A Planet of Viruses

by Carl Zimmer

Viruses are unseen but dynamic players in the ecology of Earth. They move DNA between species, provide new genetic material for evolution, and regulate vast populations of organisms.

Willner discovered that, on average, people have 174 species of viruses in the lungs.

To contemplate the size of viruses, tap out a single grain of salt onto a table. Stare at the tiny cube. You could line up about ten skin cells along one side of it. You could line up about a hundred bacteria. And you could line up a thousand tobacco mosaic viruses, end to end, alongside that same grain of salt.

Rhinoviruses are remarkably simple, with only ten genes apiece. (Humans have about twenty thousand genes.) And yet their haiku of genetic information is enough to let rhinoviruses invade our bodies, outwit our immune system, and produce new viruses that can escape to new hosts.

Rhinoviruses infect relatively few cells, causing little real harm. So why can they cause such miserable experiences? We have only ourselves to blame. Infected cells release signaling molecules, called cytokines, which attract nearby immune cells. Those immune cells then make us feel awful. They create inflammation that triggers a scratchy feeling in the throat and leads to the production of a lot of mucus around the site of the infection. In order to recover from a cold, we have to wait not only for the immune system to wipe out the virus, but also for the immune system itself to calm down.

Parents often give children cough syrup for colds, but studies show it doesn’t make people get better faster. In fact, cough syrup also poses a wide variety of rare yet serious side effects, such as convulsions, rapid heart rate, and even death.

The diversity of human rhinoviruses makes them a very difficult target to hit. A drug or a vaccine that attacks one protein on the surface of one strain may prove to be useless against others that have a version of that protein with a different structure.

If scientists can figure out ways to attack the rhinovirus’s genetic core, they may be able to stop the disease.

Most colds finish in under a week, and 40 percent of people who test positive for rhinoviruses suffer no symptoms at all.

Human rhinoviruses may help train our immune systems not to overreact to minor triggers, instead directing their assaults to real threats. Perhaps we should not think of colds as ancient enemies but as wise old tutors.

In 1918, a particularly virulent outbreak of the flu infected 500 million people—a third of humanity at the time—and killed an estimated 50 million people. Even in years without an epidemic, influenza takes a brutal toll. The World Health Organization estimates that each year the flu infects 5 to 10 percent of all adults and 20 to 30 percent of all children. Somewhere between a quarter and half a million people die of the flu each year.

Like cold-causing rhinoviruses, influenza viruses manage to wreak their harm with very little genetic information—just thirteen genes.

Once the influenza lawnmower has cut away that protective layer, pathogens can slip in and cause dangerous lung infections, some of which can be fatal.

One theory holds that certain strains of the flu provoke the immune system to respond so aggressively that it ends up devastating the host instead of wiping out the virus. But some scientists doubt this explanation and think the true answer lies elsewhere. It’s possible, for example, that in 1918, older people carried protective antibodies from a similar pandemic in 1889.

Birds carry all known strains of human influenza viruses, along with a vast diversity of other flu viruses that don’t infect humans.

Reassortment allows flu viruses to mix genes together into new combinations of their own.

In the 1980s, a teenage boy in Indonesia named Dede began to develop warts on his body, and soon they had completely overgrown his hands and feet. Eventually he could no longer work at a regular job and ended up as an exhibit in a freak show, earning the nickname “Tree Man.”

HPV uses a radically different strategy. Instead of killing its host cell, it causes the cell to make more copies of itself. The more host cells there are, the more viruses there are.

The viruses sense when their host cells are getting close to the surface and shift their strategy. Instead of speeding up cell division, they issue commands to their host cell to make many new viruses. When the cell reaches the surface, it bursts open with a big supply of HPV that can seek out new hosts to infect.

Never underestimate the evolutionary creativity of a virus that can transform rabbits into jackalopes or men into trees.

Herelle had found a vicious form, called a lytic phage, which kills its host as it multiplies.

Temperate phages treat bacteria much like human papillomaviruses treat our skin cells. When a temperate phage infects its host microbe, its host does not burst open with new phages. Instead, the temperate phage’s genes are joined into the host’s own DNA, and the host continues to grow and divide. It is as if the virus and its host become one.

