Evil Tendencies Cancel

In 1936 Robert Frost wrote the poem "Evil Tendencies Cancel." The poem concerns the chestnut blight, though as the title suggests, it is also about much more:

Will the blight end the chestnut? The farmers rather guess not. It keeps smouldering at the roots And sending up new shoots Till another parasite Shall come to end the blight.

Frost scholars don't pay a lot of attention to the poem—it's not considered one of his major works. But scientists like Dennis Fulbright do. In six brief lines, the poet not only succinctly captured the chestnut's plight, but also accurately predicted a discovery that would fuel a whole new round of efforts to rescue the American chestnut. "It's pretty amazing, isn't it?" says Fulbright, a plant pathologist at Michigan State University. "It tells the whole story."

Fulbright is tall and has an athletic build. With his tousled dark hair and boyish grin, he looks a good bit younger than his fifty-three years. He grew up in Southern California, far beyond the chestnut's native home, so he wasn't weaned on the kinds of fond reminiscences that inspire many would-be saviors of the tree. He was twenty-nine years old before he even saw his first American chestnut tree. But after decades of chestnut research, he's developed a deep sense of kinship with the tree. "I'm not someone who gets into these kinds of things," he says. "But when it comes to chestnut, I really feel like I have an intimate understanding of what the trees are going through and that I can help to solve it." He's worked on wheat and tomatoes, oaks and Christmas trees, but none have sparked the kind of emotional attachment he feels for chestnut trees. His wife jokingly calls herself a "chestnut widow."

Like any love-struck admirer, he can't help looking for chestnuts wherever he goes, and he invariably finds them, even in unlikely places, such as when he stumbled across a chestnut in Mexico, or when a chestnut sapling was spotlighted by his headlights as he pulled into a campground in Massachusetts. Even after twenty-five years, the romance is still growing as he branches out from disease-oriented research into new chestnut ventures, working with growers to develop a Michigan chestnut industry and innovating new, weird chestnut products, like chestnut chips and chestnut beer.

But Fulbright has also developed an appreciation for the tree's foe, the Cryphonectria parasitica fungus: "You have to give it its due. . . . It's the perfect killer, like a shark." (Another veteran researcher confesses similar admiration for the fungus, though he admits "it's like admiring the Boston Strangler.") The more Fulbright has studied the organism, the more he's become enthralled: "If you're going to be wowed by a fungus, it's one to be wowed by. It's a beautiful color, it grows in culture in the laboratory, it's easy to isolate. Sometimes I think I'm more in love with the fungus than the tree. I call it the Stockholm syndrome, like when a hostage starts pulling for his kidnappers."

It's not surprising Fulbright has fallen for both the tree and its enemy. Plant pathologists don't tend to think about just one or the other. Rather, they approach the diseases they study as a triangle, with one point the host, one point the parasite, and one point the environ ment. Change any of those points and you can potentially change the course of the disease. In afflictions of food crops, the first line of attack is often the environment—improving the soil, adding irrigation, spacing plantings so the plant gains an edge over its pathogen. But there's no environmental fix for a pandemic like the chestnut blight, which sprawls over millions of acres of wild forest land. That leaves just two points of the triangle to deal with. You can work on the host, the tree, so that it can put up a better fight, as generations of breeders have tried. Or you can tackle the parasite, the fungus, to render it less lethal. That's where Fulbright has focused his work.

It's an approach made possible thanks to a serendipitous discovery in Europe, where the blight touched down in the 1930s. (Some say it arrived on chestnut mine timbers imported from America to Genoa; others think it sneaked in on chestnut trees planted in botanical gardens.) At first it appeared that the European chestnuts were destined for the same tragic fate as their American cousins. But twenty years into the epidemic, an Italian scientist noticed that sprouts growing from the remains of dying chestnuts had begun showing signs of spontaneous recovery. They developed cankers, but then the cankers stopped growing and actually appeared to be closing. He speculated that the trees had somehow acquired an immunity to the fungus—an idea other scientists dismissed as a biological impossibility, because it would take centuries for the trees to evolve that kind of protection.

The observation intrigued Jean Grente, a French agronomist who had made his name in domesticating the production of truffles. Grente worked for the French equivalent of the USDA, in a lab he called "Le Laboratoire de Lutte Biologique," the Laboratory of Biological Struggle. In 1965, after studying samples of fungus taken from the healing trees, Grente discovered the real reason for their recovery: the trees hadn't changed, but the fungus had. These strains of the fungus were a sickly white, instead of their normal vibrant orange. They also grew far more slowly than usual. He speculated that the blight was afflicted by a blight of its own that dramatically retarded the fungus's ability to grow and spread. Here was Frost's other parasite.

