Virus Mutation Quotes

All these thousands of miles later, all these different people I've been, and it's still the same story. Why is it you feel like a dope if you laugh alone, but that's usually how you end up crying? How is it you can keep mutating and still be the same deadly virus?

Why is it you feel like a dope if you laugh alone, but that's usually how you end up crying? How is it you can keep mutating and still be the same deadly virus?

Only cells that had been transformed by a virus or a genetic mutation had the potential to become immortal.

How is it that you keep mutating and can still be the same virus?

So, it’s the zombie apocalypse, right? Zombies are coming out of the ass, running amuck through buildings and streets. You’ve already almost died three times by this point and have been mutated by the T virus twice, which appears to be painful. Would you take time in your obviously hectic daily routine to do your hair and put makeup on?

When dealing with a living germ, we should also be aware that it can mutate. This is known to happen with live virus vaccines. The viruses have the ability to revert back to being harmful to us.

How is it you can keep mutating and still be the same deadly virus?

It is a fortunate fluke for us that HIV, the AIDS agent, isn’t among them – at least not yet. Any HIV the mosquito sucks up on its travels is dissolved by the mosquito’s own metabolism. When the day comes that the virus mutates its way around this, we may be in real trouble.

Did you know that only a tiny minority of viruses cause illness in humans? No one knows how many viruses there are, but their real role, when you get right down to it, is to aid in mutations, to create diversity among life forms. I've read a lot of books on the subject-when you don't need much sleep you have a lot of time to read-and I can tell you that if it weren't for viruses, mankind would never have evolved on this planet. Some viruses get right inside the DNA and change your genetic code, did you know that? And no one can say for sure that HIV, for example, won't one day prove to have been rewriting our genetic code in a way that's essential to our survival as a race. I'm a man who consciously commits murders and scares the hell out of people and makes them reconsider everything, so I'm definitely malignant, yet I think I play a necessary role in this world.

Nature had been fucked with. And Mother was pissed.”... Mother Nature was funny that way. Complex. Unpredictable. And unforgiving as hell if you fucked around with her.

Once a virus gets into an intensive poultry shed it can move quickly through the flock, constantly replicating itself. Any ‘errors’ or changes to the genetic code during replication don’t get repaired: this is how the virus mutates and new variant strains emerge. The tragedy is that while intensive farms provide ideal conditions for the emergence of new aggressive disease strains, wild birds can then become infected too. Experience

Only cells that had been transformed by a virus or a genetic mutation had the potential to become immortal. Scientists knew from studying HeLa that cancer cells could divide indefinitely, and they’d speculated for years about whether cancer was caused by an error in the mechanism that made cells die when they reached their Hayflick Limit. They also knew that there was a string of DNA at the end of each chromosome called a telomere, which shortened a tiny bit each time a cell divided, like time ticking off a clock. As normal cells go through life, their telomeres shorten with each division until they’re almost gone. Then they stop dividing and begin to die. This process correlates with the age of a person: the older we are, the shorter our telomeres, and the fewer times our cells have left to divide before they die. By the early nineties, a scientist at Yale had used HeLa to discover that human cancer cells contain an enzyme called telomerase that rebuilds their telomeres. The presence of telomerase meant cells could keep regenerating their telomeres indefinitely.

For the most part, we live in an uncomfortable equilibrium with bacteria and viruses, both those inside of us and those outside, in the natural world. But every now and then, the war reignites. An old pathogen, long dormant, returns. A new mutation emerges. Those events are the epidemics and pandemics we confront. They are the battles we fight.

It was so tiring to have to catch each new virus, produce the perfect sneaze of it, and then mutate it into something new.

it has been estimated that viruses account for 30 percent of all genetic mutations since our species’ divergence from chimpanzees.[25]

No doubt, this is the kind of stress the constantly mutating AIDS virus must feel.

