In the wake of my story in the Times on zombies and today in Slate on our inner viruses, I figured I had stirred up enough questions to try out Reddit’s feature, Ask Me (Almost) Anything. So I’ll be there
tomorrow Monday 12/10 at 3 pm ET. See you then!
I was recently interviewed by a BBC reporter about viruses and their potential to devastate or help us in years to come. The video is now posted, and you can watch it here.
Slate is running a “pandemics” series, and I’m offering up the view from deep time. Koalas are getting hammered by a viral epidemic right now, and we’d do well to understand their woes. Because over the past 60 million years, we’ve experienced much the same thing, and it’s helped make us who we are today. Check it out.
I recently gave a talk in San Francisco about the future of viruses, based in part on my book, A Planet of Viruses. I talk about how deadly new outbreaks may emerge, how we may harness viruses for technology and medicine, and just how many viruses there are out there (hint: 10000000000000000000000000000000).
On Tuesday I’ll be in Hartford to participate in the Science on Screen series. It started in Boston last year, and now it’s spreading across the country. Each evening consists of a science-themed movie paired with a talk about some of the science involved. On Tuesday, Real Artways in Hartford will be screening the virus-zombie movie, 28 Days Later. And I’ll talk about what real viruses can do to their hosts. Details here.
As I was putting together a talk today about our microbial world, I just came across this interesting paper in the August issue of The Journal of Virology.
A team of Korean scientists set up some traps to catch viruses and bacteria floating in the air. They set up their traps in Seoul, in an industrial complex in western Korea, and in a forest. Based on their collection, they came up with the following estimates…
**In each cubic meter of air, there are between 1.6 million and 40 million viruses.
**In each cubic meter of air, there are between 860,000 and 11 million bacteria.
Given that we breathe roughly .01 cubic meters of air each minute, a simple calculation based on these results suggests we breathe in a few hundred thousand viruses every minute.
Half of the viruses the scientists trapped didn’t match any known virus species. But most belong to groups that infect plants or mammals.
A note to hypochondriacs: holding your breath may keep viruses from coming into your body, but as a lifestyle choice, it has some drawbacks.
The virus known as XMRV does not cause chronic fatigue syndrome.
Achieving this particular bit of knowledge has taken a pretty spectacular couple of years.
In October 2009, Judy Mikovits, a scientist then at the Whittemore Peterson Institute in Reno, Nevada, and her colleagues published a startling paper. They found that 68 out of 101 people suffering from chronic fatigue syndrome (also known as myalgic encephalomyelitis) carried a virus called XMRV. Only 8 out of 218 healthy people had it. That’s 67% versus 3.7%. Mikovits and her colleagues raised the possibility that the virus played a part in the disorder, which affects an estimated 60 million people. If that were true, then there might be a straightforward way to treat people: wipe out the offending virus.
Very quickly, a number of other scientists replicated the experiment. One team found evdience of a different virus in some of their subjects–not XMRV. The other scientists couldn’t find any virus at all that was present in any significant number of people with chronic fatigue and not in people without it.
With remarkable speed, the study and the follow-up research gave rise to a fierce controversy. Critics dismissed Mikovits’s work as nothing more than contamination (the virus is common in mice). Mikovits dismissed her critics becasue they hadn’t replicated her experiment closely enough to really test it. Many people with chronic fatigue syndrome, embittered by years of suffering (and suggestions that it was all in their head) rallied around Mikovits. (To get a sense of the back story, see the comments many people left on a blog post I wrote about this controversy last year.)
A few months into the controversy, I was at Columbia University to interview a scientist named Ian Lipkin for a profile for the New York Times. I focused mainly on his research linking viruses to new diseases. But Lipkin also does the reverse–what he likes to call “de-discovery.” When someone makes a controversial claim that virus X causes condition Y, Lipkin sometimes puts the claim to the test. Lipkin explained to me how it’s important to get everyone on board with such a replication study–both the original scientists and their critics. And he told me that he had launched a big study on XMRV, in collaboration with a team of scientists that included Mikovits, scientists who failed to find a link, and others. (I wrote more generally about de-discovery last year in the Times.)
The study would take a lot of time. The scientists and doctors would examine 147 people with chronic fatigue and 146 normal people, giving them thorough medical exams and a close inspection of their blood. Several labs would use identical methods to search for XMRV. And in that time a lot happened.
More scientists investigated XMRV on their own and found still more evidence that the viruses had likely contaminated Mikovits’s cell cultures. Mikovits wouldn’t budge, even as Science retracted the paper in December 2011. Meanwhile, Mikovits got into a battle royale with her institute, getting locked out of her office, sneaking in a grad student in to get her notebooks (possibly to work on Lipkin’s study), and spending five days in jail.
Today, nearly three years after the start of the XMRV affair, the big study came out in the journal mBio. The scientists found no evidence of XMRV in people with chronic fatigue. Mikovits fully endorsed the conclusion.
I am curious how people with this condition view this finding. I find it pretty depressing. It’s taken up plenty of money along with the valuable time of lots of talented researchers. It’s raised and then dashed hopes. And all we have to show for it is the lack of a link. What causes chronic fatigue syndrome? Your guess is as good as mine.
It would be nice if there was a simple set of instructions for finding the cause, but that’s probably just a fantasy. Perhaps the best we can hope for is to avoid these expensive, time-consuming wrestling matches in the first place. That’s why I find projects like the Reproducibility Intiative so interesting. When scientists make mistakes, let’s find out as fast as possible.
Here’s some more information on the saga:
[Apologies for a few typos, now fixed–I hit “publish” instead of “save draft”!]
Next Friday (August 31) I have the honor of taking part in the Kristine Bonnevie Lecture, an annual lecture held at the University of Oslo to honor the first female professor in Norway. I’ll be speaking along with Cori Bargmann of Rockefeller University, who has done hugely important research on the links between the anatomy of the brain and how animals behave. Details are here.
If there are any Loom-readers in Norway (perhaps a few?), I hope to see you in Oslo.
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]
Last September, harbor seal pups in Massachusetts and New Hampshire started to die in droves. In today’s New York Times, I write about what killed them: a new influenza strain that evolved from shorebirds to seals, possibly as recently as last summer. While controversy swirls around scientists experimentally nudging flu viruses across the evolutionary between birds and mammals, Nature has been doing some experiments of its own. Check it out.