It was the same virus that was killing birds: West Nile. And once again, it took researchers by surprise. No human in North or South America had ever suffered from it before.
The United States is home to many viruses that make people sick. Some are old and some are new. When the first humans made their way into the Western Hemisphere some fifteen thousand years ago, they brought a number of viruses with them. Human papillomavirus, for example, retains traces of its ancient emigration. The strains of the virus found in Native Americans are more closely related to each other than they are to HPV strains in other parts of the world. Their closest relative outside of the New World are strains of HPV found in Asia, just as Native Americans are most closely related to Asians.
Columbus’s discovery of the New World triggered a second wave of new viruses. Europeans brought viruses causing diseases such as influenza and smallpox that wiped out most Native Americans. In later centuries, still more viruses arrived. HIV came to the United States in the 1970s, and at the end of the twentieth century, West Nile virus became one of America’s newest immigrants.
It had only been six decades since West Nile virus was discovered anywhere on the planet. In 1937, a woman in the West Nile district of Uganda came to a hospital with a mysterious fever, and her doctors isolated a new virus from her blood. Over the next few decades, scientists found the same virus in many patients in the Near East, Asia, and Australia. But they also discovered that West Nile virus did not depend on humans for its survival. Researchers detected the virus in many species in birds, where it could multiply to far higher numbers.
At first it was not clear how the virus could move from human to human, from bird to bird, or from bird to human. That mystery was solved when scientists found the virus in a very different kind of animal: mosquitoes. When a virus-bearing mosquito bites a bird, it sticks its syringe-like mouth into the animal’s skin. As the mosquito drinks, it squirts saliva into the wound. Along with the saliva comes the West Nile virus.
The virus first invades cells in the bird’s skin, including immune system cells that are supposed to defend animals from diseases. Virus-laden immune cells crawl into the lymph nodes, where they release their passengers, leading to the infection of more immune cells. From the lymph nodes, infected immune cells spread into the bloodstream and organs such as the spleen and kidneys. It takes just a few days for the viruses in a mosquito bite to multiply into billions inside a bird. Despite their huge numbers, West Nile viruses cannot escape a bird on their own. They need a vector. An mosquito must bite the infected bird, drawing up some of its virus-laden blood. Once in the mosquito, the viruses invade the cells of its midgut. From there they can be carried to the insect’s salivary glands, where the viruses are ready to be injected into a new bird.
Vector-borne viruses like West Nile virus require a special versatility to complete their life cycle. Mosquitoes and birds are profoundly different kinds of hosts, with different body temperatures, different immune systems, and different anatomies. West Nile virus has to be able to thrive in both environments to complete its life cycle. Thanks to their versatility, vector-borne viruses also pose special challenges to doctors and public health workers who want to stop their spread. They don’t require people to be in close contact to spread from host to host. Mosquitoes, in effect, give the viruses wings.
Studies on the genes of West Nile virus suggest that it first evolved in Africa. As birds migrated from Africa to other continents in the Old World, they spread the virus to new bird species. Along the way, West Nile virus infected humans. In Eastern Europe, epidemics broke out, producing some cases of encephalitis. In a 1996 epidemic in Romania, ninety thousand people came down with West Nile, leading to seventeen deaths. These new epidemics, first in Europe and later in the West, may have been the result of the virus infecting people who populations had not experienced it before. In Africa, by contrast, people may be immunized against West Nile virus after being infected while they’re young.
It is striking that the New World has been spared West Nile virus for so long. The flow of people across the Atlantic and Pacific was not enough to carry the virus to the Americas. Scientists cannot say exactly how West Nile virus finally landed in New York in 1999, but they have a few clues. The New World strain of West Nile virus is most closely related to viruses that caused an outbreak in birds in Israel in 1998. It’s possible that pet smugglers brought infected birds from the Near East to New York.
On its own, a single infected bird could not have triggered a nationwide epidemic. The viruses needed a new vector to spread. It just so happens that West Nile viruses can survive inside 62 species of mosquitoes that live in the United States. The birds of America turned out to be good hosts as well. All told, 150 American bird species have been found to carry West Nile virus. A few species, such as robins, blue jays, and house finches, turned out to be particularly good incubators.
Moving from bird to mosquito to bird, West Nile virus spread across the entire United States in just 4 years. And along the way, people became ill with West Nile virus too. About 85 percent of infections in the United States cause no symptoms. The other 15 percent of infected people develop fevers, rashes, and headaches, and 38 percent of them have to go to a hospital, where they stay for about 5 days on average. About 1 in 150 infected people end up developing encephalitis. Between 1999 and 2008, U.S. doctors recorded 28,961 cases of West Nile virus. Of those victims, 1,131 died.
Once West Nile virus arrived in the United States, it settled into a regular cycle, a cycle set by the natural history of birds and mosquitoes. In the spring, robins and other birds produce new generations of chicks that are helpless targets for virus-carrying mosquitoes. By the summer, many birds are positively brimming with West Nile virus, raising the fraction of mosquitoes that carry it. It’s at that time of year that most human cases of West Nile virus emerge. When the temperature falls, mosquitoes die, and the viruses can no longer spread. It’s not clear how the virus survives North American winters. It’s possible that they survive in low levels among mosquitoes in the south, where the winters aren’t so harsh. It’s also possible that mosquitoes infect own their eggs with West Nile virus. When infected eggs hatch the next spring, the new generation is ready to start infecting birds all over again.
West Nile virus has fit so successfully into the ecology of the United States that it’s probably going to be impossible to eradicate. Unfortunately, doctors have no vaccine to prevent West Nile virus and no drugs to treat an infection. If you get sick, you can only hope that you are among the majority who suffer a fever and then recover. And in the future, West Nile virus may become even more entrenched in its new home.
Jonathan Soverow of Beth Israel Deaconess Medical Center and his colleagues examined sixteen thousand cases of West Nile virus that occurred between 2001 and 2005, noting the weather at the time of each outbreak. They found that epidemics tended to occur when there was heavy rainfall, high humidity, and warm temperatures. Warm, rainy, muggy weather makes mosquitoes reproduce faster and makes their breeding season longer. It also speeds up the growth of the viruses inside the mosquitoes.
Unfortunately, we can expect more of that sort of weather in the future. Carbon dioxide and other heat-trapping gases are raising the average temperature in the United States, and climate scientists project that the temperature will continue to rise much higher in decades to come. Now that West Nile virus has made a new home here, we’re making that home more comfortable.
[Originally published in A Planet of Viruses. Copyright 2011 Carl Zimmer]
[Photo by eyeweed via Creative Commons]