Or actually, as later research established, a virus. Incredibly enough, Cryphonectria parasitica had come down with the fungal equivalent of a bad cold. And the fungus responded in just the same way humans respond to a rotten case of the flu: it became sluggish and listless, and lost its appetite.

Like the flu, this virus could be passed around, as Grente found when he placed a culture of healthy fungus in the same petri dish with a sickly strain. Filaments from the two grew together and formed a new mycelial fan. But instead of the normal sunshine hue, this was the pale-orange color of sherbet. When Grente injected strains of ailing fungus into blight cankers on trees, the parasite infiltrated the uninfected fungus and the overall infection on the trees slowed down.

Grente termed the phenomenon "hypovirulence," for the way that the virus saps the blight's normal virulence. It's not a cure for the blight, but slowing the fungus's assault buys time for an infected tree. The tree has the chance to rally its natural defenses, growing a thick wall of callus tissue around the deadly canker to block the further spread of the advancing mycelial wedge. It's the same kind of scab trees form in response to any wound, whether the cause is a swipe from a car or the cut of a saw. You can see when a tree is winning its fight—healing cankers often have a gruesome, swollen appearance, like arthritic joints. One researcher calls them "big uglies." Instead of the usual flat or sunken patches on the bark that signify dead tissue underneath, healing cankers are bulging and distended by the tree's struggle for life beneath.

Grente began treating French chestnut orchards with strains of hypovirulent fungus. The strains steadily spread, and within ten years the blight epidemic there had ground to a halt. Proud as he was of his discovery, Grente also acknowledged that the credit was not his alone: "The blight has been defeated by nature, not me," he explained. "I just found the way to do in 10 years what nature does in 50 or 60." Grente's discovery pointed to a wholly new strategy for defeating the chestnut blight—the use of a biological control, much like ladybugs can be deployed to rid a garden of pesky aphids.

The discovery had come none too soon. By this time, forestry experts had all but given up on the American chestnut. The USDA had abandoned its breeding program. Plant pathology departments ruefully taught that the blight marked the field's greatest failure. There were probably fewer than a dozen American scientists doing anything remotely related to the American chestnut. One of the few places where chestnut research was still proceeding was at the Connecticut Agricultural Experiment Station, Arthur Graves's old stomping grounds. There, Richard Jaynes was still pressing ahead with Graves's breeding program, pulling in occasional help from Sandra Anagnostakis, a young mycologist.

A Kansas native, Anagnostakis had begun working on her doctorate at the University of Texas in the early 1960s, but cut her studies short when her husband landed a job at Yale University. Despite having only a master's degree, she was hired by the Connecticut Agricultural Experiment Station in 1966. "In those days it didn't really matter what sort of degree you had," she says. "Now you would have to have a PhD." (In fact, she adds, she got so tired of people mistakenly calling her "doctor" that she spent a year in Germany writing up her research to acquire a doctorate degree. She returned with the added credential in hand only to discover that "nobody cared.")

Anagnostakis spent her first two years at the station working on fungal diseases of tomatoes and corn, until one day Jaynes placed a blight-ridden chestnut branch on her desk and told her, "Here—you're a mycologist, why don't you do something about this?" She was soon hooked. Other colleagues like Jaynes have since moved on to other jobs or other fields of research, but forty years later, Anagnostakis is still passionately trying to do something about the chestnut. She hit retirement age in 2004, but cheerfully insists she has no intentions of ever retiring; she recently told her boss, "I intend to drop dead in the woods someday."

Anagnostakis is a small, sturdy woman with a round face, short salt-and-pepper hair, and the brisk air of a schoolmarm. She quickly warms up, though, when the subject is chestnuts. Her cluttered office is filled with chestnut memorabilia—photos, a painting of children gathering chestnuts, slices of wood. The license plate on her car reads "CHSNUT." She is, she says, one of three "chestnut ladies": the other two are researchers in Italy and China. Anagnostakis describes herself as a "terminal introvert," but she actually has a pretty forceful personality—and that, as much as her scholarship and longevity, maintains her authority in the field. As one colleague observed, even when she's saying something that you suspect is wrong, she says it with such assurance you begin to be persuaded.

