The Autoimmune Epidemic: Bodies Gone Haywire in a World Out of Balance--and the Cutting-Edge Science that Promises Hope (No Series) (20 page)

In a sense, then, today’s emerging relationship between common viruses and autoimmune disease merely mirrors what is coming to be better understood in all areas of health research: infectious pathogens play a far greater role than scientists once surmised in the onset of diseases, including cancer, heart disease, psychiatric illness, and autoimmune diseases, from Guillain-Barré syndrome to type 1 diabetes to lupus.

A WALK ON THE WILD SIDE: CHANGING VIRUSES AND GLOBAL WARMING

One can hardly talk about viruses in the twenty-first century without grappling with the emergence of a number of virulent new pathogens such as the H5N1 virus (avian or bird flu), West Nile virus, Ebola virus, and severe acute respiratory syndrome, or SARS.

These new potential plagues tend to result, in part, from the global spread of industrialization, which pushes humans toward ever-closer contact with wildlife as we encroach into what were once solely wildlife habitats. Ebola virus outbreaks are linked to mining development in previously untouched areas as well as hunters looking for exotic bush meat; the AIDS pandemic is believed to have originated from human encroachment into African forests where wild chimpanzees were a reservoir for the virus; and fruit bats in remote areas are thought to be the original source of several high profile zoonotic pathogens which have spread to humans, the most recent of which is SARS.

Similarly, H5N1 virus, or avian flu, is often the result of farmers and infected fowl crowding together in prime living space. Andrew Cunningham, a zoologist with the Zoological Society of London, recently raised a red flag about new viruses emerging from global encroachment into wildlife in an essay in the British medical journal
BMJ,
arguing that while this has probably happened many times in the past, such viruses failed to spread because those infected lived in remote enough areas that they either died or got well before they interacted with larger human populations. In today’s world, however, the increases in international trade and travel make any kind of virulent new flu outbreak an overnight global emergency. The international trade in wildlife is now enormous, with hundreds of millions of wild animals and their products being transported around the world every year. The emergence of West Nile virus in North America, and AIDS and SARS globally, Cunningham points out, arose from such travel and trade in an age when “travelers can be in the middle of a tropical jungle one day and commuting to their desk in London the next.” With world air travel expected to grow at about 5 percent a year for at least the next twenty years, the global crisis of newly emerging infectious diseases is unlikely to disappear anytime soon.

Others argue for the impact of global warming and hotter weather on growing rates of infectious diseases. In Al Gore’s 2006 movie
An Inconvenient Truth,
a disturbing chart cites rising rates of illnesses, among them SARS, malaria, Ebola virus, and avian flu. The documentary’s accompanying Web site states that with continued warming, deaths from climate-related illness are expected to rise sharply over the next two decades, according to projections by the World Health Organization. The question emerges: As the planet warms from pollution and infection-bearing mosquitoes and ticks proliferate in more temperate climates, how much will illness rates rise? Mosquitoes that transmit diseases such as West Nile virus thrive in warm weather. Simply lengthening the warm season will allow mosquitoes more time to reproduce, which means more generations of mosquitoes each year. Warmer climates may also allow mosquitoes to expand into areas that were too cold for them before. To make matters worse, the heat could also speed up the reproduction of the viruses the mosquitoes transmit.

Some viruses thrive in colder climates, others in warmer ones. In fact “colds” were first given that name because researchers were trying to grow a common cold virus in the lab and no one could manage it. One day, a researcher accidentally left the door ajar on the incubator and the temperature dropped. When the scientist came back the next day he discovered to his astonishment that the virus was now growing. That’s how researchers came to understand that “cold” viruses grow better at cooler temperatures.

Other viruses, like coxsackievirus, however, favor warmer conditions. These viruses don’t replicate over the winter, but neither do they die. They lie in wait until temperatures are warmer and suitable for their growth. If temperatures are consistently warmer, that allows viruses that grow in warmer temperatures to abound. Common viruses such as RSV, or respiratory syncytial virus, a major cause of respiratory illness in young children, also thrive in warmer weather. If both viral and chemical triggers of autoimmunity are mounting simultaneously, what exactly will that mean for today’s already disturbing increase in autoimmune disease?