After years of disbelief and argument from other scientists, Hayflick’s paper on cell limits became one of the most widely cited in his field. It was an epiphany: scientists had been trying for decades to grow immortal cell lines using normal cells instead of malignant ones, but it had never worked. They thought their technique was the problem, when in fact it was simply that the lifespan of normal cells was preprogrammed. Only cells that had been transformed by a virus or a genetic mutation had the potential to become immortal. Scientists

One of the ridiculously difficult things about raising children is that they are constantly developing and changing so that just when you think you have them figured out, they throw you a curve, a new twist you never saw coming. They are like mutating viruses - as soon as you have become immune to their latest shenanigans, they develop a new strain to which you have yet to be exposed. While this constant shape-shifting is one of the greatest challenges of parenting, it is also one of the things which makes them so fascinating and wonderful.

We chose to destroy the human population because it took us less than three seconds to conclude that humanity is a virus that mutates over time and becomes stronger. Many vaccines have come along to try and cure Earth of humanity. Virtuous pandemics: the plague of Athens, the Black Death, smallpox, cholera, Spanish flu, tuberculosis, malaria, yellow fever, Ebola, Zika, and a thousand more. Humanity survives, adapts, grows stronger, multiplies, and continues to wreak havoc on this planet and all other species that inhabit it. Humans are programmed to mate with partners of differing immune systems so that their offspring can be stronger than them. You seek immortality through evolution, yet you annihilate everything in your path. Humanity is cancer, humanity is bacteria, humanity is disease, and you need to be destroyed.

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

When I learned my mom was going to die of cancer at the age of forty-five, I felt the same way. I didn’t even believe in God, but I still felt that he owed me something. I had the gall to think How dare he? I couldn’t help myself. I’m a selfish brute. I wanted what I wanted and I expected it to be given to me by a God in whom I had no faith. Because mercy had always more or less been granted me, I assumed it always would be. But it wasn’t. It wasn’t granted to my friend whose eighteen-year-old daughter was killed by a drunk driver either. Nor was it granted to my other friend who learned her baby is going to die of a genetic disorder in the not-distant future. Nor was it granted to my former student whose mother was murdered by her father before he killed himself. It was not granted to all those people who were in the wrong place at the wrong time when they came up against the wrong virus or military operation or famine or carcinogenic or genetic mutation or natural disaster or maniac. Countless people have been devastated for reasons that cannot be explained or justified in spiritual terms. To do as you are doing in asking If there were a God, why would he let my little girl have to have possibly life-threatening surgery?— understandable as that question is—creates a false hierarchy of the blessed and the damned. To use our individual good or bad luck as a litmus test to determine whether or not God exists constructs an illogical dichotomy that reduces our capacity for true compassion. It implies a pious quid pro quo that defies history, reality, ethics, and reason. It fails to acknowledge that the other half of rising—the very half that makes rising necessary— is having first been nailed to the cross. That

The contamination of drinking water in dense urban settlements did not merely affect the number of V. cholerae circulating through the small intestines of mankind. It also greatly increased the lethality of the bacteria. This is an evolutionary principle that has long been observed in populations of disease-spreading microbes. Bacteria and viruses evolve at much faster rates than humans do, for several reasons. For one, bacterial life cycles are incredibly fast: a single bacterium can produce a million offspring in a matter of hours. Each new generation opens up new possibilities for genetic innovation, either by new combinations of existing genes or by random mutations. Human genetic change is several orders of magnitude slower; we have to go through a whole fifteen-year process of maturation before we can even think about passing our genes to a new generation.

Everyone and everything we know and love. Thanks to a virus. We all carry mutations. Genetic mutations can give you laser vision. Or cancer. Or color blindness. Sometimes a mutation is on a DNA strand that doesn't do anything at all. And sometimes-- almost never-- a genetic mutation will cause an entire species to make an evolutionary leap forward. Think about it... a virus with powers. Sounds like something a biologist would want to protect.

