Immortal (7 page)

‘Move another step and I’ll send you home with buckshot in your ass!’

Five pairs of hands shot into the air. A sixth scientist, a woman with her hair coiled in a bun behind her head, covered her mouth to prevent a scream and promptly collapsed. As her colleagues
moved to her aid, Saffron lunged forward, ramming the barrel of the shotgun in their faces.

‘Don’t move!’ she screamed, prodding them backward and looking at a meek man with a narrow nose and quivering jowls. ‘You – open the fucking door, now!’

The man stared at her, his face trembling, beads of sweat spilling into his eyes, but he stood his ground and shook his head. Saffron changed her stance, took one pace toward him and flipped the
barrel of the shotgun toward her as she spun the stock. The heavy butt of the weapon smashed up into the scientist’s jaw with a dull crack and sent him spinning away onto the lawns amid
blood-spattered cries.

Saffron didn’t give the man’s colleagues the chance to respond, shoving the shotgun toward them again.

‘The door! Now!’

‘Okay!’ one of them shouted, turning and walking back to the entrance door and sliding his card through a reader mounted on a panel. He keyed in his access code and the door slid
open.

‘Back inside, all of you!’ Saffron shouted, turning and gesturing for Manx to grab the incapacitated scientists and drag them into the building.

She watched as the pathetic huddle shuffled past her into the building before hurrying after them and closing the door from the inside. She turned to her captives.

‘The labs. Take me there, now.’

The scientist who had opened the door smiled grimly, and shook his head.

‘You’re screwed,’ he said with cold delight. ‘The cameras will have seen you, and I set my code to lock us in reception here. The police will already be on their way and
there’s nothing you can do about it.’

Saffron glanced at the door as Manx pushed the button desperately before looking at her and shaking his head.

‘We’re stuck,’ Ruby Lily uttered in despair.

Saffron glared at the scientists and cocked the shotgun.

‘Then we’ve got nothing to lose.’

Colin Manx’s jaw dropped and he raised a hand to stop her.

‘Saff, no!’

Saffron ignored him and pulled the trigger.

‘What others?’

Tyler Willis sighed as he realized he had been cornered. He reached up and rubbed his wounded shoulder, shaking his head as he spoke, ‘Hiram Conley was one of seven men I’ve been
studying over the past eight weeks.’

Ethan looked at Lopez, who had now begun recording the conversation using a portable device in her pocket. She nodded once at him, and Ethan turned his attention to Willis.

‘Tell us everything, from the beginning,’ he said. ‘If there’s some kind of danger in this for you, then the more we know, the better we can protect you.’

Willis stared at Ethan.

‘I want your word. You’re government, right? I want your word, both of you, that you can protect me if this gets out.’

Ethan was about to speak, but Lopez beat him to it.

‘We’ll cover your back, Tyler,’ she assured him. ‘That’s why we’re here.’

Ethan swallowed, uncertain of how they could possibly guarantee his safety when they had no clear idea of who was threatening him and why.

Willis sighed, and gestured around him at his office.

‘This has been my work for the past three years. Along with Werner syndrome, I’ve been studying the effects and causes of cellular senescence, seeking ways in which to delay the
deleterious effects of human aging.’

‘Why?’ Lopez asked. ‘What’s the purpose exactly? Everybody dies eventually.’

‘Yes, they do,’ he agreed. ‘But the purpose of my work is to understand how we age and how to try to develop medicines that will ensure that people age comfortably, without the
debilitating diseases that afflict the elderly. By studying things like cellular apoptosis – programmed cell death – it’s theoretically possible to reverse the process of
aging.’

‘Surely that can’t work,’ Ethan said. ‘People have to age in order to die, and nothing is immortal.’

Tyler Willis smiled broadly.

‘In fact, that’s not entirely true. We see aging as a process that takes place across our own lifespans, and we see others age as we do. It’s something we’re used to, but
in nature not every species ages at the same rate, and for some there is no aging process at all.’

Lopez raised an eyebrow.

‘You mean that some animals live forever?’

