Virus: The Day of Resurrection (13 page)

As he peered into his microscope, Professor Kaji of Osaka University’s Research Institute for Microbial Diseases muttered, “This is bad. This is very, very bad.”

To stop the spread of Tibetan flu, universities and laboratories throughout Japan were working frantically on a vaccine for the influenza A-Minus virus. But more than actually working on the vaccine itself, they had been reduced to sending research staff out to secure the fertilized eggs needed to do the work. Throughout the latter half of April, shipments of chicken eggs had plummeted to two thirds of what they had been, and with the spread of Newcastle disease, further declines were expected. Already, eggs were selling for forty yen apiece on the retail market. In the poultry industry, one dealer after another was going bankrupt, watching helplessly as entire flocks were wiped out in a matter of days. The government announced that they were considering importing eggs from abroad, but already Newcastle disease had appeared in Europe and America, and with the entire world in a scramble to deal with the influenza, a ruckus over imports hardly seemed to be in the cards. On top of this, with the “new strain” of Newcastle disease, hens didn’t just stop laying eggs; many of the females thought to have acquired immunity either laid mostly dead eggs or eggs that died around the fourth day thanks to incipient infections.

Viruses, unlike bacteria, cannot reproduce outside of living cells, so unless the cells of a living embryo were present inside a developing egg—a fertilized one that had been incubating for around ten days—it was utterly impossible to grow a culture of the influenza virus inside an egg.

In a desperate effort to keep the work of producing a vaccine going, microbiologists joined forces with Health and Welfare–related offices to scrounge for duck and quail eggs. At the same time, research continued into whether or not there was anything besides the chicken egg that could function as a unit for the mass-production of viral cultures. As for growing cultures in tissue samples, it was also possible to use living human or animal cells grown in culture solution. Cells from the kidneys of monkeys were frequently used for tissue culturing, though they were hard to handle, and there was not sufficient time to gather enough to produce millions of doses of vaccine.

In the midst of such a furor, Professor Kaji was attempting to isolate the Tibetan flu virus from the lung tissues of the first person in Osaka to have died of it. The victim was a forty-two-year-old man. Three days after contracting influenza, he had developed a violent, suffocative bronchitis and exhibited symptoms of pneumonia to go along with it. At last he had died, despite his doctor’s treatment and the medical regimen administered. The rate of death from Tibetan flu was unusually high, especially in Asia, and reports had even come in from some places telling of victims who had died
without becoming aware of any symptoms
, so Professor Kaji had focused his attention on the first person to die of an A-Minus-type infection in Osaka. He had been a salaryman in robust health with no particular problems in any of his organs. The tissue sample from his lungs was first liquefied and then run through a super-centrifuge, to which a microbe filtration device was attached to screen out the assorted germs. The filtered, germless fluid was then transferred to a culture of cells from the kidney of a Japanese macaque that were being grown in culture solution at thirty-nine degrees Centigrade. Forty-eight hours later, human blood would be used to check for corpuscular agglutination. If the influenza virus had grown inside the living cells to surpass a density of one million virions per milliliter, a phenomenon called a “crosslinking reaction” would occur, and the corpuscles would agglutinate. By diluting the culture solution in many gradual stages and studying the degree to which the blood cells were caused to agglutinate each time, it was possible to learn the number of virus particles present. After that, the culture would be mixed with antibodies for the A-Minus type, obtained from the lymph of house mice that had been infected beforehand—to observe the neutralization effect. Prior to that, however, at the stage of estimating viral density by way of the corpuscular agglutination reaction, the professor had tried adding drops of blood not only to the culture solution, but also to the liver cells themselves. As soon as he peered into his microscope to look at that fluid, those muttered words had escaped from the professor’s mouth.

“This is bad!”

A part-time lab assistant—a young coed who had just started medical school—turned around to look at him. “What’s wrong?”

“I’m seeing
corpuscular adhesion
.”

The apple-cheeked woman peeked at what he was doing from over his shoulder. “What does that mean?” she asked. “Flu viruses always make blood condense, right?”

“This isn’t simple condensation. It’s adhesion. Have a look. You see? The corpuscles are being adsorbed onto the surface of the kidney cells.”

“No kidding,” the med student said, fascinated, as she looked through the eyepiece of the microscope.

“So basically,” Professor Kaji said, “what we’ve got here is an influenza A-Minus virus with characteristics of the HA type.”

“The HA type?” she said, her voice rising half an octave. “Is there such a thing?”

“You’ve never heard of it? It’s the contagion that causes a bug called parainfluenza. Tohoku University first discovered a strain of its virus group in 1953. It’s the one that’s also been called ‘Sendai virus’ and ‘influenza D.’ ”

“Influenza
D
?” Her eyes widened at that. “Flu just has the A and B types, doesn’t it?”

Professor Kaji stared for a moment at the face of this young student—if she were any younger, he thought she’d probably reek of baby formula—and then just shook his head and resignedly began to speak. “Now, see here. Just because it’s called influenza, it doesn’t mean there are only two kinds. What we usually call influenza actually comes in three types: A, B, and C.”

“Well, I didn’t know about C.”

“That’s because it never causes any major epidemics. It’s constantly going around here and there, but most people have antibodies for it, so it doesn’t get far. Even within the influenza A species, there are various types of flus, flus that people get, that horses get, that pigs get, that ducks get, et cetera et cetera.”

“Wow, so even pigs can catch the flu?”

