Influenza Virus Quotes

Awas! Cinta itu pembawa virus gila!

Every age has its signature afflictions. Thus, a bacterial age existed; at the latest, it ended with the discovery of antibiotics. Despite widespread fear of an influenza epidemic, we are not living in a viral age. Thanks to immunological technology, we have already left it behind. From a pathological standpoint, the incipient twenty-first century is determined neither by bacteria nor by viruses, but by neurons. Neurological illnesses such as depression, attention deficit hyperactivity disorder (ADHD), borderline personality disorder (BPD), and burnout syndrome mark the landscape of pathology at the beginning of the twenty-first century.

فيروس الزكام من السهل إلتقاطه لكن من الصعب العثور عليه !

Stomach flu” isn’t an influenza virus at all, but the term has entered the vernacular and helps perpetuate the pesky misconception.

Viruses are themselves an enigma that exist on the edges of life. They are not simply small bacteria. Bacteria consist of only one cell, but they are fully alive. Each has a metabolism, requires food, produces waste, and reproduces by division. Viruses do not eat or burn oxygen for energy. They do not engage in any process that could be considered metabolic. They do not produce waste. They do not have sex. They make no side products, by accident or design. They do not even reproduce independently. They are less than a fully living organism but more than an inert collection of chemicals.

What we really need is a game-changing influenza vaccine that will target the conserved—or unchanging—features of the influenza viruses that are more likely to cause human influenza pandemics and subsequently seasonal influenza in the following years.

And although better coverage of the outbreak’s evolution in the press couldn’t have stopped the influenza virus, a single newspaper headline in Philadelphia saying “Don’t Go to Any Parades; for the Love of God Cancel Your Stupid Parade” could have saved hundreds of lives. It would have done a lot more than those telling people, “Don’t Get Scared!” Telling people that things are fine is not the same as making them fine. This failure is in the past. Journalists and editors had their reasons. Risking jail time is no joke. But learning from this breakdown in truth-telling is important because the fourth estate can’t fail again. We are fortunate today to have organizations like the Centers for Disease Control and Prevention and the World Health Organization that track how diseases are progressing and report these findings. In the event of an outbreak similar to the Spanish flu, they will be wonderful resources. I hope we’ll be similarly lucky to have journalists who will be able to share necessary information with the public. The public is at its strongest when it is well informed. Despite Lippmann’s claims to the contrary, we are smart, and we are good, and we are always stronger when we work together. If there is a next time, it would be very much to our benefit to remember that.

The CDC and three other research groups submitted a paper for publication in the journal Science detailing how they had reconstructed the 1918 H1N1 influenza virus, using virus genes that had been identified in lung samples of patients who died during the 1918 pandemic.

new influenza virus emerges, it is highly competitive, even cannibalistic. It usually drives older types into extinction. This happens because infection stimulates the body’s immune system to generate all its defenses against all influenza viruses to which the body has ever been exposed. When older viruses attempt to infect someone, they cannot gain a foothold. They cease replicating. They die out. So, unlike practically every other known virus, only one type—one swarm or quasi species—of influenza virus dominates at any given time. This itself helps prepare the way for a new pandemic, since the more time passes, the fewer people’s immune systems will recognize other antigens.

Influenza. If you close your eyes and say the word aloud, it sounds lovely. It would make a good name for a pleasant, ancient Italian village.

For instance, one reason that the Ebola virus doesn’t spread widely among humans is that it is too efficient—mortality is as high as 90 percent—which

the CDC estimates an average of 34,000 Americans die from influenza each flu season.

The 1918 epidemic came in two waves, a mild flu in the spring of 1918 followed by the killer flu in the fall.

in Australia, India, New Zealand, South Africa, and the United Kingdom, where 45 percent of all civilian deaths were people aged fifteen to thirty-five.97 Death was not caused by the influenza virus itself so much as by the body’s immunological reaction to the virus. Perversely, this meant that individuals with the strongest immune systems were more likely to die than those with weaker immune systems.

All rather humbling, she added ruefully. Here we are in the golden age of medicine - making such great strides against rabies, typhoid fever, diphtheria - and a common or garden influenza is beating us hollow.

Influenza transmission is legendary. The dying cells in the respiratory tract trigger an inflammatory response, which triggers the cough reflex. The virus thus uses the body’s own defenses to infect other potential hosts.

Should we add the 40 to 50 million victims of the 1918 influenza pandemic to the 15 million who were killed in World War I, because the flu virus would not have evolved its virulence if the war hadn’t packed so many troops into trenches?

But it’s not just me, you know. The whole world’s sad,” I said. “It’s like a virus. It’s going to end badly. Glaciers melting, ozone depleted. Terrorists blowing up buildings, nuclear rods infecting the aqueducts. Influenza hopping from the pigeons to the humans, killing millions. Billions. People rotting in the street. The sun bursting open, shattering us eight minutes later. If not that, starvation. Cannibalism. Freakish mutated babies with eyeballs in their navels. It’s a terrible place to bring a child into,” I said. “This world. It is terrible. Just terrible.” I

At least etymologically speaking, when we talk about influenza we are talking about the influences that shape the world everywhere at once. Today’s bird flu or swine flu viruses or the 1918 Spanish flu virus are not the real influenza — not the underlying influence — but only its symptom.

But as the program got going, the smallest details became issues, even the very name of the disease. Pig farmers complained to the Centers for Disease Control that the name “swine flu” might frighten people away from eating pork. They asked, to no avail, that the flu’s name be changed to “New Jersey

What are the odds that a killer flu virus will spread around the world like a tidal wave, killing millions? “The burning question is, will there be a human influenza pandemic,” Secretary Leavitt told reporters. “On behalf of the WHO, I can tell you that there will be. The only question is the virulence and rapidity of transmission from human to human.

