I didn’t need to finish the sentence; Wally was already punching something into his phone. Within a few minutes two people appeared, a prematurely balding man in his thirties and a similar-aged woman with prematurely gray hair. It was unfortunate, I thought, that they’d been partnered, since together they gave the impression that enrollment in the Epidemic Intelligence Service sucked the life out of you. Or perhaps that was an accurate impression; these two were already overburdened to the point of exhaustion. Nonetheless, they attended to Wally’s instructions with rapt attention, both of them taking notes.

“So . . . we’re looking for ART survivors who return to an emergency department—what, months later?” the woman—Erica Ogino—asked.

I nodded. “Yes. At least three or four months out from recovery—we think these are all people who got sick early on, in the very first wave, and came back months later with sudden neurological symptoms. Start a database and get every shred of detail you can about them—the time course, gender, age, presenting symptoms, progression, outcome, location, treatment, confounding factors, general health, what treatment they received during ART; everything. Maybe these posts are a case of true-true-and-unrelated, but we need to look for patterns.”

A look of intrigue lit the balding guy’s face. “What could cause symptoms that late? Is this some kind of reinfection?”

“We don’t have any—” I began, but Erica interrupted me, tapping a finger against her chin. “The herpes virus.”

“What, you think these people have herpes?”

“No, I don’t think they have herpes. But that virus family is known for establishing a dormant presence in nerve cells. It hangs out in your neurons until something reactivates it, right? That’s why people who’ve had chicken pox are at risk for shingles later on. Or think about herpes simplex: years and years later it can cause encephalitis. These patients present with dramatic onset of fever, seizures, and altered mental status, and nobody has any idea why at first because the original infection was often so long ago. Maybe this virus can do the same thing. Maybe it causes some form of cerebral inflammation when it reemerges.”

If Wally’s expression was anything to judge by, he found this idea as unsettling as I did. Over the centuries, viruses have evolved different mechanisms of survival. Some, like influenza or Ebola, replicate in an explosion—possibly killing their hosts in the process but relying on the afflicted person to first pass them on to others by way of coughing or sneezing or bleeding or diarrhea. But some, as Erica had correctly stated, have engineered an even more ingenious means of survival. They bide their time by setting up long-term residency in the cells of their hosts, waiting for some stressor to jolt them back into action. Close to one hundred percent of the world’s adult population harbor at least one of the eight members of the Herpesviridae family in their bodies, for example, putting them at risk of recurrent mononucleosis or herpes or shingles. Occasionally, such a virus could affect the brain, either directly or by causing the body’s immune system to inflict its own form of terrible collateral damage.