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I shook my head.

“Would you like to? Because I have it all right here.”

“Yes.”

“Then answer my question. What does the inhibition of PDE4B do?”

I shouldn’t have known, but as I considered the question, I remembered reading an article eight years ago in Scientific American, where PDE4B had been discussed in the context of gene therapies for mental illness.

I said, “It’s linked to low anxiety and high problem solving. Well, at least in mice.”

“Correct. It’s been inhibited in you. What if I were to tell you that your entire IGF system had also been altered and your GRIN2B gene mutated?”

Four years ago (and six months, eleven days to be exact—How did I know that?) I’d read an abstract on the IGF system. In fact, I could see a perfect image of it in my mind’s eye.

“High learning and memory,” I said.

“You just know that off the top of your head?”

“I remember reading about it.”

“FOXP2?”

I shook my head, certain I had never heard of that gene before.

“It’s linked to learning stimulus-response associations faster. How about NLGN3?”

I said, “Enhanced learning and spatial-learning abilities.”

“GluK4.”

“Low bipolar risk and higher cognitive function.”

Edwin looked up at me. “Your cognition, memory, concentration, pattern recognition—it’s all been targeted for enhancement. Have you experienced gains across these areas?”

“Yes.”

“Since when?”

“Over the last three weeks.”

“Do you get how astounding this is?”

For a moment, I couldn’t speak. I had suspected that something had been done to me, but to hear it confirmed knocked the wind out of me.

“Why did you have Dr. Strand run another genome analysis?” Edwin asked.

Interesting. They had intercepted my new analysis before my doctor could even tell me the results. They must have been monitoring me closely after Denver.

I said finally, “I told you. I wanted the evidence for myself. And because I suspected my LRP5 gene had been upregulated, and perhaps modified.” In the context of genetics, upregulation means the gene has increased its expression or effect. Downregulation means the opposite. If you have OPN1MW, you can see color. If it’s downregulated, you’re colorblind.

Edwin looked at his tablet for a moment, quickly scrolling the pages.

“LRP5 is increased bone density?” he asked.

I nodded.

“When did you begin to suspect?”

“Five weeks after Denver, I started experiencing a deep pain throughout my body.”

“Why did you hide this from me?”

“Again, I wasn’t hiding it. I wasn’t sure what was happening, which is why I asked Dr. Strand—”

“We could’ve run a new analysis. You work for the Gene Protection Agency, for chrissake.”

“I wanted to know if it was just some weird side effect of the virus or something worse before panicking my employer. I wanted to come to you with information, not conjecture. I haven’t even told Beth yet.”

“I’m going to read you a hit list of the other genes that were targeted for down-or upregulation. In most cases, they’ve been mutated to previously unknown polymorphisms. In a few cases, short, novel DNA sequences have been edited in, presumably to improve their function.”

“There’s more?”

“Oh, yeah.”

I leaned forward.

“SOST.”

I said, “Bone-loss resistance.”

“MSTN.”

“Lean, large muscles.”

“SCN9A, FAAH-OUT, and NTRK1. Do you know any of those?”

I shook my head.

“They’re associated with a higher pain tolerance.” He went on: “HSD17B13. That’s low risk of chronic liver disease. CCR5.”

“HIV resistance?”

“Yep. FUT2, IL23R, HBB, PKU, CFTR, HEXA, PCSK9, GHR, GH, SLC30A8, IFIH1=MDA5, NPC1, and ANGPTL3.”

I said, “In the order you read them…resistance against norovirus, Crohn’s disease and ulcerative colitis, malaria, ochratoxin, TB, coronary disease, cancer, the next four types one and two diabetes, Ebola, and I believe the last one reinforces lipid and cardiac health.”

“Wow. Okay. These next few are kind of weird. EGLN1, EPAS1, MTHFR, and EPOR.”

“I read an article about that gene system a couple of years ago. It’s typically found in Tibetans, right?”

“That’s right. They support life and body function at high altitude. BHLHE41=DEC2, NPSR1, and ADRB1.”

“I don’t know those.”

“They lower your sleep requirements. APOE, APP, NGF, NEU1, NGFR.”

I knew these genes. I’d read an article about them in Nature Genetics during a flight to Minneapolis, seven years ago.

“Lower Alzheimer’s risk,” I said.

“CTNNB1.”

“Don’t know that one.”

“Radiation resistance. CDKN2A and TP53?”

“Low cancer risk,” I said.

“TERT.”

“Isn’t that related to aging?”