* * *
Martin’s first thought was to let the phone ring, since it couldn’t possibly be as important as what he was doing right now, but then someone answered it.
“Dr. Martin,” some vaguely familiar lab tech called from Martha’s desk. “I have a Dr. Rucker for you. He says it’s important.”
The name sounded familiar, but his focus was on the young girl in front of him, and he didn’t want the distraction of searching his memory. “It’s always important. Tell him we’re closed,” he said gruffly, and then thought better of it. “Don’t tell him were closed, take a number and someone will call him back.” He turned back to Martha. “What do we do now?”
Before Martha could respond, they were interrupted again. “I’m sorry, Dr. Martin,” said the lab tech, “but I think you need to take this phone call. He says he’s infected with the Hybrid virus.”
The name Rucker finally made a connection in his brain: Colorado Springs.
“This is Nathan Martin.”
“Phillip Rucker; I am the Coroner for Colorado Springs. I’m calling because I have information about both the Colorado Springs virus and the Hybrid virus.”
“How do you know those names?” asked Martin.
“I got them from Klaus Reisch.”
“That means nothing to me,” Martin said. “I’ve already been duped once this week, and my suspicion level is running at an all time high.”
“How about Amanda Flynn?” Rucker said with obvious annoyance. The phone line was silent and Phil went on. “The Colorado Springs virus incites a severe encephalitic process; it’s as bad as herpes encephalitis,” Phil said.
Martin’s mind raced with the mention of herpes.
“A mixture of herpes and Ebola,” Phil said suddenly.
“How do you know that?” Martin said angrily.
“That’s not important. Look for a third component. The infection stimulates the formation of a thick layer of stem cells lining the ventricles. The Colorado Springs virus stimulates cell growth in the brain. It’s that growth that kills people.”
“Germinal matrix?” Martin said skeptically. “There has to be another explanation. No one has ever found viable stem cells in an adult brain.”
“That’s not correct. There have been several reports dating back to 1957.” Phil said. “There are large pluripotential cells interspersed among the ependymal cells and the subependymal layers below. Whether we call them stem cells or not is irrelevant. I believe that this virus interacts with those cells and stimulates their growth.”
“Interesting theory. I haven’t seen any specimens, but you have, so for the moment I’ll entertain it. Any clue what this third component might be?”
“It has to be human DNA.”
“Possible,” Martin said thoughtfully. “The original virus was created under less than optimal conditions. It’s possible that their herpes specimen came by scraping someone’s mouth. The herpes virus inserts itself in the donor’s DNA, and when they tried to recover the virus, they got a little more than they had expected. Gene therapy.” It had taken billions of dollars and millions of hours and experiments to trick small viruses into incorporating pieces of human chromosomes, and then delivering those genes to specific sites. Avanti had managed it without even trying.
Adam Sabritas had followed Martin to the phone and had been quietly listening. “I found it,” he said, vibrating with nervous energy from head to toe. Martin turned towards the young man. “I finished sequencing part of the Colorado Springs virus. About half of the DNA is human.”
“Did you get that?” Martin asked into the phone, watching the frequency of Sabritas’s vibration increase. He looked like an elementary student who had an answer and would explode if his teacher didn’t call on him quickly. “What else did you find, Adam?”
“It’s the short arm of chromosome eleven.” Sabritas was breathless with excitement. “It’s a purine receptor locus, but it’s incomplete.”
“A purine receptor?” Martin questioned thoughtfully. It was possible; purine receptors were small protein complexes within the cell membrane. When the correct key was fitted into the receptor, a cascade of chemical reactions within the cell occurred, most of which were involved with cell survival.
“That would account for the various presentations,” Phil said into the phone.
Sabritas had spread out his computer sheets across Martha’s desk and kept stabbing parts of them with a thick, stubby finger, saying, “Look at this,” over and over again. “I’m sorry, what did you say, Dr. Rucker?”
“I said that an incomplete purine receptor gene would explain the various presentations. In most people, the virus acts in typical fashion. It invades the cell, inserts its DNA into the host’s DNA, creates millions of new copies of itself, and then destroys the cell. The immune system does the rest. As other cells become infected, they begin to display bits of the virus on their MHC proteins, and the cells are destroyed by immune cells. That’s what causes all the destructive changes and the inflammation. The psychiatric presentation makes sense as well, because the cells most vulnerable to these viruses are located primarily in the limbic system.”
Martin had pushed aside Sabritas’s chart and turned the speakerphone on. “I’ve put you on speaker phone. I want some of my staff to hear this,” he said while sitting in Martha’s chair.
“The limbic system?” A Ph.D. candidate had overheard part of the conversation and had drifted closer to the phone and Adam Sabritas.
“Emotional centers of the brain,” Sabritas answered automatically.
“I know that—” the student answered defensively, but Martin’s glare cut off the rest of his thought.
A crowd had gathered around the speaker. “Go on, Dr. Rucker,” he said.
“I’m guessing that in a few cells the purine receptor gene is repaired and activated. Instead of producing viable viral particles, the cell produces the actual receptors.”
“This sounds a little like Borna Disease,” the graduate student said much too loudly. Every head turned towards him. Even Phil hadn’t heard of Borna Disease. The student’s face flushed with the sudden attention. “It’s a viral infection in sheep and cattle. It causes unusual behaviors in the animals.” He stammered a little. “Years ago people thought that it might cause depression in humans.” A dozen faces stared at him, waiting for the relevance of his interruption. “It’s an RNA virus that replicates in the cell nucleus, but it doesn’t destroy the cell. It causes unusual proteins to be elaborated across the cell membrane.”
Satisfied, people started looking at one another.
“Interesting. .” Martin said stammering over the grad student’s name.“Yes, it is,” Phil added. “Most of the purine receptors are associated with apoptosis of neuronal cells, but some, instead of initiating programmed cell death, cause the normally inert neurons to either grow or to differentiate. It stands to reason that with the additional receptors, the cells become hypersensitive to their ligands. That’s what causes the reformation of a germinal matrix, and it is this unrestrained and rapid growth at the base of the brain that kills people.”
Everyone was silent for a moment, digesting Phil’s theory. “I have to tell you, I’ve barely heard of purine receptors.” Martin looked around the crowded office. “So now we know how it kills, what do we do about it? Fighting the encephalitic process with the usual anti-inflammatory agents isn’t going to help. How do we stop these cells from dividing?”
“I don’t think we can,” Phil said.
Most of Martin’s staff nodded their heads.
Phil continued, “The key is to start treatment before the combination of inflammation and growth are fully developed.”