Upgrade(65)

Humans are 99.9 percent identical in their haploid DNA/genome sequence of approximately 3.2 billion base pairs. However, while we all have roughly the same genes, there are polymorphisms—small differences in the sequence of these genes—that lead to changes in expression levels, and even alter a gene’s function. These subtle differences are what make us each unique from other members of our species.

I had coded my program to find and highlight these differences.

I dropped the huge files containing Tiffany’s raw DNA sequence into my program query.

As it went to work, I got a can of soup down from the cabinet and heated it in a saucepan on my stovetop.

I was ravenous.

I read the results of Tiffany’s DNA analysis as I ate.

Just as I’d expected, the same genes that had been altered in my genome had also been altered correspondingly in hers.

Even the modifications tracked.

These DNA payloads were already beginning to exercise their edits to myriad genes, involving multiple cascades of pathways—each a light touch to the genome, almost a butterfly effect that would have, over time, changed Tiffany’s genome and led to augmentation of her intelligence, longevity, and resilience, finally lifting her to some version of my level of being.

After seeing Kara and Andrew, I was beginning to suspect that, while the upgrade altered expressions of intelligence, memory, and physical prowess across the board, it could exponentially ramp up preexisting proclivities—strength, agility, and coordination for people like Andrew and Kara. Pattern recognition and people reading for the more intellectually inclined like me.

Tiffany had been on the same journey toward becoming an enhanced form of Homo sapiens that I had taken when Andrew shot her at the top of those stairs.

Using the software, I began to isolate the genetic codes of multiple viral packages, which had delivered the upgrade to her. Each was an eight kilobase sequence—such an insignificant piece of DNA, but it carried a code. While it had replicated, it didn’t appear to be packaged and secreted to the point of becoming transmissible.

Tiffany had never been contagious.

But the real question was what was happening with Sequence B.

I heard the DNA sequencer make a beep that indicated it was now uploading Sequence B into LifeCode.

Since it didn’t appear that Kara’s virus could spread from person to person, I wondered how she had managed to infect so many of Glasgow’s residents. Had she sent a team to infiltrate the city several months ago and manually infect as many people as possible? She could’ve targeted just a handful of locations and had pretty good odds of infecting at least half the population.

My laptop flashed a message, alerting me that Sequence B (Chris’s DNA) had finished uploading to LifeCode.

I dropped the files into my custom program query, then stepped outside to pee.

The sky was overcast and starless.

The crisp scent of snow permeated the air, and darkness crowded up against the lighted areas of the rest stop.

I returned to the van and quickly scanned the initial findings from Sequence B.

Right away, I could see that something was amiss in the code.

While Chris had also received the viral upgrade package, only some of the upgrades had occurred. In many cases, they were only partial, having failed to complete the changes and instead scrambling sections of vital genes.

Instead of initiating the upgrade, the viral package had lit the fuse on a new genetic fragment and begun a series of genetic off-targeting.

I copied the new sequences and dropped them into a general query to see if I could find a match and possible interactions.

Unsurprisingly, no exact genomic matches came back.

But I watched in horror as the list of “50%—95% overlap” results scrolled by: scrapie, mad cow disease, camel spongiform encephalopathy (CSE), transmissible mink encephalopathy (TME), chronic wasting disease (CWD), feline spongiform encephalopathy (FSE), exotic ungulate encephalopathy (EUE), spongiform encephalopathy, Creutzfeldt-Jakob disease (CJD), iatrogenic Creutzfeldt-Jakob disease (iCJD), variant Creutzfeldt-Jakob disease (vCJD), familial Creutzfeldt-Jakob disease (fCJD), sporadic Creutzfeldt-Jakob disease (sCJD), Gerstmann-Str?ussler-Scheinker disease (GSS), fatal familial insomnia (FFI), kuru, variably protease-sensitive prionopathy (VPSPr).

Fuck me.

These were all forms of prion disease.

Prions are misfolded proteins that carry a horrifying ability to catalytically transmit their misfolded shape onto normal variants of the same protein. These mutations cause normal proteins in the brain to misfold. They literally shred brain matter and cause a handful of horror-show neurodegenerative diseases. Victims lose their ability to recognize people and places and to take care of themselves. In the final stages, they cease to think at all.

Normally, prion diseases are exceedingly rare—fewer than three hundred cases reported in the United States each year—and proceed slowly. And the method of contagion is highly specific. You could only contract it one of three ways—genetically inherited, from contaminated corneal transplants or medical equipment, or, as in the case of kuru, which plagued the Fore people of Papua New Guinea: cannibalism.

I closed my laptop, powered off the sequencer, and started the Sprinter.

My mind raced.

For people like Tiffany and me, the upgrade was performing as intended.

But if the upgrade had gone terribly wrong somehow, a prion disease was exactly the type of malfunction you’d expect to see.