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Dicken nodded absently.

The five large primate cages had most of the amenities: tree limbs, swings and rings, floors covered with rubber matting, multiple levels for pacing and climbing, a wide selection of plastic toys. Dicken counted six howler monkeys segregated male and female in two cages, with perforated plastic sheeting between: They could see and smell each other, but not touch.

They walked on and paused before a long, narrow aquarium containing a happily swimming platypus and several small fish. Dicken loved platypuses. He smiled like a little boy at the foot-long juvenile as it breached and dove several times through the clear green water, silvery lines of bubbles streaming from its slick fur.

“Her name is Torrie,” Presky said. “She’s pretty, no?”

“She’s wonderful,” Dicken said.

“Anything with fur, scales, or feathers, has viral genes of interest,” Jurie said. “Torrie’s rather a dud, at the moment, but we like her anyway. We’ve just finished sequencing and comparing the allogenomes of echidnas and, of course, platypuses.”

“We’re taking a census of monotreme ERVs,” Turner explained. “ERVs are useful during viviparous development. They help us subdue our mothers’ immune systems. Otherwise, her lymphocytes would kill the embryos, because in part they type for the father’s tissue. However, like birds, monotremes lay eggs. They should not use ERVs so extensively during early development.”

“The Temin-Larsson-Villarreal hypothesis,” Dicken said.

“You’re familiar with TLV?” Turner asked, pleased. TLV stood for a theory of virus-host interactions concocted from work done over decades, at different institutions, by Howard R. Temin, Eric Larsson, and Luis P. Villarreal. TLV had gained a lot of favor since SHEVA.

Dicken nodded. “So, do they?”

“Do who, what?” Presky asked.

“Do echidnas and birds express ERV particles to protect their embryos?”

“Ah,” Presky said, and smiled mysteriously, then wagged his finger. “Job security.” He faced Turner. Wherever his head moved, his body moved as well, like a clocktower figure. “Torrie will have a mate soon. That effects many changes intriguing to us.”

“Intriguing to Torrie, as well, presumably,” Jurie added, deadpan.

They moved on to a concrete enclosure with a convincing, though small grove of conifers. “No lions or tigers, but we have bears,” Presky said. “Two young males. Sometimes they’re out sparring with each other. They are brothers, they like to play fight.”

“Bears, raccoons, badgers,” Turner added. “Peaceful enough critters, virally, at least. Apes, including us, seem to have the most active and numerous ERV.”

“Most plants and animals have their own capabilities in biological propaganda and warfare. War happens only if the populations are pressed hard,” Jurie said. “Shall we hear Dr. Turner’s favorite example?”

Turner took them across to a large enclosure containing three rather mangy-looking European bison. Four large, shaggy animals, fur hanging in patches, regarded the human onlookers with ageless placidity. One shook its head, sending dust and straw flying. “Fresh in modern memory, for hamburger eaters anyway: Toxin gene transfer to E. coli bacteria in cattle,” Turner began. “Modern factory farming and slaughterhouse technique puts severe stress on the cattle, who send hormonal signals to their multiple tummies, their rumen. E. coli react to these signals by taking up phages—viruses for bacteria—that carry genes from another common gut bacteria, Shigella. Those genes just happen to code for Shiga toxin. The exchange does not hurt the cow, fascinating, no? But when a predator kills a cow-like critter in nature, and bites into the gut—which most do, eating half-digested grass and such, wild salad it’s called—it swallows a load of E. coli packed with Shiga toxin. That can make the predators—and us—very sick. Sick or dead predators reduce the stress on cows. It’s a clever relief valve. Now we sterilize our beef with radiation. All the beef.”

“Personally, I never eat rare meat,” Jurie said with a contemplative arch of his brows. “Too many loose genes floating around. Dr. Miller, our chief botanist, tells me I should be concerned about my greens, as well.”

Orlin Miller raised his hands in collegial defense. “Equal time for veggies.”

They entered Building Two, the combination aviary and herpetarium. Mounted on benches beside the large sliding warehouse door, glass boxes housed king snakes coiled beneath red heat lamps.

“We have evidence of a slow but constant lateral flow of genes between species,” Jurie said. “Dr. Foresmith is studying transfer of genes between exogenous and endogenous viruses in chickens and ducks, as well as in the Psittaciformes, parrots.”

Foresmith, an imposing, gray-haired fellow in his early fifties, formerly of the Massachusetts Institute of Technology—Dicken knew him for his work on minimum genome bacteria—took up the topic. “Flu and other exogenous viruses can exchange genes and recombine within host or reservoir populations,” he said, his voice a bass rumble. “New strains of flu used to come rumbling out of Asia every year. Now, we know that exogenous and endogenous viruses—herpes, poxviruses, HIV, SHEVA—can recombine in us. What if these viruses make a mistake? Slip a gene into the wrong location in a cell’s DNA… A cell starts to ignore its duties and grows out of control. Voilà, a malignant tumor. Or, a relatively mild virus acquires one crucial gene and flips from a persistent to an acute infection. One really big mistake, and pow,” he slapped his fist into his palm, “we suffer one hundred percent mortality.” His smile was at once admiring and nervous. “One of our paleo guys figures we can explain a lot of mass extinctions that way, in theory. If we could resurrect and reassemble the older, extremely degraded ERVs, maybe we would learn what actually happened to the dinosaurs.”

“Not so fast,” Dicken said, raising his hands in surrender. “I don’t know anything about dinosaurs or stressed cows.”

“Let’s hold off on the wilder theories for now,” Jurie admonished Foresmith, but his eyes gleamed. “Tom, you’re next.”

Tom Wrigley was the youngest in the group, in his mid-twenties, tall, dark-haired, and homely, with a red nose and a perpetually pleasant expression. He smiled shyly and handed Dicken a coin, a quarter. “That’s roughly what a birth control pill costs. My group is studying the effect of birth control on endogenous retrovirus expression in women between the ages of twenty and fifty.”

Dicken rolled the quarter in his hand. Tom held out his palm, lifting his eyebrows, and Dicken returned the coin.

“Tell them why, Tom,” Jurie prodded.

“Twenty years ago, some researchers found that HIV infected pregnant women at a higher rate. Some human endogenous retroviruses are closely related to HIV, which goes after our immune systems with a vengeance. The fetus within the mother expresses lots of HERV from its placenta, which some think helps subdue the mom’s immune system in a beneficial way—just enough so that it won’t attack the developing fetus. TLV, as you know, Dr. Dicken.”

“Howard Temin is a god in this place,” Dee Dee Blakemore said. “We’ve set up a little shrine in C wing. Prayers every Wednesday.”

“Birth control pills produce conditions in women similar to pregnancy,” Wrigley said. “We decided that women on birth control would make an excellent study group. We have twenty volunteers, five of them our own researchers.”

Blakemore raised her hand. “I’m one,” she said. “I’m feeling testy already.” She growled at Wrigley and bared her canines. Wrigley held up his hands in mock fright.