Influenza is caused by three types of viruses, of which the most worrisome and widespread is influenza A. Viruses of that type all share certain genetic traits: a single-stranded RNA genome, which is partitioned into eight segments, which serve as templates for eleven different proteins. In other words, they have eight discrete stretches of RNA coding, linked together like eight railroad cars, with eleven different deliverable cargoes. The eleven deliverables are the molecules that comprise the structure and functional machinery of the virus. They are what the genes make. Two of those molecules become spiky protuberances from the outer surface of the viral envelope: hemagglutinin and neuraminidase. Those two, recognizable by an immune system, and crucial for penetrating and exiting cells of a host, give the various subtypes of influenza A their definitive labels: H5N1, H1N1, and so on. The term “H5N1” indicates a virus featuring subtype 5 of the hemagglutinin protein combined with subtype 1 of the neuraminidase protein. Sixteen different kinds of hemagglutinin, plus nine kinds of neuraminidase, have been detected in the natural world. Hemagglutinin is the key that unlocks a cell membrane so that the virus can get in, and neuraminidase is the key for getting back out. Okay so far? Having absorbed this simple paragraph, you understand more about influenza than 99.9 percent of the people on Earth. Pat yourself on the back and get a flu shot in November. At

In 1918 fear moved ahead of the virus like the bow wave before a ship. Fear drove the people, and the government and the press could not control it. They could not control it because every true report had been diluted with lies. And the more the officials and newspapers reassured, the more they said, There is no cause for alarm if proper precautions are taken, or Influenza is nothing more or less than old-fashioned grippe, the more people believed themselves cast adrift, adrift with no one to trust, adrift on an ocean of death.

We follow what is happening with influenza virus strains in the Southern Hemisphere when it is their fall (our spring) to predict which influenza viruses will likely be with us the next winter. Some years that educated guess is more accurate than others. So is it worth getting the vaccination each year? I give that a qualified yes. It might or might not prevent you from getting flu. But even if it is only 30 to 60 percent effective, it sure beats zero protection. What we really need is a game-changing influenza vaccine that will target the conserved—or unchanging—features of the influenza viruses that are more likely to cause human influenza pandemics and subsequently seasonal influenza in the following years. How difficult would such a game-changing influenza vaccine be to achieve? The simple truth is that we don’t know, because we’ve never gotten a prototype into, let alone through, the valley of death. We need a new paradigm—a new business model that pairs public money with private pharmaceutical company partnerships and foundation support and guidance.

No medicine and none of the vaccines developed then could prevent influenza. The masks worn by millions were useless as designed and could not prevent influenza. Only preventing exposure to the virus could. Nothing today can cure influenza, although vaccines can provide significant—but nowhere near complete—protection, and several antiviral drugs can mitigate its severity. Places that isolated themselves—such as Gunnison, Colorado, and a few military installations on islands—escaped. But the closing orders that most cities issued could not prevent exposure; they were not extreme enough. Closing saloons and theaters and churches meant nothing if significant numbers of people continued to climb onto streetcars, continued to go to work, continued to go to the grocer. Even where fear closed down businesses, where both store owners and customers refused to stand face-to-face and left orders on sidewalks, there was still too much interaction to break the chain of infection. The virus was too efficient, too explosive, too good at what it did. In the end the virus did its will around the world.

Viruses like symmetrical shapes because symmetry provides a very simple means for them to multiply, and that is what makes viral diseases so infectious—in fact, that’s what ‘virulent’ means. Traditionally, symmetry has been something people have found aesthetically appealing, whether it is seen in a diamond, a flower or the face of a supermodel. But symmetry isn’t always so desirable. Some of the most deadly viruses on the biological books, from influenza to herpes, from polio to the AIDS virus, are constructed using the shape of an icosahedron. Is

But it's not just me, you know. The whole world's sad," I said. "It's like a virus. It's going to end badly. Glaciers melting, ozone depleted. Terrorists blowing up buildings, nuclear rods infecting the aqueducts. Influenza hopping from the pigeons to the humans, killing millions. Billions. People rotting in the street. The sun bursting open, shattering us eight minutes later. If not that, starvation. Cannibalism. Freakish mutated babies with eyeballs in their navels. It's a terrible place to bring a child into," I said. "This world. It is terrible. Just terrible.

If they would have acknowledged this [SARS] early, and we could have seen the virus as it occurred in south China, we probably could have isolated it before it got out of hand,” explained one infectious disease expert. “But they completely hid it. They hide everything. You can’t even find out how many people die from earthquakes.”2438 The foundation of the theoretical models is openness and cooperation for rapid detection of outbreaks of influenza. “Would they admit to it if it was here?” one Asian diplomat asked. “That’s the big question, since they deny everything left, right and center.

This is something that has been going on forever,” Craig Spencer, the director of global health in emergency medicine at Columbia University, says about the variability of human response to infection. “I wouldn’t be surprised if people are walking about with long Epstein-Barr virus, or long influenza. We all know someone who is low energy, who’s told to work harder. We have all heard about chronic Lyme sufferers, and those with ME/CFS. But they get written off.” Spencer understands something about how infections can do long-term damage, because he contracted Ebola while working in Guinea, fell ill upon his return to New York City, and then struggled with the virus’s ongoing effects. (Studies have suggested that the Ebola virus may linger in the body for years.) The difference between long COVID and other infection-associated illnesses is that it is happening “on such a huge scale—unlike anything we’ve seen before. It is harder for the medical community to write off,” Spencer told me. Indeed, many researchers I spoke with for this book hope that the race to understand long COVID will advance our understanding of other chronic conditions that follow infection, transforming medicine in the process.