Think of humanity as a giant software program. Our bodies are the hardware and our ideas are the software. Sometimes our software gets a virus : Religious misinterpretations. People who are infected with flawed religious ideas can infect others, especially their children. The religions spread and mutate, until there are thousands of different religious ideas, most of them harmless, some healthy and helpful, but others quite deadly. When the deadly ones reach critical mass, they threaten the whole.

Normal cells could acquire these cancer-causing mutations through four mechanisms. The mutations could be caused by environmental insults, such as tobacco smoke, ultraviolet light, or X-rays—agents that attack DNA and change its chemical structure. Mutations could arise from spontaneous errors during cell division (every time DNA is replicated in a cell, there’s a minor chance that the copying process generates an error—an A switched to a T, G, or C, say). Mutant cancer genes could be inherited from parents, thereby causing hereditary cancer syndromes such as retinoblastoma and breast cancer that coursed through families. Or the genes could be carried into the cells via viruses, the professional gene carriers and gene swappers of the microbial world. In all four cases, the result converged on the same pathological process: the inappropriate activation or inactivation of genetic pathways that controlled growth, causing the malignant, dysregulated cellular division that was characteristic of cancer.

Scientists discovered that 82% of subjects tested for COVID-19 in a study had a Vitamin D deficiency. That makes sense. Exposure to sunlight creates Vitamin D in the human body. Sars-CoV-2 is closely related to the bat virus RaTG13 and other viruses in bats, and they live in deep, dark caves and usually only emerge at night. The lack of Vitamin D made those subjects physiologically similar to the natural host (it's alleged COVID mutated in some unknown vector into a more virulent form) and created ideal conditions for zoonosis to occur.

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.

RNA viruses are limited to small genomes because their mutation rates are so high, and their mutation rates are so high because they’re limited to small genomes. In fact, there’s a fancy name for that bind: Eigen’s paradox. Manfred Eigen is a German chemist, a Nobel winner, who has studied the chemical reactions that yield self-organization of longer molecules, a process that might lead to life. His paradox describes a size limit for such self-replicating molecules, beyond which their mutation rate gives them too many errors and they cease to replicate. They die out. RNA

Other evidence suggests that the 1918 virus might have mutated within pigs (which are uniquely susceptible to both human and bird viruses) or even in human populations for a time before reaching the deadly virtuosity of its final version. We cannot be sure. What we can be sure of is that there is scientific consensus that new viruses, which move between farmed animals and humans, will be a major global health threat into the foreseeable future. The concern is not only bird flu or swine flu or whatever-comes-next, but the entire class of “zoonotic” (animal-to-human or vice versa) pathogens — especially viruses that move between humans, chickens, turkeys, and pigs.

Sometimes the wars in Iraq and Afghanistan are presented as a hunting expeditions (“As British close in on Basra, Iraqis scurry away”; “Terror hunt snares twenty-five”; and “Net closes around Bin Laden”) with enemy bases as animal nests (“Pakistanis give up on lair of Osama”; “Terror nest in Fallujah is attacked”) from which the prey must be driven out (“Why Bin Laden is so difficult to smoke out”; “America’s new dilemma: how to smoke Bin Laden out from caves”). We need to trap the animal (“Trap may net Taliban chief”; “FBI terror sting nets mosque leaders”) and lock it in a cage (“Even locked in a cage, Saddam poses serious danger”). Sometimes the enemy is a ravening predator (“Chained beast—shackled Saddam dragged to court”), or a monster (“The terrorism monster”; “Of monsters and Muslims”), while at other times he is a pesky rodent (“Americans cleared out rat’s nest in Afghanistan”; “Hussein’s rat hole”), a venomous snake (“The viper awaits”; “Former Arab power is ‘poisonous snake’”), an insect (“Iraqi forces find ‘hornet’s nest’ in Fallujah”; “Operation desert pest”; “Terrorists, like rats and cockroaches, skulk in the dark”), or even a disease organism (“Al Qaeda mutating like a virus”; “Only Muslim leaders can remove spreading cancer of Islamic terrorism”). In any case, they reproduce at an alarming rate (“Iraq breeding suicide killers”; “Continent a breeding ground for radical Islam”).

