HOMETOWN VIRUS

Marburg’s Got a Level-4 Pathogen

When people ask where I’m from, my stock response is: “A sleepy little German university town called Marburg, where the deadly virus of the same name first broke out in 1967, infecting 31 people and killing seven.” If that doesn’t register, I explain that my hometown is an hour or so north of Frankfurt.

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Marburg—the virus, not the town—is basically just like Ebola. When it’s not busy putting people in their graves, it’s causing blood to leak out of each of the body’s main holes and even new ones of its own creation. For residents and scientists, the virus remains an important part of Marburg’s lore. Like a Lovecraftian fishgod who dwells in the city’s charnel fundament, it is ingrained in the region’s psyche and largely unspoken of.

At the time of the first infections, the Marburg virus had a recorded fatality rate of 25 percent, a number that–given the village’s small population and the hysterical reception of its otherwise sleepy local media–was amplified to elicit quarantine-level fear in the city’s residents, despite the disease being relatively manageable. By the time outbreaks were noticed in the Democratic Republic of Congo in 1998 and Angola in 2004, the lethality had risen to between 80 and 90 percent. Put another way, the Marburg virus is today defined as a Biosafety Level 4 pathogen; HIV is Level 2.

Michael Hilberger, 82, is a survivor of the original outbreak of the Marburg virus back in the Summer of Love. Hilberger remains a robust and hearty man, despite a heart attack he suffered just four weeks prior to my visit and the devastating loss of his wife just eight weeks before that. He wasn’t too excited about telling the story of his experience with Marburg and kept pointing at old newspaper clippings he’d prepared for my visit. “This’ll tell you all you need to know about the monkey disease.”

Marburg’s earliest symptom is a boiling-hot fever that resembles your basic flu, so it took a couple days of people getting sick for local doctors to realize something was fishy. By the time four people had been hospitalized, it became clear that the epicenter of infection was Behringwerke, a pharmaceutical corporation named after Emil von Behring, the first Nobel laureate in the field of physiology and medicine. It was then narrowed down further—all the victims worked in Behringwerke’s monkey lab.

At the time, Hilberger was working as a research scientist developing new thickening agents for human blood by taking samples from monkey brains. “I would walk over to the monkey house from our lab at nine or ten in the morning, and the monkeys would already be dead and laid out for me,” Hilberger said. “I’d cut open their heads and remove the brains. It was a little strange when I first started doing it, but I thought, ‘What the hell, I’ll just pull through it.’” Given the messy nature of his work, it isn’t exactly surprising in hindsight that Hilberger was among the first to contract the virus.

In the 60s, monkeys used for European research were often hunted in Uganda and exported to the continent. Instead of destroying a primate if it was sick, monkey farmers simply shipped it off to a place on Lake Victoria in Kenya that came to be known as Monkey Island, where they figured the monkey would either die or go on living in feeble misery—it didn’t matter which. Eventually though, because of surging medical demand, monkey suppliers short on inventory started returning to Monkey Island and grabbing monkeys that, by virtue of not being dead, appeared to be in good enough shape for the lab.

Shortly after the disease was connected to Behringwerke’s primates, hysteria set in. National tabloids such as the Bild-Zeitung squirted out daily headlines about the “Green Monkey disease.” A desperate, and futile, search for a cure got under way. According to Hilberger’s niece, a small team of scientists flew to the Congo in the hopes of learning more about Marburg, consulting indigenous witch doctors and every other local expert in the process. When the European doctors showed photos of the diseased to the natives, they were plainly told the culprit was vampirism.

Marburg virus spreads through direct contact with blood or bodily fluids. Its high lethality results from infecting the macrophages, which is what your white blood cells turn into to devour pathogens, and additionally disturbing blood coagulation and infecting the vascular walls, which then become permeable to all sorts of weird, foreign, and disgusting intruders. Severe hemorrhagic fever syndrome sets in, furthering the monstrous disturbances in the vascular system. Those who died in Marburg bled from the genitals, mouth, nose, eyes, and through the skin. Necessary blood infusions resulted in unstoppable bleeding from the needle pricks.