More vigorous yet is the strategy practiced by the influenza, common cold, and pertussis (whooping cough) microbes, which induce the victim to cough or sneeze, thereby launching a cloud of microbes toward prospective new hosts. Similarly, the cholera bacterium induces in its victim a massive diarrhea that delivers bacteria into the water supplies of potential new victims, while the virus responsible for Korean hemorrhagic fever broadcasts itself in the urine of mice. For modification of a host’s behavior, nothing matches rabies virus, which not only gets into the saliva of an infected dog but drives the dog into a frenzy of biting and thus infecting many new victims. But for physical effort on the bug’s own part, the prize still goes to worms such as hookworms and schistosomes, which actively burrow through a host’s skin from the water or soil into which their larvae had been excreted in a previous victim’s feces. Thus, from our point of view, genital sores, diarrhea, and coughing are “symptoms of disease.” From a germ’s point of view, they’re clever evolutionary strategies to broadcast the germ.

Because the second wave was so much more severe than the first, a lot of people refused to believe it could be the same disease. It had to be terrorism. They didn't care what medical experts kept telling them, about how it was the nature of influenza to occur in waves and that there was nothing about this pandemic, terrible though it was, that wasn't happening more or less as had long been predicted. No, not bioterrorism, others said, but a virus that had escaped from a laboratory. These were the same people who believed that both Lyme disease and West Nile virus were caused by germs that had escaped many years ago from a government lab off the coast of Long Island. They scoffed at the assertion that it was impossible to say for sure where the flu had begun because cases had appeared in several different countries at exactly the same time. Cover-up! Everyone knew the government was involved in the development of bioweapons. And although the Americans were not the only ones who were working on such weapons, the belief that they were somehow to blame--that the monster germ had most likely been created in an American lab, for American military purposes--would outlive the pandemic itself. In any case, according to a poll, eighty-two percent of Americans believed the government knew more about the flu than it was saying. And the number of people who declared themselves dead set against any vaccine the government came up with was steadily growing.

A highly regarded infectious-disease epidemiologist named Donald S. Burke, presently dean of the Graduate School of Public Health at the University of Pittsburgh, gave a lecture (later published) back in 1997 in which he listed the criteria that might implicate certain kinds of viruses as likeliest candidates to cause a new pandemic. “The first criterion is the most obvious: recent pandemics in human history,” Burke told his audience. That would point to the orthomyxoviruses (including the influenzas) and the retroviruses (including the HIVs), among others. “The second criterion is proven ability to cause major epidemics in non-human animal populations.” This would again spotlight the orthomyxoviruses, but also the family of paramyxoviruses, such as Hendra and Nipah, and the coronaviruses, such as that virus later known as SARS-CoV. Burke’s third criterion was “intrinsic evolvability,” meaning readiness to mutate and to recombine (or reassort), which “confers on a virus the potential to emerge into and to cause pandemics in human populations.” As examples he returned to retroviruses, orthomyxoviruses, and coronaviruses. “Some of these viruses,” he warned, citing coronaviruses in particular, “should be considered as serious threats to human health. These are viruses with high evolvability and proven ability to cause epidemics in animal populations.” It’s interesting in retrospect to note that he had augured the SARS epidemic six years before it occurred. Much more recently, Burke told me: “I made a lucky guess.” He laughed a self-deprecating hoot and then added that “prediction is too strong a word” for what he had been doing.

It may seem paradoxical to claim that stress, a physiological mechanism vital to life, is a cause of illness. To resolve this apparent contradiction, we must differentiate between acute stress and chronic stress. Acute stress is the immediate, short-term body response to threat. Chronic stress is activation of the stress mechanisms over long periods of time when a person is exposed to stressors that cannot be escaped either because she does not recognize them or because she has no control over them. Discharges of nervous system, hormonal output and immune changes constitute the flight-or-fight reactions that help us survive immediate danger. These biological responses are adaptive in the emergencies for which nature designed them. But the same stress responses, triggered chronically and without resolution, produce harm and even permanent damage. Chronically high cortisol levels destroy tissue. Chronically elevated adrenalin levels raise the blood pressure and damage the heart. There is extensive documentation of the inhibiting effect of chronic stress on the immune system. In one study, the activity of immune cells called natural killer (NK) cells were compared in two groups: spousal caregivers of people with Alzheimer’s disease, and age- and health-matched controls. NK cells are front-line troops in the fight against infections and against cancer, having the capacity to attack invading micro-organisms and to destroy cells with malignant mutations. The NK cell functioning of the caregivers was significantly suppressed, even in those whose spouses had died as long as three years previously. The caregivers who reported lower levels of social support also showed the greatest depression in immune activity — just as the loneliest medical students had the most impaired immune systems under the stress of examinations. Another study of caregivers assessed the efficacy of immunization against influenza. In this study 80 per cent among the non-stressed control group developed immunity against the virus, but only 20 per cent of the Alzheimer caregivers were able to do so. The stress of unremitting caregiving inhibited the immune system and left people susceptible to influenza. Research has also shown stress-related delays in tissue repair. The wounds of Alzheimer caregivers took an average of nine days longer to heal than those of controls. Higher levels of stress cause higher cortisol output via the HPA axis, and cortisol inhibits the activity of the inflammatory cells involved in wound healing. Dental students had a wound deliberately inflicted on their hard palates while they were facing immunology exams and again during vacation. In all of them the wound healed more quickly in the summer. Under stress, their white blood cells produced less of a substance essential to healing. The oft-observed relationship between stress, impaired immunity and illness has given rise to the concept of “diseases of adaptation,” a phrase of Hans Selye’s. The flight-or-fight response, it is argued, was indispensable in an era when early human beings had to confront a natural world of predators and other dangers. In civilized society, however, the flight-fight reaction is triggered in situations where it is neither necessary nor helpful, since we no longer face the same mortal threats to existence. The body’s physiological stress mechanisms are often triggered inappropriately, leading to disease. There is another way to look at it. The flight-or-fight alarm reaction exists today for the same purpose evolution originally assigned to it: to enable us to survive. What has happened is that we have lost touch with the gut feelings designed to be our warning system. The body mounts a stress response, but the mind is unaware of the threat. We keep ourselves in physiologically stressful situations, with only a dim awareness of distress or no awareness at all.