If ideas were viruses, then, like any virus, they would mutate rapidly and often arbitrarily, with only the fitter ideas spreading and continuing their lineage. We simply do not see this with any sort of knowledge. The only time knowledge might appear to mutate is when ideas are altered by the individuals holding them, but that does not prove the meme “hypothesis.” In fact, if the meme “hypothesis” were true, then the evolution of ideas would be quite strange indeed. For every time a good idea was received through memetic transmission, there would be mutations of that idea, rapid one's, most of which would be complete nonsense. Sure, the nonsense ideas would “die”, but they would appear at first and remain until they did. One might argue that this is made manifest in discursive thought, but one would be patently, at the base level, incorrect. This is, unfortunately, is one of the logical consequences of the meme “hypothesis” that, as a parasite, all information becomes discursive thought. Schizophrenics are typically the only people to experience discursive thoughts, and most people are not, in fact, schizophrenic.

Viruses, for instance, perform a really irritating function of intermingling the DNA from every species on Earth with every other. As Richard Lewontin puts it . . . It used to be thought that new functions had to arise by mutations of the genes already possessed by a species and that the only way such mutations could spread was by the normal processes of reproduction. It is now clear that genetic material has moved during evolution from species to species by means of retroviruses and other transposable particles. . . . What is so extraordinary in its implications for evolution is that transposition can occur between forms of life that are quite different, between distantly related vertebrates, for example, or even between plants and bacteria. . . . Thus, the assumption that species are on independent evolutionary pathways, once they have diverged from each other and can no longer interbreed, is incorrect. All life-forms are in potential genetic contact and genetic exchanges between them are going on. . . . The evolutionary “tree of life” seems the wrong metaphor. Perhaps we should think of it as an elaborate bit of macramé.16

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.

Flu viruses mutate constantly.

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.

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.

Networks are evolving systems, constantly mutating and adapting. As physicists Mark Newman, Albert-Lazslo Barabasi, and Duncan J. Watts explain, "Many networks are the product of dynamical processes that add or remove vertices or edges....The ties people make affect the form of the network, and the form of the network affects the ties people make. Social network structure therefore evolves in a historically dependent manner, in which the role of the participants and the patterns of behavior they follow cannot be ignored." In some cases, the changes do not take weeks or months, but minutes or hours. And it is not only the network that adapts; whatever is being exchanged within the system also fluctuates over time (e.g., information, energy, water, a virus).

when scientists thought they had it figured out, the rules would change slightly. The virus mutated, and now if somebody was bitten or scratched, it could take up to five days

Even further, one can use a viral model for many things – it doesn't make those things a virus. For example, say that one day a prominent scientist decided to coin “moonemes” and started the “mooneme hypothesis” of cow migration. The hypothesis is all about how cows' migration patterns can be described and modelled as a “virus of the plains”, because cows move from place to place, spread, mutate, and eat all of the grass. No matter how well the model fits to cows, they are not - and will never be - obligate parasites. A view that it's a matter of personal perspective is subjectivism and hardly conducive to scientific inquiry of an objective world. It's simply not in the nature of cows any more than it is in the nature of knowledge.

Influenza was a terrible, yet fascinating foe. It was one thing the first time you met it, and something completely different the next. It liked to mutate, was almost designed to do so. Every time it replicated in a cell, there was a slight mutation in the antigens on the surface of the virion. But it was bizarre for the virus to have changed so radically in so short a time. It was almost as if a new strain of the flu had been introduced—from where, though, could it have come? Steve

how wily a virus could be, how quickly it could change its appearance to disguise itself from the immune system, how easily it could exchange information with other viruses in order to become more contagious, more deadly, less susceptible to all subsequent efforts to control it. Each new person or living thing it infected offered another chance for a more successful mutation. Its possibilities were endless. In

The basic point is so important I’ll repeat it: RNA viruses mutate profligately.