Because of the fever, Hilberger spent most of the time he was infected in a state of delirium. The acute phase of his infection lasted about 12 weeks and was followed by nearly a full year of recovery. When he was released from the hospital, however, he and his family were confronted with an alternate consequence of having been exposed to the virus: Fellow residents no longer wanted anything to do with them. Storeowners were paranoid about “the people from Behringwerke’s bringing the disease into their shops,” as Hilberger put it.

Hilberger did eventually return to work, though he never dealt with monkeys again. The company, I guess oblivious to potential bovine infection, soon after made the switch to cow blood in the quest for valuable blood-thickening solutions.

At the Behring archive, where everything related to the scientist and his famous laboratory is housed, I rifled through the massive array of press clippings from that era. Ulrike Enke, a lovely lady whose field is the study of the art of medical illustrations, oversees the archive and had prepared two folders for me. The folders contained articles as well as a couple dozen dramatic tabloid headlines featuring all kinds of off-putting combinations of the words death, dead, monkey, disease, mystery, kill, infection, victims, and virus.

Not surprisingly, I would eventually find peppered in other, non-Behring-owned literature several instances of Marburg’s potential use as a biological weapon. Ken Alibek, who used to run the Soviet biological-weapons program before he defected to the United States, wrote about the Marburg virus in his book Biohazard. He explains that the Soviets had been working on enhancing the virus to create insidious airborne artillery. One important scientist on the case was Dr. Nikolai Ustinov, who would eventually die after contracting the disease during his research. He left behind an even more powerful strain, however, called “Variant U,” so named in an aptly backhanded homage to the man. Alibek also claims that Dr. U.’s strain was turned into a weapon and ultimately approved by the Soviet Ministry of Defense in 1991. Around the same time, according to scientists and researchers familiar with the subject, the Russians were also experimenting with developing an Ebola-Marburg-smallpox chimera virus that built on Ustinov’s research.

These transmission electron micrographs depict typical strains of the Marburg virus, whose discovery in 1967 made a whole new classification of RNA viruses necessary: Filoviridae, named so for their threadlike appearance. To this day, Marburg and Ebola are the only known viruses of this kind.

Werner Slenczka is the scientist who first identified the mysterious Marburg pathogen. He lives at the top of a steep, curvy driveway on a hill just a few miles from where I grew up. He met me halfway on the path leading up to his house, wearing shorts and enjoying his newest habit: smoking cigarettes. I was escorted through his living room on the way to a terrace of limited natural light and furnished with dark wood.

When asked how realistic the weaponization of Marburg is, Slenczka was blunt: “Biological-weapons strategists must be pretty damn desperate if they jump at something just because it has a high lethality,” he said. “You have to know how to disperse it first, and that’s not an easy thing to do with Marburg.” He explained to me that, theoretically, the most efficient way to spread pathogens is via aerosols. But the Marburg virus can’t survive in this compressed environment, he added, so essentially the only way to contract the disease is via direct contact. Here’s the rub: Marburg can, however, be passed along via asymptomatic people or primates who once exhibited signs of the infection but currently appear to be in remission. Meaning the virus lies dormant somewhere in your body, undetected by the immune system, but still entirely infectious. This is known as reservoir hosting. In one case, a Marburg outbreak survivor infected his wife a couple months after his symptoms had disappeared, probably from fucking her. Monkeys that were dead and butchered remained infected as well, passing the virus on to lab workers like Hilberger charged with handling the internal organs. Interestingly, none of the handlers of the live animals ever transmitted the disease.

Addressing the topic of cross-species infection, Slenczka noted, “Yes, theoretically anything can happen, and Marburg could change. But even if that happened, which people have been speculating about a lot, that doesn’t mean it will easily spread from one person to the next.” There are several factors involved, but primary is that of the virus’s receptors. Measles and influenza, for example, are highly contagious because the cells in your nose are like a glue trap for bacteria, and that’s where their cellular receptors are conveniently located. Other viruses, like Marburg, have to get to certain cells inside the body before they can infect anyone. Judging from its particle makeup, there’s no real reason Marburg isn’t as contagious as measles, but it most likely has to do with the absence of any hyper-effective receptors.

As for the smallpox-Ebola-Marburg-Chimera rumor, quoth Slenczka: “Smallpox is a DNA virus, Marburg an RNA virus—how is that supposed to go together?”