AVIAN FLU: AN AUTOIMMUNE-INDUCING VIRUS

The most feared of these new pathogens is no doubt the H5N1 virus, headlined, at this writing, to be the cause of the next flu pandemic. Because of the unusual way in which the virus can cause the body’s immune system to rapidly turn from friend to foe, the avian flu is particularly troublesome for the quarter of the population that possesses the genetic predisposition to autoimmunity. Avian flu is feared because it could provoke a repeat of the influenza pandemic of 1918. The 1918 flu, or H1N1 virus, was—like the avian flu—an influenza A virus. Like that earlier flu, avian flu unleashes an unusual hurricanelike storm of immune-system signaling proteins called cytokines, which signal the immune system to combat microbial invaders. Cytokines signaling to the immune system to fight disease is a good thing, but when cytokine levels are elevated for too long and their signaling becomes uncontrolled, they can hijack the body’s immune system to turn against the body itself. In avian flu, just as in autoimmune disease, too many cytokines are released, stimulating the immune system troops to run amok, killing not just avian flu–infected cells but healthy cells throughout virtually every organ of the body. In avian flu the result is fast, furious, and all too often deadly.

Moreover, one doesn’t need to possess a genetic predisposition to autoimmunity for the avian flu to unleash its autoimmune-like cytokine fire. The H5N1 virus is so virulent that it bypasses the need for any genetic predisposition; anyone can suffer avian flu’s severe friendly-fire effect. In 1918, those most likely to die were people with strong immune systems rather than the elderly and very young. Whether those with a predisposition to autoimmunity—who by the very nature of the disease have overly strong immune system responses—are in some way more at risk is a question researchers and patients alike can hope they only have to answer hypothetically.

VACCINATION STATION: AUTOIMMUNITY GETS A SHOT IN THE ARM?

As anyone who watches the six o’clock news well knows, the emergence of pathogens with the potential to become global pandemics is driving a frenzied search for new vaccines for avian flu and viruses such as SARS. For those with autoimmune disease, however, these vaccines might prove just as worrisome as they are reassuring. Although individuals with an unrecognized genetic predisposition to autoimmunity or who have an autoimmune disease may be more in need of protection against flu pandemics and infectious-disease outbreaks than others with less overexcitable immune systems, vaccines may in and of themselves prove to be dangerous for them.

Just over thirty years ago, in 1976, the Centers for Disease Control investigated and confirmed that a severe influenza outbreak at Fort Dix, New Jersey, had been caused by the “swine flu”—an influenza A–type virus. The Department of Health, Education, and Welfare grew concerned that the United States might be about to see another large national flu pandemic, involving numbers of influenza deaths reminiscent of the flu pandemic of 1918. The federal government deemed it prudent to vaccinate all Americans. In October 1976, the National Influenza Immunization Program officially began. Initially, nearly 1 million Americans were vaccinated each week, with the number growing to more than 4 million a week by the end of that first month. By the middle of November, 6 million Americans were being vaccinated each week. From the very start of the campaign, the National Influenza Immunization Program ran a well-organized surveillance system, monitoring for adverse side effects. Within the first two months, concerns from that early warning system began to emerge. More than ten states reported cases of Guillain-Barré syndrome in individuals who had been vaccinated recently. The relationship was so profound that the vaccination program stopped cold on December 16, 1976. By January 1977, more than five hundred cases of Guillain-Barré syndrome had been reported as a direct result of the vaccine. People were being vaccinated to protect against the influenza A swine flu, but literally hundreds of them were ending up with an uncommon neurological disorder leading to acute paralysis, from which some recovered wholly, others partially, and twenty-five died. Later calculations showed that the relative risk of acquiring GBS during the six weeks after the vaccination was ten times higher if you had been vaccinated than if you had never received the swine flu vaccine.

The cases of GBS that resulted from the swine flu vaccine were no different, in terms of the severity of paralysis and weakness, from those that had emerged in nonvaccinated individuals, except for the fact that those who developed GBS without having been vaccinated were, as in my own case, far more likely to have had an acute illness in the month preceding GBS.