Like many chestnut researchers, she has a strong affinity for the tree and a sense of its having a distinct personality. "It's vital, with a strong life force," she says, adding with a laugh, "and I'm not one of the sentimental ones."

"Have you read A Feeling for the Organism?" she asks, referring to Evelyn Fox Keller's biography of Nobel Prize—winning plant geneticist Barbara McClintock. McClintock maintained that years of standing in the fields, carefully studying individual corn plants, gave her the intimate knowledge and understanding—the feeling for the organism— that allowed her landmark insights into how corn genes operate. "I know what she meant," says Anagnostakis. "If I go out and really look at the trees, I find out all kinds of things."

In addition to her scientific work on Castanea dentata, Anagnostakis has become something of a historian of the species and its nemesis. She has immersed herself in the old literature in an effort to trace the entry of chestnut blight in the United States and to gain as precise a picture as possible of what the tree was once like. She has acquired, for instance, all the USDA records documenting importations of Asian and European chestnuts and is able to tell, with a quick glance at the well-thumbed index cards, the precise history of a particular tree. "Someone will call me up and say they live in Washburn, Illinois, and there's a beautiful American chestnut tree in their yard and I should be interested. So I look in my records and find out someone from Washburn, Illinois, got fifty Chinese chestnuts in 1912 and it happens to be their street address. I'm breaking hearts everywhere." Though she says she's not a confrontational person, she rarely hesitates to correct someone if she thinks they are wrong. She has contacted mail order companies to ask them to correct misleading claims about the chestnut trees offered in their catalogs. "They were not happy, of course," she recalls. "I do try to keep my mouth shut, but it's very hard."

Around 1972, Jaynes showed her Grente's paper and suggested they take a look at his approach. She agreed that it looked interesting and wrote the Frenchman in English, asking for samples of his fungus cultures, but got no response. So she contacted a friend who taught high school French and asked her for help in writing him again. "Within about a week I got cultures back in the mail. He had been intending to get my letter translated but just hadn't gotten around to it," she recalls.

Anagnostakis, Jaynes, pathologist Neal Van Alfen, and geneticist Peter Day began a series of experiments to try to understand the phenomenon Grente had described and to see if the same miracle could be replicated in this country. They tested the strains Grente had sent, first in the lab; then in trees growing in greenhouses; and last, in trees planted at the station's farm. They inserted plugs of the European hypovirulent fungus into the edges of cankers formed by the virulent American fungus. When they later sampled the cankers, they found that the different strains had joined and the new growth of fungus was now hypovirulent. The research team reported their Wndings in a landmark article in 1975 in the prestigious journal Science: "Our results in the laboratory, greenhouse, and field .. . suggest that this fungal strain [the hypovirulent fungus from Europe] may become a control for the disease in the United States." The article was accompanied by a copy of Frost's poem.

The paper ignited a new wave of interest in rescuing the American chestnut. Forget about breeding hybrids to achieve victory against the blight; here was a weapon that just might bring a swift end to the protracted war. It also offered an infinitely more elegant and simple resolution: spread hypovirulent fungus in a forest of chestnut sprouts and let it take off, like a swarm of aphid-hungry ladybugs. If Europe was any indication, the saplings would recover and the chestnut forest would come roaring back. It is no wonder one forest researcher declared that hypovirulence represented "the most exciting event in chestnut blight research in recent years."

"It really was responsible for bringing chestnut back on to the playing field," says William MacDonald, a plant pathologist at West Virginia University and one of a number of researchers who jumped into the field in the wake of the discovery. Suddenly there was more money for chestnut research (though never enough, the scientists would complain). At the Connecticut Agricultural Experiment Station, Jaynes noticed there were now four or five other scientists interested in pursuing chestnut studies. When MacDonald hosted a symposium on chestnut research at his university in 1978, about 125 scientists, foresters, and others showed up, the largest gathering of people with an interest in the American chestnut since the Pennsylvania Chestnut Tree Blight Commission conference more than sixty years before.

Although the promise of hypovirulence was widely recognized, it presented bedeviling mysteries and a new disease triangle to be probed and understood. What was the biology of the blight's own blight? How exactly did it infect and affect its host, the Cryphonectria fungus? Did American chestnut trees offer the same microenvironment for this new host-parasite relationship as the European trees?