Nevertheless, Marburg is extremely lethal and therefore worked on only in labs, like the one found at Philips University in Marburg, that meet BSL-4 requirements. Nothing is allowed to leave these labs that has been in contact with a pathogen. All liquids, containers, and tools have to go through an autoclave, and the air is heated before it goes out through the filters to make sure nothing can escape. The research staff wear full body suits during a shift and undergo a detailed security procedure involving multiple sterilizing showers afterward. Somehow there remains a large pool of students who would kill to work with Ebola or Marburg. “It appears to be sexy somehow,” Slenczka laughed.

Werner Slenczka holding a copy of —a compendium on zoonoses he wrote with fellow scientists. The picture on the right shows one of the patients of the initial outbreak during the “pre-final” stage.

Slenczka began his studies in Marburg and went on to universities in Munich and Zurich, studying a wide range of subjects, from biochemistry to human medicine, including a full year in the pathology department of Frankfurt University. He explained that when he first got into virology he wasn’t certain he’d stick with it, but his work on Marburg changed all that, pigeonholing him as a type of fearless virus commando. “The Marburg virus came along,” he told me, “and after that I couldn’t change to another institution because wherever I applied they said, ‘If you started working here, we’d need to build a maximum-security lab especially for you.’” It was as though he’d caught the virus simply by identifying it.

When Marburg first came around, there was a fairly uninformed and misguided “vaccination” used on residents—no such vaccination was thoroughly tested, and to this day no approved combative injection exists. Dr. Pierre Formenty, a World Health Organization scientist and expert on the Marburg virus, explained to me that though there are several candidate vaccines in development, bringing one to market is an extremely time-consuming and costly process. Slenczka put it more plainly: “You always need a clientele for a vaccine.” His point is that no one in the Western world would use the vaccine, and even in Africa it’s not such a massive risk considering its limited ways of transmission. The problem with diseases like this is that you can’t really test it on humans, and without testing you’re not likely to get an effective vaccine. And even when there is a successful vaccine implemented, there are adverse effects.

Slenczka went on at length about the smallpox vaccine in particular, discussing how it ultimately gave rise to several other lethal diseases, among them HIV. His argument is that if smallpox were still around it would have expedited the deaths of people who had contracted HIV, thereby preventing the massive numbers of infections and eventual deaths the world experienced throughout the 80s and 90s. He says most aren’t eager to publish contrarian ideologies of this nature because it’s awkward (some might also say wrong) to sound critical of the smallpox vaccine. But he believes this “sociology of pathogens,” as he refers to it, is what prevented an HIV epidemic in humans from existing centuries before it actually did. Which, OK—I’m just not sure that’s the end of the argument. To nonscientists, Slenczka’s tune plays out in a sort of choose-your-own-death scenario.

His point, though, is important: While vaccines are obviously critical and save lots of lives, they also pave the way for diseases to mature in people with weaker immune systems—like the folks who were vaccinated and didn’t have the decency to die of smallpox, or later tuberculosis or diphtheria. “If you close one hole, it’ll spill from another one,” Slenczka said, referring to this phenomenon.

The author Richard Preston contacted Slenczka twice when he was conducting research for his book The Hot Zone (which served as a loose basis for the Dustin Hoffman/Rene Russo vehicle Outbreak) and other novels, but Slenczka claims he didn’t have the apocalyptic vision Preston was hoping he would deliver. Slenczka is emphatic, making sure to note that he always tries to communicate a realistic picture of the virus but that people are more inclined to hone in on the worst possible scenario. Slenczka tells a quick, true story from long ago: Two young brothers from Marburg used to share a double bed each night. One brother eventually contracted and died from Marburg. The other didn’t miss a single day of school.

A disease like the Marburg virus is an example of what often happens in research labs working with limited resources and under extreme pressure to produce results. Alternative disease-ridden subjects—rodents, felines, and primates, imported and domestic—necessarily stand in for humans, with mixed and occasionally mortifying results. “The threat with Marburg, or Ebola for that matter, is that they can emerge in remote places and be amplified in health-care settings,” Dr. Formenty of the WHO said, “sometimes without being recognized.”