Unlocked: An Oral History of Haden’s Syndrome Read Free Page A

the Black Death usually only attacked each of its victims once.
    Monique Davis:
    After the first several days of the Super Bowl flu we started getting some of the same patients back into the ER, only this time suffering from symptoms that resembled meningitis. After the first few, those of us on staff started looking at each other like,
you have got to be kidding me
. There was no way it could be coincidence that the same people who had been coming in for the flu were coming back with meningitis-like symptoms. The patients were different races, sexes, economic classes—the only thing they had in common was that they had the Super Bowl flu first.
    We started checking around at the other ERs to see if they had the same thing happening, and they did. Patients were coming back with what looked like meningitis. A lot fewer of them than in the first round. Maybe one in four or five. But it was definitely a second stage of some sort. Now, it’s possible for meningitis to be diagnosed as a flu. They share some initial symptoms. But for the same virus to exhibit flu-like symptoms, recede in most patients and then return like meningitis in a select few, that was new. And really sort of frightening.
    Benjamin Moldanado:
    One of the things that researchers don’t want to admit, because it sounds more than a little bit sociopathic, is how interesting the Haden’s virus was and what things we were hypothesizing in order to explain how it was doing what it was doing. With the meningitis-like symptoms we were confronted with the idea that a virus would attack a body, have the body’s immune response beat it back to greater or lesser extent and then as a result
wholly reconfigure
the way it was attacking the body—but only in a small number of the infected.
    Some of the early hypotheses included reactions to blood type or specific antibodies, a signal dependent on total viral load, or a response to specific environmental inputs, like temperature or air quality or even wireless signal. The last of those is an example of how just because it’s a hypothesis doesn’t mean it’s good, or useful. The point was that we were looking for some reason for the virus to apparently mutate, and that led us to be occasionally wildly imaginative in our speculation. It was the most intriguing puzzle that most of us had worked with, and we’re talking about a room full of people whose job it is to work on genetic material and other natural puzzles every day. It was fun—or as fun as anything could be up to the point when you remembered people were out there dying from the thing, and you were supposed to be putting a stop to that.
    Our problem was that none of our hypotheses fit the data. There was no obvious single environmental or physical factor we could find that would precipitate the change we saw in the virus. At least not in the short term. This was a problem because everyone wanted to know what they could do to counteract or at least avoid the second phase of the virus attack. And we had nothing to tell them. The only way you’d know whether or not you’d get the second phase of the attack was the headache, the stiff neck, and the other symptoms. You got it or you didn’t.
    This was widely considered an unhelpful response from the CDC researchers, and I don’t disagree with that. We were some of the smartest scientists, geneticists, and virologists in the world. We were working as hard as we could on the problem. And it seemed like the problem was working equally hard to elude us.
    Natasha Lawrence:
    The meningitis phase affected substantially fewer people than the flu phase but the mortality rate was substantially higher. About a quarter of the deaths associated with Haden’s came from people who died in the second phase. That’s because the phase didn’t just present meningitis-like symptoms. The virus invaded deep into the brain and started altering brain structure in significant ways. It was literally making the brain rewire its own