But as Bill Gates said to us when Mark and I met with him in his Seattle-area office, “People invest in high-probability scenarios: the markets that are there. And these low-probability things that maybe you should buy an insurance policy for by investing in capacity up front, don’t get done. Society allocates resources primarily in this capitalistic way. The irony is that there’s really no reward for being the one who anticipates the challenge.” Every time there is a new, serious viral outbreak, such as Ebola in 2012 and Zika in 2016, there is a public outcry, a demand to know why a vaccine wasn’t available to combat this latest threat. Next a public health official predicts a vaccine will be available in x number of months. These predictions almost always turn out to be wrong. And even if they’re right, there are problems in getting the vaccine production scaled up to meet the size and location of the threat, or the virus has receded to where it came from and there is no longer a demand for prevention or treatment. Here is Bill Gates again: Unfortunately, the message from the private sector has been quite negative, like H1N1 [the 2009 epidemic influenza strain]: A lot of vaccine was procured because people thought it would spread. Then, after it was all over, they sort of persecuted the WHO people and claimed GSK [GlaxoSmithKline] sold this stuff and they should have known the thing would end and it was a waste of money. That was bad. Even with Ebola, these guys—Merck, GSK, and J & J [Johnson & Johnson]—all spent a bunch of money and it’s not clear they won’t have wasted their money. They’re not break-even at this stage for the things they went and did, even though at the time everyone was saying, “Of course you’ll get paid. Just go and do all this stuff.” So it does attenuate the responsiveness. This model will never work or serve our worldwide needs. Yet if we don’t change the model, the outcome will not change, either.

Today, such studies are illegal. Medical scientists cannot offer inducements like pardons to persuade prisoners to take part in their studies. Although they can award small cash payments to research subjects, they are forbidden from giving anyone so much money or such tempting favors that their compensations might constitute what ethicists term an inappropriate inducement, an irresistible temptation to join the study. Now, more than eighty years after the 1918 flu, people enter studies for several reasons—to get free medical care, to get an experimental drug that, they hope, might cure them of a disease like cancer or AIDS, or to help further scientific knowledge. In theory at least, study participants are supposed to be true volunteers, taking part in research of their own free will. But in 1918, such ethical arguments were rarely considered. Instead, the justification for a risky study with human beings was that it was better to subject a few to a great danger in order to save the many. Prisoners were thought to be the ideal study subjects. They could offer up their bodies for science and, if they survived, their pardons could be justified because they gave something back to society. The Navy inmates were perfect for another reason. Thirty-nine of them had never had influenza, as far as anyone knew. So they might be uniquely susceptible to the disease. If the doctors wanted to deliberately transmit the 1918 flu, what better subjects? Was influenza really so easily transmitted? the doctors asked. Why did some people get it and others not? Why did it kill the young and healthy? Could the wartime disruptions and movements of troops explain the spread of the flu? If it was as contagious as it seemed, how was it being spread? What kind of microorganism was causing the illness? The normal way to try to answer such questions would be to study the spread of the disease in animals. Give the disease to a few cages of laboratory rats, or perhaps to some white rabbits. Isolate whatever was causing the illness. Show how it spread and test ways to protect animals—and people—against the disease. But influenza, it seemed, was a uniquely human disease. No animal was known to be susceptible to it. Medical researchers felt they had no choice but to study influenza in people. Either the Navy doctors were uncommonly persuasive or the enticement of a pardon was overwhelmingly compelling. For whatever reason, the sixty-two men agreed to be subjects in the medical experiment. And so the study began. First the sailors were transferred to a quarantine station on Gallops Island in Boston Harbor. Then the Navy doctors did their best to give the men the flu. Influenza is a respiratory disease—it is spread from person to person, presumably carried on droplets of mucus sprayed in the air when sick people cough or sneeze, or carried on their hands and spread when the sick touch the healthy. Whatever was causing the flu should be present in mucus taken from the ill. The experiments, then, were straightforward. The Navy doctors collected mucus from men who were desperately ill with the flu, gathering thick viscous secretions from their noses and throats. They sprayed mucus from flu patients into the noses and throats of some men, and dropped it into other men’s eyes. In one attempt, they swabbed mucus from the back of the nose of a man with the flu and then directly swabbed that mucus into the back of a volunteer’s nose.

In most life forms, genes are stretched out along the length of a filament-like molecule of DNA, deoxyribonucleic acid. But many viruses—including influenza, HIV, and the coronavirus that causes SARS (severe acute respiratory syndrome)—encode their genes in RNA, ribonucleic acid, an even simpler but less stable molecule.

NATURE CHOSE to rage in 1918, and it chose the form of the influenza virus in which to do

Like cold-causing rhinoviruses, influenza viruses manage to wreak their harm with very little genetic information—just thirteen genes.

Perhaps, in some innocent encounter in China between a child and a bird, a new killer flu is on its way. Or perhaps, even now, a young man or a young woman has become infected with two different strains of flu viruses. They are mixing together in the person’s lungs, their genes reassorting. Emerging from that witches’ brew is a new virus, a chimera, that, like the 1918 flu virus, is perfectly suited for destruction. Perhaps, as we grow almost smug about influenza, that most quotidian of infections, a new plague is now gathering deadly force. Except this time we stand armed with a better understanding of the past to better survive the next pandemic.

influenza viruses manage to wreak their harm with very little genetic information—just thirteen genes.