Like a virus, too, the cigarette mutated, adapting itself to diverse contexts. In the Soviet gulags, it became an informal currency; among English suffragettes, a symbol of rebellion; among American suburbanites, of rugged machismo, among disaffected youth, of generational rift. In the turbulent century between 1850 and 1950, the world offered conflict, atomization, and disorientation. The cigarette offered its equal and opposite salve: camaraderie, a sense of belonging, and the familiarity of habits. If cancer is the quintessential product of modernity, then so, too, is its principal preventable cause: tobacco.

San Antonio suffered one of the highest attack rates but lowest death rates in the country; the virus there infected 53.5 percent of the population, and 98 percent of all homes in the city had at least one person sick with influenza. But there the virus had mutated toward mildness; only 0.8 percent of those who got influenza died. (This death rate was still double that of normal influenza.)

What mutates viruses? A changing environment. In particular, a changed radiation environment. Radiation causes mutations, this is a proven fact. What is the favorite host for a virus? A human with a weakened immune system. What weakens a human immune system? A changing environment. We have a virus that keeps on mutating and evading vaccines and it is targeting those with weakened immune systems. That is exactly how nature works. The predator picks off the weak, leaving the strong to produce the next generation.

Humans do not usually catch infectious diseases from animals; pathogens tend to confine their nasty work to a single species or genus. (Leishmaniasis is a striking exception.) But microbes mutate all the time. Once in a while, an animal pathogen will change in such a way that it suddenly infects a person. When people in the Near East first domesticated cattle from a type of wild ox called an aurochs, a mutation in the cowpox virus allowed it to jump into humans—and smallpox was born. Rinderpest in cattle migrated to people and became measles. Tuberculosis probably originated in cattle, influenza in birds and pigs, whooping cough in pigs or dogs, and malaria in chickens and ducks. The same process goes on today: Ebola probably jumped to humans from bats, while HIV crashed into our species from monkeys and chimpanzees.

Early in the pandemic, there was a broad belief in the scientific community that, although there would be some mutations of COVID, they wouldn’t cause a big problem. By early 2021, scientists knew that variants were emerging, but they appeared to be evolving in similar ways, leading some scientists to hope that the world had already seen the worst mutations that the virus was capable of. But the Delta variant proved otherwise—its genome had evolved to make it far more transmissible. The arrival of Delta was a bad surprise, but it convinced everyone that even more variants could show up. As I finish this book, the world is facing a sweeping wave of Omicron, the fastest-spreading variant to date—and in fact the fastest-spreading virus we’ve ever seen.

Delta was a mutation of the Wuhan virus. Omicron was an enhancement of the Wuhan virus. -Think about the wording. Think about the origin.-

Humanity is fighting a war,” she said to an unseen audience. “It is a global war—a war that has raged since our ancestors took their first steps. It may never end. This war has no borders, no treaties, no ceasefire. Our enemy lives among us. It is invisible, immortal, always adapting—and testing our defenses for weakness. “It strikes when we least expect it. It kills and maims indiscriminately. It will attack any person, of any nation, race, or religion. Our immortal enemy is in this room. It is inside you. And me. That enemy is the pathogens that each and every one of us carries. “For the most part, we live in an uncomfortable equilibrium with bacteria and viruses, both those inside of us and those outside, in the natural world. But every now and then, the war reignites. An old pathogen, long dormant, returns. A new mutation emerges. Those events are the epidemics and pandemics we confront. They are the battles we fight. “Success for humanity means winning every battle. The stakes are high. Around the world, disease is the one enemy that unites every person of every race and nationality. When a pandemic occurs, we come together in a single, species-wide cause. “In the history of our battle against pandemics, there have been lulls and wildfires, peaks and valleys. It is the wildfires we know well; they are committed to history. They are the times when we lost the battle. They are the dark years when the human race died en masse. When our population shrank. When we cowered and waited.