‘Perhaps not forever, but for long enough that to a human perspective they would appear immortal,’ Willis said. ‘The hydrozoan species
Turritopsis nutricula
is able to
return from a mature adult to an immature polyp stage and back again, effectively meaning that it is considered biologically immortal and has no maximum lifespan. Colonies of sea anemones have been
kept in laboratories for close to a century, can regenerate any body part and show no signs of aging. Some koi fish, a much larger and more complex species, have lived beyond two hundred
years.’

‘That’s not quite the same as a mammal living for that long,’ Ethan pointed out.

‘But that’s my point,’ Tyler insisted, ‘delayed senescence isn’t species specific and can occur in mammals too. In May 2007, a fifty-tonne Bowhead whale caught off
the coast of Alaska was found to have the head of an explosive harpoon embedded within its neck blubber. The four-inch arrow-shaped projectile had been manufactured in New Bedford, Massachusetts
around 1890, making the whale a minimum of one hundred seventeen years old.’

‘A bit like Hiram Conley,’ Lopez said. ‘He had a Minie musket ball lodged in his right femur. According to analysis the wound was around one hundred forty years old.’

Tyler Willis grasped the edge of his desk.

‘You’re sure? You actually have evidence of this?’

‘It’s locked up,’ Lopez replied quickly, cursing inwardly at having revealed too much. ‘But our source is reliable. The main reason we’re here is to find out what
the hell’s been going on with this Conley and how he could have ended up not just with that wound but with a fresh Minie ball in his shoulder.’

Willis seemed momentarily distracted, whispering to himself.

‘I’ll be damned, it’s true then.’ He looked at them. ‘Conley had been shot before I met him in the pass, before the ranger arrived. Somebody else shot him with a
musket, maybe one of the others.’

‘When you were found,’ Ethan said, ‘you told Patrol Officer Zamora that Hiram Conley was too old to die, that you didn’t want him killed. You knew that he was very old
then, didn’t you?’

Willis seemed to come back to the present. He looked at both Lopez and Ethan as though weighing them up, and then finally nodded.

‘I didn’t at first,’ he said simply.

‘What was wrong with him, exactly?’ Lopez asked.

Willis sighed heavily.

‘It’s very difficult to explain,’ he said. ‘You need to think differently about life and what it is before you can understand what happened to Hiram Conley. What you need
to know is that nobody ever dies of old age, ever. What happens to us, and to all other species, is that the ability of our cells to divide without generating errors decreases the more times those
cells are forced to divide. The gradual building up of cellular errors eventually results in programmed cell death, apoptosis, which leads to a specific cause of death such as organ failure, cancer
and so on. We die as a result of illness brought on by age, but not by age itself.’

‘So technically people could live forever?’ Lopez asked, ‘if their cells could divide without errors.’

‘It’s possible,’ Willis nodded, ‘even as crazy as it sounds. But unfortunately it’s not quite as simple as that. Like everything else, aging is something that has
evolved through natural selection. Most of the earliest forms of life on our planet were bacterial colonies and such like, forms which don’t necessarily suffer senescence because, as a
colony, they survive for millions of years and continue the genetic heritage of the colony as a whole. However, with most forms of life aging has evolved because the longer something lives, the
more likely it is to encounter a fatal incident, be it predation or an accident.’

‘We die just in case we have an accident?’ Lopez muttered. ‘Sounds like a bum deal.’

‘Not really,’ Willis said. ‘Evolution has resulted in a situation where it has become an advantage to have higher reproductive strategies at the youngest possible age, thus
reducing the chances of some fatal event preventing reproduction and making a species extinct. Natural selection favors those species which can mate most effectively when they’re young and
fit, and so the evolution of species has resulted in forms of life who mature early and mate young, before then growing old and passing away. There’s a resources issue too – if nothing
ever died, then pretty soon all the planet’s resources would be consumed and nothing more could live. Each generation of species must thus make way for the next.’

‘So what was your angle on all of this?’ Lopez asked. ‘You were trying to eradicate age-related disease, but how?’