Pig farmers complained to the Centers for Disease Control that the name “swine flu” might frighten people away from eating pork. They asked, to no avail, that the flu’s name be changed to “New Jersey flu.

knows exactly how serious this threat could be. Nevertheless, we cannot afford to take a chance with the health of our nation.” With that preamble, Ford announced that he was asking Congress to appropriate $135 million “for the production of sufficient vaccine to inoculate every man, woman, and child in the United States,” for a disease that no one could even prove to exist.

air cannot flow out of the room, only in. There they are bathed in blue ultraviolet light, which kills viruses. After that, they tug on

There are three different types of influenza viruses: A, B, and C. Type C rarely causes disease in humans. Type B does cause disease, but not epidemics. Only influenza A viruses cause epidemics or pandemics, an epidemic being a local or national outbreak, a pandemic a worldwide one.

Many viruses, including influenza and diarrhoea-causing viruses such as rotavirus, can survive for days in the environment, building up on particular kinds of objects known as fomites. Have you noticed a sudden increase in male physicians sporting bow ties? This fashion statement is a response to health researchers’ identification of standard ties as fomites.

in 2004, the National Intelligence Council, a research organization in the U.S. intelligence community, had published a report titled Mapping the Global Future, which presented scenarios for the year 2020. One of the scenarios imagined was a pandemic in 2020. It was eerily prophetic, even as to the year: It is only a matter of time before a new pandemic appears, such as the 1918–1919 influenza virus that killed an estimated twenty million worldwide. Such a pandemic in megacities of the developing world . . . would be devastating and could spread rapidly throughout the world.

ARDS by no means accounts for all the influenza deaths in 1918 and 1919, or even for a majority of them. It explains only those who died in a few days, and it explains why so many young healthy people died. Although influenza almost certainly killed some people in ways that had little to do with the lungs—for example, someone whose already weak heart could not stand the additional strain of fighting the disease—the overwhelming majority of non-ARDS deaths came from bacterial pneumonias. The destruction of the epithelial cells eliminated the sweeping action that clears so much of the respiratory tract of bacteria, and the virus damaged or exhausted other parts of the immune system as well. That gave the normal bacterial flora of the mouth unimpeded entry into the lungs. Recent research also suggests that the neuraminidase on the influenza virus makes it easier for some bacteria to attach to lung tissue, creating a lethal synergy between the virus and these bacteria. And in the lungs, the bacteria began to grow.

For the virus had not disappeared. It had only gone underground, like a forest fire left burning in the roots, swarming and mutating, adapting, honing itself, watching and waiting, waiting to burst into flame.

In 1918 especially, this question of balance played a crucial role in the war between virus and immune system, and between life and death. The virus was often so efficient at invading the lungs that the immune system had to mount a massive response to it. What was killing young adults a few days after the first symptom was not the virus. The killer was the massive immune response itself.

Ecco a cosa sono utili le zoonosi: ci ricordano, come versioni moderne di san Francesco, che in quanto esseri umani siamo parte della natura, e che la stessa idea di un mondo naturale distinto da noi è sbagliata e artificiale. C’è un mondo solo, di cui l’umanità fa parte, così come l’HIV, i virus di Ebola e dell’influenza, Nipah, Hendra e la SARS, gli scimpanzé, i pipistrelli, gli zibetti e le oche indiane. E ne fa parte anche il prossimo virus killer che ci colpirà, quello che ancora non abbiamo scoperto.

Australia had escaped. It had escaped because of a stringent quarantine of incoming ships. Some ships arrived there with attack rates as high as 43 percent and fatality rates among all passengers as high as 7 percent. But the quarantine kept the virus out, kept the continent safe, until late December 1918 when, with influenza having receded around the world, a troopship carrying ninety ill soldiers arrived. Although they too were quarantined, the disease penetrated—apparently through medical personnel treating troops. By then the strain had lost much of its lethality. In Australia the death rates from influenza were far less than in any other Westernized nation on earth, barely one-third that of the United States, not even one-quarter that of Italy. But it was lethal enough.

Statistics also confirmed what every physician, indeed every person, already knew. In the civilian population as well, young adults had died at extraordinary, and frightening, rates. The elderly, normally the group most susceptible to influenza, not only survived attacks of the disease but were attacked far less often. This resistance of the elderly was a worldwide phenomenon. The most likely explanation is that an earlier pandemic (later analysis of antibodies proved it was not the 1889–90 one), so mild as to not attract attention, resembled the 1918 virus closely enough that it provided protection.

Societies, especially in the developed world, were thought to be on the verge of becoming invulnerable to new plagues. Unfortunately, this expectation has proved to be spectacularly misplaced. Well into the twenty-first century smallpox remains the only disease to have been successfully eradicated. Worldwide, infectious diseases remain leading causes of death and serious impediments to economic growth and political stability. Newly emerging diseases such as Ebola, Lassa fever, West Nile virus, avian flu, Zika, and dengue present new challenges, while familiar afflictions such as tuberculosis and malaria have reemerged, often in menacing drug-resistant forms. Public health authorities have particularly targeted the persisting threat of a devastating new pandemic of influenza such as the “Spanish lady” that swept the world with such ferocity in 1918 and 1919.

The last big deadly human influenza epidemic in the world was in 1918. There were about twenty million dead worldwide, including five hundred thousand in the United States. Based on our present population, the equivalent number of dead now would be approximately one and a half million people. Could you imagine such a thing today? And the 1918 virus wasn’t particularly virulent, and of course, travel was much slower then and less frequent. Today, the highways and skyways can spread an infectious virus around the world in days.