When we catch a disease naturally, we usually produce antibodies to the organism that causes it. These antibodies, or proteins in the blood, remember the organism that caused the disease and can recognize and inactivate it when we come into contact with it again. Vaccines—made up of bits of virus that have either been crippled so that they can’t trigger serious illness or have been killed before being injected—teach our body’s immune system to produce antibodies and identify the virus so that when the immune system encounters it again it will recognize it and inactivate it without our ever having to suffer the disease itself.

Epidemiologists wondered if the cause of so many people developing GBS after getting the swine flu vaccine might have been a residual protein taken from the myelin of embryonic chicks that existed in the vaccine through all its manufacturing stages, though the idea that this myelin protein had caused a case of molecular mimicry was a guess at best. Back then, investigators could not imagine that the virus in the vaccine itself was the cause. Still, it seemed a freak occurrence having to do with something unique to the swine flu vaccine.

Then, in 1992, 1993, and 1994, it all happened again. People developed Guillain-Barré after widescale influenza vaccination programs, cementing the epidemiologic evidence that influenza strains other than the swine flu could also induce GBS. This isn’t all that surprising, given Harley and James’s discovery that molecular mimicry between a protein in a virus and a protein in the body could lead to autoimmune disease. But it was a startling realization at the time.

Sadly, those most in need of protection—people susceptible to demyelination and paralysis should they come down with an acute infection—are also those most likely to be at risk of severe adverse effects from the very vaccines meant to help them. For that reason, most physicians advise those who have had Guillain-Barré syndrome not to receive flu vaccines.

While concerns over the ill effects of vaccines make up as many headlines as do our efforts to invent new ones, it nevertheless seems prudent to underscore how much society as a whole has benefited from wide-scale vaccinations before launching into a deeper examination of the growing data finding a causal link between vaccines and autoimmune disease. If you were born about a hundred years ago and came down with a case of diphtheria, your life would have been at stake. At that time, thousands of people died routinely during disease outbreaks of mumps, rubella, and diphtheria. Enough generations have passed in the interim that few of us are viscerally cognizant of how lethal these diseases once were. As a public health tool, vaccines are an astonishingly beneficial and cost-effective life-saving intervention against infectious disease.

But they have their downsides, and autoimmune disease is emerging as a potentially dark one. In 1994, the
Journal of the American Medical Association
reported a dangerous relationship between diphtheria, tetanus, and oral polio vaccines and a number of autoimmune disorders, including Guillian-Barré syndrome. Similarly, a correlation has been reported and debated in scientific journals for years between the hepatitis B vaccine and multiple sclerosis as well as rheumatoid arthritis. Other evidence links the measles vaccine to multiple sclerosis and the measles, mumps, rubella (MMR) and hepatitis B vaccines to rheumatoid arthritis. Many scientists also believe strong anecdotal evidence exists between receiving the hepatitis B vaccine and developing lupus. Yet another noted connection between vaccine and illness is evidence relating the
Haemophilus influenzae
type b vaccine, known as Hib, to type 1 diabetes. Like Epstein-Barr, however, the Hib vaccine may take time to wreak its damage and spark disease: a statistically significant association between receiving the
Haemophilus
vaccine and developing type 1 diabetes in children exists as much as three years after receiving the vaccine. More recently, reports have emerged linking the new human papillomavirus, or HPV, vaccine to a statistically significant increased risk of Guillain Barré syndrome, especially when the vaccine is co-administered with the meningococcal vaccine.

As one top researcher who prefers to speak off the record puts it, “If you are looking for what the big ‘ahas’ in autoimmune research are going to be in the next few years, you have to look at vaccines.” Since our understanding of autoimmunity in general is still relatively young compared to national research campaigns into so many other diseases, and our epidemiological data linking autoimmune disease to standard vaccination programs is even newer, it’s easy enough to dismiss most of what we do know as speculative. The frequently long time frame between getting a vaccine and developing autoantibodies as a result can make it hard to cast such associations as cause and effect. Still, the data we do have clearly shows that certain autoimmune diseases such as Guillain-Barré syndrome and type 1 diabetes can be triggered by vaccines. Is it so surprising then to consider that others can be as well?