Presumably the virus originated in Asia, like the blight fungus, and was dispersed around the world along with the fungus. But if that was the case, why had hypovirulence only come to the rescue of chestnuts in Europe? Was it possible the fungal flu was also present in the United

States but had somehow gone unnoticed? The answer came from an unlikely place, hundreds of miles beyond the chestnut's home range. In 1976, an observant cross-country skier happened by a small grove of American chestnut trees in Rockford, Michigan, likely planted by settlers long ago. The trees, she noticed, had blight cankers, but these cankers looked unusual—much like the photos she had seen in a recent news story on hypovirulence. She contacted the Connecticut researchers and sent samples to Anagnostakis, who cultured them in her lab and soon determined that they were infected with a hypovirus. But it wasn't the same as the European blight-of-the-blight. This was a homegrown hypovirus, and it seemed to be aiding these Michigan chestnut trees just as the virus in Europe had done.

Dennis Fulbright was still in graduate school when the first scientific reports on hypovirulence were published. He read the Science paper and found it interesting. But after presenting a seminar summarizing the work, he gave it little thought. He took a job at Michigan State University and planned to work on wheat diseases. But a colleague with an interest in the American chestnut soon persuaded him to take a look at the Michigan chestnut trees. The Rockford stand was not an isolated example, the colleague explained. There were similar old groves dating from the nineteenth century scattered all over the state's Lower Peninsula, and they contained an estimated six hundred to eight hundred good-sized surviving chestnut trees. Some undoubtedly had simply escaped the blight so far, but others—no one knew how many— seemed to surviving in spite of it. The trees appeared to be undergoing a European-style recovery.

One of the most heartening sites was a small woodlot in Grand Haven, owned by a man named George Unger, who used to gather the nuts every fall and sell them in Chicago. Years before, when the blight first reached Michigan, a county extension agent had urged Unger to chop down all his chestnut trees while it was still possible to sell the wood. "Everybody agreed; they said they're going, gone," Unger later recalled. But as Unger began sawing his way through the stand, he noticed that some of the trees sported bulging cankers instead of the usual flat dead spots. Unger had never heard of hypovirulence, but he trusted what his instincts told him—that these chestnuts were fighting back against the blight and maybe even winning. He decided to stop cutting down the trees.

Fulbright visited the stand in 1981. It was the first time he'd ever seen chestnut blight at work, and these were not your typical blight cankers. "I was very confused," he recalls. "Recovering cankers tend to look very ugly. They're swollen and broken up. The bark is fractured. There's lots of thickening of the bark. It doesn't look very pleasing. I kept thinking to myself: this is the good aspect of chestnut blight?" He was amazed that a layman like Unger had recognized the stirrings of recovery in the dreadful-looking growths. "It even took me, as a plant pathologist, a little bit of time to get through that."

Once he got through it, however, Fulbright was convinced that the Grand Haven trees were indeed in the midst of a naturally induced recuperation. But to his frustration, he had a hard time getting other scientists fired up about the Michigan trees. "There were all these excuses why Michigan was an anomaly and maybe it shouldn't be studied and what we're trying to work on are trees in Virginia, the backbone of the chestnut population." East Coast researchers insisted that what was happening in Michigan was due to some kind of "edge factor"—the inexplicable phenomena that often occur on the edge of natural ranges. At times he even found it difficult to persuade Michiganders of the importance of the trees. When developers bought George Unger's land and proposed plowing the stand under for housing in the early 1990s, Fulbright tried to get a local conservation group to join him in battling the plans. The group's botanist was unmoved by his pleas on the chestnuts' behalf. "Why are we trying to save these trees? They're invasive species as far as Michigan's concerned," he told Fulbright.

By the time I met Fulbright in late 2005, researchers could no longer pooh-pooh the significance of the Michigan trees. Three decades of scouring the American chestnut's natural range for other signs of hypovirulence had come up empty. The chestnut groves in Michigan are among only a few places in the United States where hypovirulence has arisen naturally and are the sole examples of American chestnuts demonstrating dramatic recovery en masse.

"What happened to Unger's stand in Grand Haven?" I ask Fulbright.

"I didn't have the heart to go there until this year," he answers. "It is houses."

No more trees. No more blight. Is this evil tendencies canceling?

Frost's poem suggests a simple leveling process. But natural systems, unlike words, aren't readily herded into the elegant forms we seek. The farmer-poet was such a close observer of nature; did he really believe it would be so easy?