Meanwhile, Herelle developed phage-based drugs sold by the company that’s now known as L’Oreal.

But by 1940, the phage craze had come to end. The idea of using live viruses as medicine had made many doctors uneasy. When antibiotics were discovered in the 1930s, those doctors responded far more enthusiastically, because antibiotics were not alive; they were just artificial chemicals and proteins produced by fungi and bacteria.

Skeptics have also argued that even if scientists could design an effective phage therapy, evolution would soon render it useless.

The advocates for phage therapy respond by pointing out that phages can evolve, too. As they replicate, they sometimes pick up mutations, and some of those mutations can give them new avenues for infecting resistant bacteria.

They can even tinker with phage DNA to create phages that can kill in new ways.

Based on the number of viruses she found in her samples, Proctor estimated that every liter of seawater contained up to one hundred billion viruses.

Viruses outnumber all other residents of the ocean by about fifteen to one. If you put all the viruses of the oceans on a scale, they would equal the weight of seventy-five million blue whales (there are less than ten thousand blue whales on the entire planet). And if you lined up all the viruses in the ocean end to end, they would stretch out 42 million light-years.

Cholera, for example, is caused by blooms of waterborne bacteria called Vibrio. But Vibrio are host to a number of phages. When the population of Vibrio explodes and causes a cholera epidemic, the phages multiply. The virus population rises so quickly that it kills Vibrio faster than the microbes can reproduce. The bacterial boom subsides, and the cholera epidemic fades away.

By one rough calculation, 10 percent of all the photosynthesis on Earth is carried out with virus genes. Breathe ten times, and one of those breaths comes to you courtesy of a virus.

They called it an endogenous retrovirus—endogenous meaning generated within.

As far as scientists can tell, no endogenous retroviruses in the human genome are active.

While most of this viral DNA is useless, our ancestors have commandeered some of it for our own benefit. In fact, without these viruses, none of us today would have been born.

It was exquisitely lethal, killing about seventy percent of the people it infected.

Hamsters and voles shared a common ancestor over 16 million years ago, which means that Ebola diverged from its closest relative—Marburg virus—at least that long ago.

We’d be better prepared for these emergencies if they didn’t always come as such surprises. The next plague may start when yet another virus in some wild animal jumps into our species—a virus we might not yet even know about.

The practice triggered religious objections that only God should decide who survived the dreaded smallpox.

Eu odeio CRENTE

He took pus from the hand of a milkmaid named Sarah Nelmes and inoculated it into the arm of a boy. The boy developed a few small pustules, but otherwise he suffered no symptoms. Six weeks later, Jenner variolated the boy—in other words, he exposed the boy to smallpox, rather than cowpox. The boy developed no pustules at all.

Os cara eram mto louco bixo

He dubbed it “vaccination,” after the Latin name of cowpox, Variolae vaccinae.

In 1803, King Carlos of Spain came up with a radical solution: a vaccine expedition to the Americas and Asia. Twenty orphans boarded a ship in Spain. One of the orphans had been vaccinated before the ship set sail. After eight days, the orphan developed pustules, and then scabs. Those scabs were used to vaccinate another orphan, and so on through a chain of vaccination. As the ship stopped in port after port, the expedition delivered scabs to vaccinate the local population.

Outbreak by outbreak, the virus was beaten back, until the last case was recorded in Ethiopia in 1977. The world was now free of smallpox.

A few other campaigns have followed in its wake, but only one other virus has been eradicated successfully so far: the rinderpest virus.

Missing from viruses were all the genes for full-blown life. Scientists could find no instructions in a virus for making a ribosome, for example, the molecular factory that turns RNA into proteins. Nor did viruses have genes for the enzymes that break down food in order to grow. In other words, viruses appeared to lack much of the genetic information required to be truly alive.

We protect our giant genomes from this risk by producing error-correcting enzymes, as do other animals, plants, fungi, protozoans, and bacteria. Viruses, on the other hand, have no repair enzymes. As a result, they make copying errors at a tremendously higher rate than we do—in some cases, over a thousand times higher.

Viruses are indeed exquisitely deadly, but they have provided the world with some of its most important innovations. Creation and destruction join together once more.