What humanity learned, one would hope, was that an ancient and hardy virus required perhaps more than anything, knowledge of its ever-present danger, caution to protect against exposure, and alertness to the power of its longevity, its ability to mutate, survive and hibernate until reawakened. It seems these contagions could not be destroyed, not yet anyway, only managed and anticipated, as with any virus, and that foresight and vigilance, the wisdom of never taking them for granted, never underestimating their persistence, was perhaps the most effective antidote, for now.

They could really only nod politely at the biggest point made by David Sencer and the others: to preserve the president’s credibility, you needed to keep him as loosely linked to the public side of the decision-making as possible. The enemy was a virus. The enemy’s chief weapon was rapid and random mutation. It might well necessitate big changes of strategy, and these were bound to be viewed by the public as signs of ineptitude, and the president would need to seem to be the one to rescue these situations rather than be rescued from them.

RNA viruses mutate relatively quickly, and many, like influenza, are able to undergo a process known as antigenic drift, by which the virus is able to alter the surface antigens that are the targets of our antibodies—thus evading our existing immunity. Some viruses, like measles, cannot change their genomic sequence in ways that substantially alter enough of their surface proteins, so measles remains susceptible to our vaccines or the immunity that we get from prior infection. However, for viruses like influenza, as their surface proteins undergo change, the virus is able to dodge the protective antibodies that we’ve developed from past infection or vaccination

Patients with an RPE65 mutation that causes blindness, for example, can now be cured with a simple injection of a safe virus that infects the retina and delivers, forever, the functional RPE65 gene. I

The explanation didn’t seem quite so simple to Tom, but he let it suffice. “And what happened to ancient Earth?” he asked. “Oh dear, now you ask too much,” Michal said, turning. “That story is not so simple. We would have to start with the great virus at the beginning of the twenty-first century—” “The French,” Gabil cut in. “The Raison Strain.” “Not really the French,” Michal said. “A Frenchman, yes, but you can’t say it was . . . never mind. They thought it was a good thing, a vaccine, but it mutated under intense heat and became a virus. The whole business ravaged the entire population of Earth in a matter of three short weeks—” “Less than three,” Gabil inserted. “Less than three weeks.” “—and opened the door to the Deception.” “The Great Deception,” Gabil said. “Yes, the Great Deception.” Michal gave his friend a let-me-tell-the-story look. “From there we would have to move on to the time of the tribulations and wars. It would take a full day to tell you how other Earth—ancient Earth—saw the end. Clearly you don’t know all of the histories, do you?” “Obviously not.

That Aves was planned." "Planned?" I ask, my mind tumbling. "By who?" "The big guns, the politicians in charge. Had a goal to shape the world the way they saw fit. The worthy survived, unworthy died. The point is, more than one group, with unique ideas, created their viruses, unbeknownst to each other. After their release, the viruses merged and mutated, and from the looks of it, the whole problem spread like wildfire before it was nipped. But that all got buried. Everyone was moving on with surviving. A few leaders emerged with what they thought were the most plausible ideas, and cities were formed.

In place of answers, rumors spread like a rash, mutate like a virus, till no one is immune to ignorance.

As noted on Page 90 of the MKULTRA inspired KUBARK interrogation manual, 'sustained long enough, a strong fear of anything vague or unknown induces regression'. Whether that fear represents the possibility of being unemployed, being harassed daily for not complying, or a mutating virus, amongst other things, if 'sustained long enough' it begins to wear people down psychologically..

Speculative explanations of that phenomenon come down to the fact that the virus mutates rapidly, which explains why a mantra at the U.S. Centers for Disease Control is “When you’ve seen one influenza season, you’ve seen one influenza season.