Sandra Anagnostakis's experience points to what American researchers have been able to achieve with Frost's other parasite. On a warm April day, we climb into her car and drive from her office in a residential neighborhood of New Haven to the station's farm in nearby Hamden. She steers the car across a bumpy, grassy field to where there are seventy American chestnut trees planted in four neat rows. The trees were inoculated with hypovirulent fungus starting in 1978. "We treated every canker we could reach for four years," Anagnostakis recalls. Then they left the trees alone. Today, the trees are still covered with blight, but hypovirulence also remains at work. As a result, most of the trees are still alive. "I think they're wonderful," she says proudly, as we walk through the rows. "They're beautiful."

Truly, beauty is in the eye of the beholder. These trees are a far cry from the thick, imposing towers of wood that fans of the tree have in mind when they talk about chestnut restoration. Many of them look more like bushes than trees; their main stems have died back and been replaced by multiple prongs of skinny sprouts. The best of the bunch are scraggly, limby specimens, averaging no more than thirty-five feet tall. As another researcher jokes, "They're apple trees." Could this really be considered success?

"It depends on what you call successful," Anagnostakis maintains. "I'm talking about trees that survive and flower." The trees blossom abundantly each summer, and every fall she collects bushels of nuts. Even now, after nearly thirty years, the cankers on the trees are still hypovirulent and the viruses are helping the trees to stay alive, allowing her to continue her efforts to breed blight-resistant trees. To her, that is proof that hypovirulence offers a viable strategy for fighting the blight. "It's a way of bringing things into balance and giving these trees a chance," she says. It's a way to preserve the species.

Yet even Anagnostakis would admit that blighting the blight in America has not been the smooth operation that it was in Europe. Try as they might, researchers generally have not been able to spark the kind of rapid tree-to-tree spread of hypovirulence that saved the European chestnut trees. And that is the essence of biological control. The achievement Anagnostakis calls success might save an orchard or a small woodlot, but it's not going to rescue millions of acres of forest.

In the years since that first paper in Science was published, it's become clear that the blight-of-the-blight is a far more complex system than initially supposed. Researchers have found, for instance, that there are at least four species of hypoviruses with widely varying levels of potency. An alphabet soup of names is used to identify the different varieties. CHVi, the virus Grente isolated, can shut the fungus down. A milder Italian variant known as CHVi-Euro7 slows the fungus's spread but doesn't stop it from producing virulent spores. The Michigan species, CHV3, falls somewhere in between. And then there's CHV4, a group found in the tree's home range in Appalachia, which appears to have virtually no effect.

The host point of this microscopic disease triangle—the Cryphonectria fungus—poses another set of complications, for it also is not a monolithic entity. There are more than two hundred strains of blight fungus, a fact which also has a bearing on the success of hypovirulence.

The hypovirus particles live in the liquid interior of a fungal cell, its cytoplasm. One way the virus is transmitted is when fungus cells share their cytoplasmic material. That can only happen if the fungi are compatible strains. In that case, it's love at first sight: the tiny threadlike hyphae of the two intertwine and their cells fuse, allowing them to share cytoplasmic material. That embrace, called anastomosis, leads to the growth of new fungal tissue. If one strain is hypovirulent, the viral particles are transmitted during that fungal kiss and the new growth becomes hypovirulent. However, if two distantly related strains are brought together, it's the equivalent of a bad date. The meeting ends in mutual rejection. No anastomosis. No viral transmission. This lack of chemistry is known as vegetative incompatibility.

The European fungus, it turns out, operates in a much more homogeneous dating scene. The trees in Europe host no more than half a dozen strains of blight fungus; in such a compatible group, the virus is easily passed around. The American population of fungus is far more diverse. In Appalachia alone—the historic heart of chestnut country and the place where enthusiasts most hoped biological control would work—there are dozens of strains of Cryphonectria parasitica hanging out on chestnut trees, a fungal tower of Babel incapable of the kinds of meet-and-greets that would permit the hypovirus to readily spread. Fulbright, Anagnostakis, and other researchers began to suspect that vegetative incompatibility was the chief stumbling block to the success of the biocontrol in this country.

In light of that suspicion, some scientists have sought a way around the problem of vegetative incompatibility by creating a new avenue for the virus to spread: via its offspring, its sexually produced spores. Virologist Donald Nuss, of the University of Maryland Biotechnology Institute, has bioengineered a Cryphonectria parasitica fungus that is genetically programmed for hypovirulence, which means that when it mates, the virus is passed on to the resulting spores. The approach offers two benefits for the price of one. The virus gets moved into a variety of Cryphonectria strains, since compatibility isn't an issue in mating. And because the powdery, sexually produced spores are dispersed by the wind, they are blown far and wide, taking the hypovirus along with them.