In more recent history, we learn from other viruses, including Measles, Ebola, Rabies, Herpes, how important it is to respond immediately to prevent the spread of infection. I was shocked when I learned more about the influenza pandemic, otherwise known as the Spanish Flu of 1918–1919. It began in the US, swiftly traveled across the world, and killed more people than any disease before or since.

Covid hasn't finished with us yet, because it's only just getting started.

Our work is not to get rid of viruses, or we would, by definition, fail. Our work is to live alongside viruses and to protect as many human lives as we can. This depends, in part, on what viral stories we tell, what viral metaphors we use. A virus killed my friend. I miss her every day. I live alongside viruses every day, missing her. Her memory will make me smile; her memory will make me cry. It will make me angry, forever, at influenza, the virus that took her away, but that anger won’t get her, or us, a second chance. As individual humans and the collective we together form, death or symbiosis are our only options. The planet cannot continue to sustain our abuse. Will we eat it alive, use up its resources, and leave it an unsuitable host for further human reproduction? What will this earn us? Continued wealth for a small number of human animals is all. Human reproduction is not driving global warming; wealth production is. Human wealth will be lytic, killing our host planet and us with it. Lysogeny may still be an option. Symbiosis. We could understand, like one of lambda’s stories, that treating the host well is treating us well. The earth’s well-being is our own well-being. Lambda has its choice made for it by molecules and circumstances and luck. We have our molecules and circumstances, but we can make more than luck. We must choose it, actively and every day, a lysogenic viral story, a living with and caring for the earth because it means caring for ourselves. A virus is not an enemy; if it is, we will only lose. Viruses aren’t the problem, they’re a fact of the world. We are the problem when we refuse to protect one another’s lives as the most precious things we have. You are precious to me. We might well prefer a world without viruses, their everyday annoyances, the fever or runny nose, the cold sores, the never-ending possibility of pandemic. We won’t get a day without them. I miss Sarah every day. Viruses aren’t going anywhere. We get to choose what we become. For my part, I live to be lysogenic. Won’t you join me here?

The National Institutes of Health in Maryland keeps samples of the 1918 flu virus in a freezer at an undisclosed location. It’s not easy to get anywhere near that locked freezer, let alone inside it. First, you have to get onto the campus of the NIH, which requires identification, a reason to be admitted, and a PhD, preferably in one of the life sciences. Once you get through and find the building, a guard has to buzz you in via an airlocked entrance with double doors. Inside, you will pass through a metal detector and then be firmly guided toward a locker, where your cell phone, thumb drive, computer, pager, and camera must be deposited. Then, and only then, will you be escorted farther into the building.

All this tinkering was creating superviruses that did not exist outside the lab and that might be more easily transmissible between different species, or more virulent, or more resistant to any influenza vaccine. Most researchers were insistent that these “gain of function” studies were needed to better understand how the flu virus might evolve, but the federal government saw things differently. These experiments were a security risk.

labs that enrolled in the FluNet Global Influenza Surveillance System—a network of reference labs that sample for flu as a way to track its global spread—recorded 4,623 cases of flu in 2019 but just 53 in 2020. In Chile, there were 5,000 cases in 2019 and 12 in 2020; and in South Africa, the network’s labs detected 1,094 cases in 2019 and just 6 in 2020.53 In New Zealand there was a “near extinction” of influenza.54 With so little flu virus migrating, a similar scenario played out in the US during our fall and winter. By the end of January 2021, the CDC had recorded only 1,316 positive flu cases in its surveillance network, compared to 129,997 they had recorded over the same time frame in 2019.55 The mitigation we put into place was designed to deal with a pandemic flu, not COVID, and it worked much better against its intended viral target.

common cold virus; from chickens came “bird flu,” chickenpox, and shingles; pigs and ducks donated influenza; and from cattle arose measles, tuberculosis, and smallpox.

The characteristic of the influenza virus that makes it so dangerous and gives rise to epidemic after epidemic is its extreme mutability. It perpetually is changing the nature of its outer surface, which antibodies, the body’s most important defense system, must zero in on to be effective.

In its first Spanish influenza pamphlet, issued in September, the USPHS recommended that those nursing flu patients wear gauze masks.37 Soon laymen decided that what was a sensible caution in the sickroom would be just as sensible in every situation. Gauze masks became a common sight in the streets and department stores of communities in the eastern United States. People could and did honestly believe that a few layers of gauze would keep out flu bugs, just as screens kept the flies off the front porch. The influenza virus itself is, of course, so infinitely tiny that it can pass through any cloth, no matter how tightly woven, but a mask can catch some of the motes of dust and droplettes of water on which the virus may be riding. However, to be even slightly effective during a flu epidemic masks must be worn at all times when people are together, at home and at work and in between, must be of a proper and probably uncomfortable thickness, must be tied firmly, and must be washed and dried at least once daily. Enforcement of such conditions is impossible and so the communities where masking was compulsory during the Spanish influenza pandemic almost always had health records the same as those of adjacent communities without masking.

Today, we know that viruses are submicroscopic entities twenty times smaller than a bacterium. They contain a core of genetic material covered by a protein capsule, and they reproduce exclusively within living cells.

Antigenic shift generated the deadly 1918 influenza virus and the swine flu outbreak of 2009.

We now think that the majority of deaths in the 1918 pandemic resulted from these secondary infections, not from the flu virus itself.

The third explanation for 1918’s lethality is that the flu virus triggered an overreactive immune response that turned the body against itself.

But the 1920 edition of the Spanish influenza virus was an attenuated variant of the original strain, and the human population was more resistent than in 1918 and 1919.