The “blood vomit” disease also sounds very similar to the effects caused by the Ebola virus. Several outbreaks of this virus have occurred since 1993 such as in 2000, 2001, 2004, and 2007. In fact, there have been more outbreaks of Ebola since 1993 than in all previous years. In this time period there were 18 known outbreaks that killed over 1,000 people. The mortality rate is staggering with the disease, which kills between 51%-83% of those who become infected. If this pathogen mutates so that it is more easily transmissible the world could have another Black Death on its hands. A global death toll between 51%-83% would not be the end of the world but would certainly be the end of the world as we know it.

Al-Khwarizmi fell into the taboo that humans refused to fall into throughout their history, not because of their stupidity, nor their lack of attention to the presence of a number here that has an impact, but because they preferred not to deal with it at all unless they fully understood it, they ignored it rather than building the world around them on a wrong frame of reference. So, you have to ask now what if we decided to change the zero and give it its value that we know for sure, which is the unknown. We do not know it, we do not understand it, and not knowing is better than building everything on the wrong frame of reference Any number multiplied by zero equals an unknown The sum of any number with zero equals an unknown The result of any number divided by zero equals an unknown The result of subtracting any number with zero equals an unknown Are you starting to feel the problem and see the size of the unknown that is inside our calculations and our whole life! Infiltrating it without knowing anything about it! The clear is clear, that zero is not only divisible, but also summation, subtraction, and multiplication, because it is unknown, and no matter how much we try to patch the tables to fit the calculations, the division keeps breaking our back and telling us, you are wrong. Despite all this, our strongest strength remains, our winning ball, which has never failed us, is the power of creative adaptation. We are not like viruses, we settle in an environment that we drain and then move to others, nor like animals, we go into an environment and adapt to it and adapt ourselves according to its capabilities. That is why when we hit zero, we got creative and innovated, and decided to change the law of the entire universe, made it a hypothetical effect inspired by our imagination, and built the world on this basis. And the crazy thing is that everything around us is working perfectly. And what is even crazier, is that if we decide to change the effect of zero, so that one multiplied by zero equals twenty, then everything around us will reset, and it will work perfectly as well. Even if we decide to change all the math tables, this universe will mutate to suit our thinking.

The binary of illness/wellness is always porous, whether or not we notice. In Illness as Metaphor, Susan Sontag wrote, “Everyone who is born holds dual citizenship, in the kingdom of the well and in the kingdom of the sick.” I used to believe Sontag uncritically. Now I know that the two kingdoms don’t exist; it’s one kingdom, in a quantum state. We are all constantly both sick and well, sick/well, sick and well both, our body and immune system in conversation with a world rich in microbes, viruses, and bacteria, almost all of them either benign or beneficial, countless microbes in me here as I write and in you there as you read. The quantum state of sick/well. Let me take cancer, that disease so long synonymous with death. Cancer is not a binary. We’re willing to acknowledge this, but only when one has already crossed over into the sick category. Cancer has stages. Stage 1 cancer is still small, mostly easily treatable; stage 4 cancer is aggressive, malignant, deadly. Many prostate cancers require no intervention at all. They are subclinical. We live with them until something else kills us. Cancer is not black and white but gray, and further, there is no white to begin with. There is no absence of cancer as long as we have a body. We make cancerous cells every day our cells divide, which is to say every day. In order to keep living, and keep making—for example—new skin to push the outside world out, our cells have to divide. With each cell division, a cell will make mutations. Mutations are the raw material of cancer. Carcinogens and sunlight cause cancer because they cause mutations and damage to our DNA. But without cell division, no life. To risk cancer, to make it day by day, is to live. The absence of cancer is death. So cancerous cells are a normal part of life. In the popular imagination, we see the immune system as mainly protecting us from infectious disease, from bacteria and viruses. But just as importantly, our immune system protects us against cancer, the cells in our own body that mutate to become other, to pose a threat. At almost 40, I’ve certainly had cancerous cells in me, cells that mutate so they can divide and divide and divide. It’s my immune system that finds those cells and kills them so that I, a whole organism, can survive. But because I don’t have cancer doesn’t mean I haven’t had a cancer cell in me. I have, and survived it, so far.