"On paper it looked like that might increase the spread [of hypovir-ulence]," says Nuss. That theory is now being tested in a forest in West Virginia, where two strains of transgenic fungus have been released. Whether they succeed in spreading better than normal hypovirulent strains is still unknown. In fact, Nuss notes, chestnut experts aren't even sure whether the sexually produced spores play an important role in perpetuating the blight. Ironically, although the tools of modern science have allowed researchers to penetrate the fungus's deepest recesses and tinker with its genes, they still don't know some of the most basic things about its natural history.

When I first read the Frost poem, I read it literally. I saw it as a neatly done act of scientific prophecy. But in reading it over and over and consulting with Frost scholars, I began to see that the poem contains a certain deliberate ambiguity. "It keeps smouldering at the roots/And sending up new shoots." I at first assumed "it" referred to the chestnut. But "smouldering" is an odd word choice—not a word one would normally use to conjure the bright promise of a tree springing back to life. So what is smoldering? Something more than just the chestnut's imperative for survival? Could it be hope—for ourselves, as much as for the tree?

Despite the repeated failures of hypovirulence, Fulbright and other scientists were unwilling to give up on the possibility that the blight-of-the-blight could be harnessed to save the American chestnut. Given the dramatic recoveries he'd seen firsthand in Michigan, Fulbright remained convinced that hypoviruses could work as a biological control, if only there was a way around the problem of vegetative incompatibility. In 1991, he got a chance to test the theory when he learned about a remarkable stand of chestnut trees growing in West Salem, Wisconsin. The grove was started in the early 1900s when a farmer named Martin Hicks planted a handful of East Coast chestnut seeds on the ridge overlooking his farm. Though chestnut is not native to the area, the trees flourished and multiplied into a dense stand of some five thousand trees. It is the largest remaining chestnut forest in the United States, and until the mid-1980s, it was happily free of the blight. Ron Bockenhauer, a retired dairy farmer whose family owns the stand, didn't even realize there was anything special about the place he calls "Chestnut Hill" until he read a news article in the 1980s quoting an expert who described the chestnut as extinct. "I wrote him and said, 'Come on up,'" Bockenhauer recalls. "From then on everybody started coming." Scientists, reporters, and chestnut pilgrims visited, eager to see hale and hearty examples of their beloved tree.

The West Salem stand was a perfect location to test the power of hypovirulence to act as an effective biological control. There were none of the complications that had muddied the results of other experiments with hypovirulence. The blight was not widespread. The trees were mature. And most important, an analysis showed that only one strain of the fungus was present in the stand. (That in itself is testimony to the disease's virulence, for, according to Fulbright, it means the outbreak was probably lit by a single spore, one lonely microscopic particle dropped from a migrating bird onto a luckless tree.) Vegetative incompatibility would not be an obstacle. If hypovirulence was going to work anywhere, it ought to work on Chestnut Hill. Here was a tantalizing chance to do what no one had ever done: stop an outbreak of the blight before it got rolling.

In 1991, Fulbright, MacDonald, and Jane Cummings-Carlson, a pathologist from the Wisconsin Department of Natural Resources, quickly drew up a plan for deploying a hypovirus in the stand. Fulbright was full of optimism, certain that this strategy could save a good part of the stand. In ten years' time, he confidently told one reporter, half the trees in the stand would be alive because of hypovirulence.

Today he cringes when recalling that brash prediction. Even in West Salem, the biocontrol has proved trickier than any of the researchers expected. The first virus strain used—taken from recovering trees in Michigan—turned out to be far too debilitating to its fungal host. It left the fungus like a bedridden invalid, too sick to budge from the spot where it was placed. After three years, the researchers decided to switch to another hypovirus, one of the European strains. This strain spread more readily over the next few years, and by 1997 it had infiltrated more than a third of the cankers into which it was placed.

Still, it wasn't moving fast enough. Though the hypovirus has spread well on individual trees, there's been limited tree-to-tree spread. As a result, even in this optimal setting, the hypovirulent fungus has not been able to keep up with the explosive growth of virulent fungus. (And the site is no longer so optimal: in recent years, two more strains of the fungus have been found there, further complicating the effort at biocontrol.) By 2002, approximately six hundred trees in the stand were infected with the virulent fungus, and many had died. Parts of the forest resemble photographs from the heyday of the blight—one path is lined by a somber row of standing skeletons. Assessing the results of the experiment, Cummings-Carlson concludes that "the fungus outsmarted us."