“Absolutely. Swine flu is a lot like the kinds that humans get, especially the A types. During the time of the Spanish flu, pigs frequently got ill. By the way, one relative of the influenza A virus is the virus that causes fowl plague.”

“Oh? That bug that all the chickens are catching now?”

“No, what’s going around now is
false
fowl plague. Newcastle disease. It’s a relative of these, but a little different. By the way, even among the influenza A contagions, the antigens aren’t all the same. Influenza A—the one that caused the Spanish flu back at the end of World War I, the A1 subtype which tore through Europe between ’45 and ’48, the A2 subtype that caused the Asian flu, and now this new A-Minus too—the structure of each and every one of these antigens is a little different from all the others.”

The girl was watching his eyes carefully, a look of surprise on her face.

“In the same way, the influenza B viruses have two subtypes: the B1 and B2 forms. And in just the same way that a new strain of influenza A developed recently, it’s possible as well for new B subtypes to emerge. And C subtypes too—”

“So, I see,” the girl began fearfully. “The HA type is another different kind?”

“Yes, just like there’s a paratyphus that acts a lot like the real typhus, there’s also a disease called ‘parainfluenza’ that has the same kinds of effects as flu. The HA virus is the contagion for that. The first type of parainfluenza virus includes the HA2 virus and the Sendai virus. The second type includes the California Group virus, which Dr. Robert Chanock isolated. The third type includes the HA virus and the Shipping Fever virus that hits livestock. Finally, the fourth kind is the M-25 virus. Out of all those, only HA 1 and 2 cause adsorption reactions like we’re seeing here.”

The girl’s mouth had fallen open. “And all those are flu viruses?” she asked.

“They are. Along with mumps and Newcastle disease, they’re all myxoviruses, relatives of flu.”

The coed shuddered in disgust. “There are that many kinds of flu out there?”

“There are,” Professor Kaji said with a glum little sniff. “I don’t know why, but these myxoviruses—especially the influenza kind—mutate into new types very, very easily. The virus that causes measles? Doesn’t change at all. You get it once as a child, and you’ll never have it again for the rest of your life. Polio viruses have Type I, Type II, and Type III, but it’s just one of them that spreads, so we don’t see new kinds popping up all the time like we do with the flu.”

“So this virus …” the student began as she gestured over to the microscope. “Is it Type 1 of HA? Or Type 2?”

“We don’t know yet.” Professor Kaji shook his head. “From here on, we’ve got to use all kinds of lymph to study the neutralization reactions. We’ll have to order a variety of lymph samples, though my gut is somehow telling me this is a new type.”

“I hate this,” the student said, her face twisted like she was about to start crying. “
Yet another
flu might be going around.”

“Parainfluenza usually causes serious suffocative bronchitis in children, but this one is taking down adults.”

“Is it possible to get a double infection of this with influenza A-Minus?”

“Probably,” Professor Kaji replied. “There have been quite a few cases where people got both A1 and A2 together. These little guys are very contagious and their rate of mortality is high, so that would make for one heck of a problem. The effectiveness of each vaccine is completely different from one to another, so we’d have to make vaccine for both the A-Minus and the HA types.”

The girl sneezed.

I wonder if she isn’t predisposed to allergies?
Professor Kaji wondered.
She could be one of those types
who can develop symptoms of a disease just by listening to a detailed description of it.

“Professor, I’m going home now,” she said, her face turning pale as she spoke. “My head hurts. I wonder if I’ve caught it just by being here.”

“Did you get sick when the Asian flu was going around?”

“I did,” she said, getting up. “I was still in elementary school. They closed the school, but most of us got it anyway.”

“We ought to take early measures this time too,” the professor murmured, “but since the new semester’s just started …”

The virus Professor Kaji had discovered was a completely new kind. It was classified as a Type 6 parainfluenza and given the name HA3 Kajivirus. It caused serious respiratory disease in adult men and women. Not only was it extremely contagious, another horrifying fact soon became clear: it was confirmed that when double infections of HA3 and A-Minus viruses occurred, the rate of mortality skyrocketed to nearly seventy percent.

On April 17, Beijing’s People’s Republic of China Chemo-Sero Vaccine Research Institute—which had once made a spectacular contribution to virology with its isolation of the trachoma virus—pointed out the sobering fact that the current vaccine for the A-Minus virus produced
unusually weak
antibodies in human lymph. Specifically, they were saying that in order to generate sufficient immunological protection, not three but almost five times as much vaccine as was needed for A2 influenza vaccination would be necessary. Further, a person who had recovered from the disease once could be infected again, and that those who were infected would be difficult to cure. Dr. Long Hai of the same institute reported that the A-Minus virus did not grow very well inside developing chicken eggs (like all influenza viruses to date, it hardly grew at all in the allantoic cavity inside the egg, preferring the amniotic cavity that enveloped the embryo), and grew better in cells from human embryos or monkey kidneys. This finding suggested that although the new virus was close to the A group in terms of antigen structure, it might rather be more appropriate to refer to it as an altogether new “Influenza E” class of virus. Also, this was accompanied by a reference opinion that said the A-Minus influenza might easily cause not only respiratory complications, but also complications of the nervous system. The virological research department at Rhône-Poulenc, one of France’s mass-producers of pharmaceuticals, reported that this “complication” could easily cause heart attacks due to the sympathetic nervous system being affected—especially in cases where patients already had heart problems.