‘Disease generally comes about when people age,’ Tyler Willis said, ‘that much we know. What people don’t realize is that human diseases should have been eradicated by
natural selection by now via inherited immunity or random mutation. The reason they haven’t been is therefore because humans mate young, and for most of our evolution have also
died
young. The presence of extensive age-related disease is a relatively new phenomenon because it’s only recently that people have reached their seventies and beyond on a regular basis. This
means that natural selection only acts weakly against age-related disease because resilience to it hasn’t yet had the chance to evolve within us. My work involved studying how genetic
manipulation might serve humanity by acting as a substitute for natural selection and creating specific genes resistant to such diseases, like Huntingdon’s or Alzheimer’s.’

‘Okay,’ Lopez said, ‘so how would you go about doing that?’

‘Well,’ Willis replied, ‘the main cause of aging in mammals is the degradation of telomeres in the nuclei of cells. Telomeres are like caps at the tips of chromosomes –
you can think of them as fuel for the accurate division and replication of cells. As cells divide, telomeres become ever shorter, and eventually they are unable to support further cellular division
without a build-up of errors or deleterious mutations, which cause the signs of aging such as muscle loss, degraded skin quality, organ failure and so on. If we can find a way of allowing cells to
divide without losing the telomeres and building up those errors, we have a possible means of extending quality of life, if not longevity itself.’

‘Doesn’t sound so hard,’ Ethan said.

‘It’s hard,’ Willis assured him. ‘Mainly because the only kind of cells that naturally undergo this transformation into biologically immortal cells are those that cause
cancer. The line between the two may be thin, but it’s the difference between curing someone and killing them.’

‘And you’ve figured out a way to do this?’ Lopez asked.

‘There are a number of potential ways,’ Willis replied, ‘to slow aging in mammals. Cell loss can be repaired via growth factors to stimulate cell division, such as stem cells,
or even by simple methods such as exercise or reduced calorie intake. Senescent cells can be removed by activating the immune system against them or via gene therapy. Extracellular materials like
amyloid can be eliminated by vaccination, while intracellular junk requires the introduction of new enzymes that can degrade the junk that our own natural enzymes cannot degrade. Mitochondrial
mutations can be handled using gene therapy via cell nuclei. For cancer the strategy is to use gene therapy to delete the genes for telomerase and to eliminate telomerase-independent mechanisms of
turning normal cells into ‘‘immortal’’ cancer cells. To compensate for the loss of telomerase in stem cells we would introduce new stem cells every decade or so.’

‘Has any of this actually been achieved?’ Ethan asked.

‘The Dana-Faber Cancer Institute managed to reverse the aging process in mice,’ Willis said, ‘by targeting the chromosomes in cellular nuclei and the telomeres. They
manipulated the enzyme that regulates these tips, telomerase, turning it on and off. When they boosted the enzyme, the mice appeared rejuvenated. There was a dramatic reversal in the signs and
symptoms of aging: the brains increased in size, cognition improved, coat hair regained a healthy sheen and fertility was restored. It was the equivalent of taking someone from their eightieth year
and bringing them back to their forties. They had in effect undergone rejuvenation, had become young again.’

‘Holy crap,’ Lopez smiled. ‘That could be worth a fortune!’

‘It was only in mice,’ Willis cautioned, ‘and there’s a lot of work to be done, mostly in figuring out how to make elderly people more comfortable and to remove the
specter of age-related disease. That said, there are people looking to make money out of this – the cosmetics industry would be severely compromised if this became a commercial
product.’

Ethan frowned.

‘How come Hiram Conley was an old man then? If he’d somehow avoided aging, why was he looking about sixty when he was killed?’

Tyler Willis shook his head.

‘You’re getting it all wrong,’ he said. ‘Forget about your preconceptions, about some magical fountain of youth from which you drink and become forever young. These
things are the stuff of science fiction, and that’s the whole point. Science has been searching for a way to modify cells in order to slow or stop aging, but we’ve been looking in
entirely the wrong place.’

‘What do you mean?’ Lopez asked.

‘Hiram Conley was not in possession of some mystical vial or potion,’ Willis replied, ‘and he wasn’t genetically altered by scientists. He was suffering from an
infection.’

The blast of the shotgun rang in Saffron’s ears as the Beretta’s powerful recoil slammed the butt into her shoulder. A cloud of choking blue smoke filled the
reception area and, as the ringing in Saffron’s ears subsided, she heard the piercing screech of an alarm and the crunch of glass beneath her feet.