"Eeeow," Fulbright winces when told of her assessment. But as he scrambles up and down the steep slopes of the West Salem woods on a crisp October day, he steadfastly refuses to be discouraged. Despite the raging epidemic, there is still a verdant layer of chestnut leaves overhead and the ground is littered with broken burs and tiny mahogany nuts. He insists he is only disappointed that, as he says, "other people might consider it a failure." At first I wonder if he is just trying to rationalize the twenty-five years he's devoted to hypovirulence. But following him through Chestnut Hill, listening to him excitedly expound on what he now thinks is happening to the trees, I come to see that as much as Fulbright loves the chestnut, he also loves the process of science. It's a process in which theories are always being knocked down; that is the definition of scientific progress.

True, the stand hasn't supported the theory that vegetative incompatibility is the chief deterrent to the success of hypovirulence. "If that's outsmarting me, yeah it didn't happen like that," he says. But he adds emphatically, "I don't consider this in any way a failure. ... I think we're finding out some really significant things about chestnut blight and chestnut trees here. And that makes me so excited that I can forget the part about the fungus outwitting me."

Fulbright is seeing something unexpected unfolding on Chestnut Hill, a turn of events that gives him a whole new reason to be optimistic. To his surprise, the trees aren't responding uniformly to the hypovirus: some are taking better advantage of the treatment than others. How can that be? "OK," he says, "this is where I stop couching my language in any way with science. Some of the trees out there seem to 'get it' and some of them don't. Some of them seem to know what we're trying to do, and others don't."

As we walk through the stand, Fulbright pauses often to point to trees that "get it" and trees that don't. Finally, he comes to a stop in front of a pair of trees about fifteen feet apart. Both were inoculated with the European hypovirus seven years ago and painted with red numbers on their trunks. Number 12 is little more than an upright carcass. Number 13, on the other hand, rises sixty feet high and is exuberantly alive, flush with shiny green leaves and bunches of nut-filled, porcupiney burs. The trunk and branches are pockmarked with cankers, but these are the healing variety, swollen by layers of protective callus tissue. The trees are the same age, the same size, and in the same location. Why is 13 bouncing back while 12 is on its deathbed?

Fulbright has a theory, though it remains unproven. He suspects that the difference has to do with the genetics of the individual trees. Number 13, he speculates, has "a smidgen more" innate resistance to the blight. If the hypovirus bought the tree some time, that trace of extra-tough DNA helped the tree to spend the time well. The tree got a chance to start healing itself. Whether it survives over the long term is uncertain, but for now, it is the incarnation of a chestnut rescuer's dream.

He pauses by another chestnut that also seems to "get it," as evidenced by a large, swollen canker that's starting to close. "This is exactly the way it happens in Michigan," he says excitedly. With any luck, this tree should be around for a long time, he thinks. Suddenly he throws his arms around the tree and embraces it in, well, a big tree hug. Pressing his cheek against the rough bark, he calls out with a grin, "Tell Jane I'm happy to be outwitted by this tree."

Halfway across the country, Anagnostakis has come to the same conclusion. She, too, has noticed varying responses to the hypoviruses in her test plot of seventy trees. In an effort to discern a pattern, she mapped out the plot on paper, with smiley faces for the trees doing well and frowning faces for those that failed to thrive. She's spent hours studying the checkerboard of smiles and frowns. "There's no pattern," she has concluded. "I think that this proves that there's a genetic difference in American chestnut in their resistance to blight. . . . I think the ones that survive in the presence of hypovirulence have some sort of Wtness genes." If she and Fulbright are right, it would help explain why hypovirulence worked so well overseas: European chestnuts are slightly more blight resistant than the American trees. Perhaps the trees in Michigan owe their recovery to similarly providential genes.

As Fulbright has begun to consider the signiWcance of the tree's genetics, he's started to see evidence for his theory throughout West Salem as the blight moves through the stand. The woods there are peppered with chestnuts—mostly young trees—that were never treated with a hypovirus, but which are nonetheless developing healing cankers. They aren't resistant enough to defeat the blight on their own, but they're putting up a stiffer fight than the average American chestnut tree. "It's funny to me that I'm starting to find these trees," he says, as he points out some chestnut saplings with healing cankers. "Why didn't I see them before?"

The presence of such "genetically superior" trees makes him hopeful about the long-term picture for the stand: "Ten years from now, out of five thousand trees, there will be 250 really good-looking trees up in the canopy and some lower numbers that are getting hypovirulence." Most of the forest will be gone, but there may be just enough survivors to repopulate Chestnut Hill.