In all, SARS-1 had been the subject of six outbreaks since its last-known natural occurrence, each one the consequence of its escape from a laboratory: one time each in Singapore and Taiwan, and then four separate escapes from the same lab in Beijing.69 Another instance where an experiment in China had gone awry, and triggered the global spread of a novel virus, had occurred in 1977 and involved a strain of H1N1 influenza.

But all that was just to buy time. It takes about two to three days until Natural Killer Cells show up and begin to alleviate your desperately fighting immune soldiers. They flood the tissue and begin killing infected epithelial cells, especially the ones that were manipulated by the influenza A virus to hide their display windows, their MHC class I molecules, but not exclusively them. The more stressed and desperate infected cells get mercifully finished off, to end their suffering but also to prevent them from causing further harm.

In 1943, while Jonas Salk was working on an influenza vaccine, there were ten thousand cases of polio in the United States; in 1948, when Salk was typing polio viruses, there were twenty-seven thousand cases of polio; in 1952, when Salk was first testing his ideas on how to make a polio vaccine, there were fifty-nine thousand cases of polio. Almost every American was directly or indirectly affected by this disease.

The 1918–19 influenza virus strain, a pandemic which killed forty million people in Europe, Asia and America, was not confined to the war areas, though it struck them hardest.

Still, this particularly virulent and infectious strain of the flu virus is thought to have killed as many as 40 million people around the world between 1918 and 1919.

….In time, the Europeans brought in pigs and horses, both of which were allowed to run wild and multiply. Pigs in the wild soon became aggressive feral boars with tusks, eating everything in sight. Corn, which the Indians depended upon, was attacked and uprooted by the pigs before maturing, thus leaving the Indians without an important source of nourishment. Although pigs provided a necessary source of protein, they were also known to host worms and parasites, and spread viruses such as influenza. If undercooked, the meat could cause trichinosis infections that, depending upon the severity, could result in death in four to six weeks. The sailors returning to Europe brought with them tobacco and syphilis, both of which could be fatal. Syphilis is the gift that keeps on giving and soon spread throughout Europe and England. Unknown prior to the discovery of America, it became another blight on the European continent. Because of their close connection, many people were convinced that pigs were the carriers of Syphilis. Perhaps they were right…. .

The results of the studies opened up a whole new avenue of research into live-attenuated vaccines: synthetic attenuated virus engineering (SAVE). A virus was created with 631 synonymous mutations in its P1 coding sequence, designed to bias it toward the use of codons that rarely preferred in human cells. The result was a highly attenuated virus that caused no disease in an animal model of virus infection, and like the naturally evolved live-attenuated polioviruses developed by Sabin, it proved to be a highly effective vaccine. Unlike Sabin's strains, however, the multiplicity of genetic changes contributing to attenuation is expected to render the phenotype far more stable and resilient to reversion in vivo. This technology could prove extremely useful in the development of safe and stable attenuated viruses that raise an immune response almost identical to that against the natural infection. There are now many examples of the genetic engineering of synthetic attenuated virus vaccines; most notably it has been employed to create a live-attenuated vaccine against a strain of human influenza, a virus that, unlike poliovirus or smallpox virus, we cannot hope to eradicate and for which vaccination remains the lynchpin of disease management.

The researchers looked deeper into these observations, in hopes of gaining insight into the mechanisms underlying the high evolutionary rate and extraordinary immunologic plasticity of influenza HA. They probed in more detail the precise codons that are used by the virus to encode the influenza HA1 protein. The discriminated between codons on the basis of volatility. Each three-nucleotide codon is related by a single nucleotide change to nine 'mutational neighbours.' Of those nine mutations, some proportion change the codon to a synonymous codon and some change it to a nonsynonymous one, which directs the incorporation of a different amino acid into the protein. More volatile codons are those for which a larger proportion of those nine mutational neighbours encode an amino acid change. The use of particular codons in a gene at a frequency that is disproportionate to their random selection for encoding a chosen amino acid is termed codon bias. Such bias is common and is influenced by many factors, but here the collaborators found strong evidence for codon bias that was particular for and restricted to the amino acids making up the HA1 epitopes. Remarkably, they observed that influenza employs a disproportionate number of volatile codons in its epitope-coding sequences. There was a bias for the use of codons that had the fewest synonymous mutational neighbours. In other words, influenza HA1 appears to have optimized the speed with which it can change amino acids in its epitopes. Amino acid changes can arise from fewer mutational events. The antibody combining regions are optimized to use codons that have a greater likelihood to undergo nonsynonymous single nucleotide substitutions : they are optimized for rapid evolution.

He estimates the number of deaths worldwide as 100 million, a larger number than the conventional estimate of 20 to 40 million. But, he said, 20 million people died in India alone, making it impossible for the 20 to 40 million figure to be correct.

Ebola, West Nile, Marburg, the SARS bug, monkeypox, rabies, Machupo, dengue, the yellow fever agent, Nipah, Hendra, Hantaan (the namesake of the hantaviruses, first identified in Korea), chikungunya, Junin, Borna, the influenzas, and the HIVs (HIV-1, which mainly accounts for the AIDS pandemic, and HIV-2, which is less widespread) are all viruses.

Instead, the dean had said, “Take a look at the person sitting to your left and to your right. Chances are that person will not be there four years from now.” Every

Two epidemics swept the world in 1918. One was Spanish influenza, the first recorded outbreak of which was at a Kansas army base in March 1918. As if to mock the efforts of men to kill one another, the virus spread rapidly across the United States and then crossed to Europe on the crowded American troopships.

experts used to believe diseases were mostly transmitted by people or animals, many now maintain that airborne dust clouds can carry viruses like influenza or SARS (severe acute respiratory syndrome) and other potentially harmful bacteria, viruses, and fungal spores over thousands of miles.