Not everyone shares Fulbright's and Anagnostakis's continued hopes for hypovirulence. At least one researcher, Michael Milgroom, a plant pathologist at Cornell University, has come to the conclusion that it will never be the panacea for American chestnuts that it was for their cousins in Europe. He believes that its promise as a biological control is built on "a lot of hype"—a position that he cheerfully admits hasn't made him very popular among his colleagues. In 2004, he published a highly critical article that challenged the claims of success for hypovirulence as being based "perhaps more on hope than reality."

Reviewing the research, he bluntly concluded that, "Deployment of hypovirulence in eastern North America has been an almost complete failure." He pointed out that the only places where hypovirulence has produced significant recoveries are either where it's arisen naturally, such as in Europe or Michigan, or when it's been deployed in an artificial setting where the trees are pampered, as in Anagnostakis's test plot. That makes hypovirulence an interesting therapy for individual trees, but not a biological control. Indeed, he has trouble understanding how colleagues like MacDonald, Fulbright, and Anagnostakis have hung in with hypovirulence given the poor results. "I would have gotten out in the mid-'8os," he says. Then again, he admits, though he's fascinated by the biology of hypovirulence, he doesn't feel any particular attachment to the tree.

Most other researchers in the field think Milgroom is being too pessimistic. They say too little time has elapsed to draw any firm conclusions. No one really knows how long it took for hypovirulence to take hold and start gaining the upper hand in Europe or Michigan. The fact that hypoviruses can still be found on trees that were inoculated years or even decades ago leaves room for hope, says MacDonald. "We may just be impatient."

"But doesn't this keep breaking your heart?" I ask, as we talk about the dismal results at West Salem. "No, it doesn't," he answers, echoing a point other researchers make. "If it did, we'd be out of the whole business. The thing that keeps me coming back is we see bits and pieces of it working. There's something biologically going on here, and we may just be missing some components of it that we don't understand."

If it is true that hypovirulence works best in trees that already have what Fulbright calls "the right genetics," then it may still have an important role to play in chestnut salvation. Hypoviruses can be used, as some researchers are doing, to keep alive the rare trees that show signs of innate resistance. More important, the use of the biocontrol could be coupled with the ongoing effort to breed blight-resistant American chestnut trees, as Anagnostakis is doing. Combine a weakened fungus and tougher trees and, says the ever-optimistic Fulbright, "that really might be the whammy the chestnut blight needs."

You can look at Frost's poem "Evil Tendencies Cancel" as a straightforward declaration of hope: "another parasite" will surface to save the American chestnut. That's certainly the meaning taken by chestnut scientists, most of whom know the lines by heart. But that simple message is belied by the puzzling title. Do evil tendencies cancel? Not really.

The more I think about it, the more I realize that Frost was driving at a deeper, more complicated message. For help in digging it out, I turned to Robert Faggen, a professor of English at Claremont College and author of Robert Frost and the Challenge of Darwin. Frost's poems, he tells me, are often portrayed as sunny paeans to nature, simple as Christmas cards. But a much darker vision lurks beneath that Norman Rockwell surface, according to Faggen. Frost, he says, saw the natural world as a Darwinian arena of warfare, chaos, and chance, as every creature, large and small, fiercely contends for life.

Humans ascribe moral values to that struggle, and in doing so, we sustain ourselves with the illusion that we can and should guide it to the outcome we desire—we'll defeat the evil to save our good. The poem invites us to adopt another view, to consider the natural world as a neutral realm in which morals have no place. The blight and the tree, the parasite and the host are simply partners thrown together by evolutionary chance in that messy, unpredictable, strife-ridden cycle of birth and death that constitutes life. Each is simply playing the role nature assigned it.

We can hope for the chestnut, Frost suggests: "Will the blight end the chestnut?/The farmers rather guess not." But the poem's title asks us to consider what that hope means. What are the consequences of imposing human values on the natural world? The blight may seem evil to us, but from the vantage point of the fungus, that other parasite we await might be considered equally evil.

Perhaps, Frost is ultimately reminding us, our tendency to view nature in terms of our notions of good and bad, desirable and undesirable, can wreak its own kind of evil. Certainly the American chestnut would never have been pushed to the brink of extinction were it not for human agency. Humans introduced the chestnut blight. The tree's plight is a direct result of our visions of what our gardens, our personal Edens, should contain. It's a lesson to bear in mind as we press forward in efforts to redress the blight and restore our perfect tree.

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