The viruses that cause smallpox, influenza, hepatitis, measles, encephalitis, and viral pneumonia; the bacteria that cause tuberculosis, diphtheria, cholera, typhus, scarlet fever, and bacterial meningitis—by a quirk of evolutionary history, all were unknown in the Western Hemisphere.

RNA viruses because I already had that list in my mind: Hendra and Nipah, Ebola and Marburg, West Nile, Machupo, Junin, the influenzas, the hantas, dengue and yellow fever, rabies and its cousins, chikungunya, SARS-CoV, and Lassa, not to mention HIV-1 and HIV-2. All of them carry their genomes as RNA. The

A virus's ability to spread is the key to its ability to create a pandemic.

Although regular human flu viruses bound easily with the receptors found in the nose and throat cells, H5N1 strains attached only to those receptors on cells found in the deepest regions of the lungs.

For the viruses to be transmitted efficiently, they have to multiply in the upper portion of the respiratory system so that they can be transmitted by coughing and sneezing.

Flu viruses mutate constantly.

Intensive monitoring of pig viruses is unlikely to come any time soon, however. Most pork-producing countries do not test their pigs at all, and in some that do—such as the U.S.—the testing is done on behalf of the pork producers, who have little economic incentive to share what they find.

Swine influenza is not even a reportable disease, a classification saved for diseases deemed a threat to the entire industry, such as foot-and-mouth disease. On the other hand, pig flu viruses can be a big problem for the general population. That is because pigs are a genetic crucible for new flu viruses. They can be infected with flu viruses from birds, other pigs and people, creating opportunities for a melding of genes in new combinations known as reassortants. The fear is these new hybrids will prove capable of infecting people readily, while being sufficiently foreign to cause serious illness once they do.

the 2009 H1N1 virus so alarming is that its recent forebears infected three species—humans, birds and pigs.

Scientists isolated an influenza strain from a human for the first time in 1933. Since then, they have learned that influenza viruses come in two main “flavors”— types A and B—that differ in certain of their internal proteins. A third type (C) does not seem to cause serious disease.

The neuraminidase molecules on the freshly made particles can cleave sialic acid. In other words, the neuraminidase spikes essentially dissolve the unwanted sialic acid “glue,” thereby enabling the viral particles to travel. The enzyme also helps the virus to plow through the mucus between cells in the airways.

These alterations arise through small mutations in the gene that constitutes the blueprint for that protein. Sometimes a mutation makes little difference in the protein’s stability or activity. Sometimes it damages the protein and reduces the viability of the virus. Other times, though, it enhances survival, such as by reconfiguring a site on hemagglutinin that was formerly recognized by an antibody.

When antigenic shift occurs, strains crop up bearing a totally new hemagglutinin spike, and sometimes also a new neuraminidase molecule, that most people have never encountered. As a result the virus may evade the antibody repertoire carried by all populations around the globe and trigger a pandemic. In today’s jet-linked world, people can spread a dangerous new virus from one part of the earth to another in a day. Such a drastic metamorphosis cannot occur through simple genetic mutation. The best-studied process leading to antigenic shift involves the mixing of two viral strains in one host cell, so that the genes packaged in new viral particles (and their corresponding proteins) come partly from one strain and partly from the other. This reassortment can take place because the genome, or genetic complement, of the influenza virus consists of eight discrete strands of RNA (each of which codes for one or two proteins). These strands are easily mixed and matched when new influenza A particles form in a dually infected cell. For instance, some influenza viruses infect both people and pigs. If a pig were somehow invaded by a human virus and by a strain that typically infected only birds, the pig might end up producing a hybrid strain that was like the human virus in every way except for displaying, say, a hemagglutinin molecule from the bird virus.

Many natural infections have at least one benefit in that a bout of illness confers lifelong immunity against the causative pathogen. An ideal vaccine would also offer such lasting protection, preferably with a single dose, and perhaps even protect against related threats, such as all members of the ever evolving family of human flu viruses.

Various pathogens that can cause life-threatening infections such as HIV, hepatitis C virus, Mycobacterium tuberculosis and Plasmodium parasites (the source of malaria) can evade antibodies, and an effective vaccine against these pathogens would need to stimulate robust T cell responses.

Systematic sampling and mandatory reporting of disease in swine herds are limited to a handful of commercially devastating illnesses, including classical swine fever and nipah virus.

The researchers, under the direction of Yoshihiro Kawaoka at the University of Wisconsin at Madison, crossed an H5N1 virus with the H1N1 pandemic virus of 2009, which spread like wildfire from one end of the world to another. The 2009 pandemic, you’ll recall, caught public health officials by surprise but luckily turned out to be mild. Kawaoka’s lab-made hybrid virus spreads among ferrets by airborne droplets expelled during the course of respiration–just as human influenza viruses such as the 2009 pandemic strain spread from person to person. Kawaoka’s concoction does not kill ferrets, and probably wouldn’t kill humans, but the feat is troubling because it demonstrates that an H5N1 virus that can spread among humans is most likely possible. (We don’t know for sure because it was tested only on ferrets, not humans, of course.)

Webster’s hunch about birds being a reservoir for precursors to human viruses is now conventional wisdom.

feces. If a wild bird infects a chicken on a poultry farm, the virus may get opportunities to interact with a range of additional viruses through close contact with pigs and other animals. This is indeed what has happened in the live animal markets and backyard farms of China and southern Asia. Influenza viruses are notorious for their ability to change, through a combination of mutation and “reassortment”—a borrowing of genes from other viruses. An open farm acts like a virus convention, where different strains swap genetic material like conventioneers swap business cards.