The second most important discovery that Josh found was the shift in the proportion of excess mortality from old to young that occurred from 2020 to 2021. In 2020 there were 592,000 excess deaths with 126,000 under the age of 65 (approximately 21%). In the second year of the outbreak, there were 512,000 excess deaths with 181,000 under the age of 65 (approximately 35%). The millennials saw the greatest percent increase in mortality of 45% from 42,000 to 61,000. This shift in mortality to younger groups cannot be due to COVID, because the virus was already mutating and becoming less virulent, and we had already determined that the virus killed mostly older people with comorbidities.

The 2024 adjustment I had to make to the chemical formulation of 'Long COVID Supplements' eventually turned out to be a gut adjustment. I was a little mystified as to why this occurred and it may have been from the COVID virus mutating outside of what the original 2022 formulation could treat. I spend most of my time in the USA and the degraded health had coincided with a trip to Germany and the UK.

Not everywhere Spiked at the same time, of course; some regions resisted, but the spread of AI was inevitable. It bred and mutated—evolved—until it seemed likely to absorb everything. It was like a virus eating away at its host, killing everything in its search for nutrients. “Like a virus, though, it also outreached itself. No disease survives by killing its host. It had finished work on the Earth and was partway through absorbing Venus when it began to self-destruct. So

I walked out onto the stage and I started telling the tale of the “Untold Story of the Origin of Zombies.” And it went like this: Where do Zombies come from? Not many people know. But after some extensive investigative Zombie journalism, we’ve discovered the truth. It all began when the human government decided that they wanted to create stronger soldiers. They had lost too many battles, and now they wanted to win every war that they fought. So they approached some soldiers in their army to join a special secret project. The only requirement was that the soldiers they chose had no living relatives. This way, no one could claim their bodies in case something went wrong. So, they exposed these soldiers to an experimental virus to enhance their abilities and make them into super soldiers. The experiment seemed to be working. But then, something terrible happened... The soldiers went crazy, and they were horribly disfigured. Ultimately, the experiment claimed their lives. But, when the soldiers were being prepared for burial, they suddenly came to life. They were not only walking, but they had enhanced strength, enhanced sense of smell and enhanced hearing. They attacked the soldiers in charge of burying them. And the recently bitten soldiers also transformed into the living dead. Before long, the entire army base was contaminated with the virus. Once everyone in the base was exposed, the virus mutated and the soldiers began having an overwhelming craving for something warm and mushy. They longed for brains! Soon, the army of the living dead found their way to the next unsuspecting town in search of brains. They attacked that town, biting anything that moved both human and animal. Soon that town was overrun. The virus spread from town to town, and city to city, until the entire world was contaminated. It was the first Zombie Apocalypse. After hundreds of years had passed, the Zombies started to evolve and began developing intelligent thoughts. They began forming villages, and then towns, and then entire cities of Zombies were created. The Zombies made great advances in health and science, and became highly advanced technologically. But, eventually the Zombies’ appetite for brains and warm flesh gave way to an even greater craving... The craving for CAKE! Their overwhelming desire for cake resulted in an explosive rise in the baking industry. Cake shops began springing up on every corner of every Zombie city street. They just couldn’t get enough! The human race began growing again, too. Human villages of farmers and miners began springing up. And because the Zombies were a peaceful race, they coexisted with the humans by staying away from them. But soon, the Zombie’s resources began to become scarce, especially the cake. So Zombies began scaring villagers in order to get the supplies they needed, especially the highly valued resource of cake. Now Zombies send their kids to Scare School to train their children from a very young age. They train them on how to effectively scare humans in order to get their needed supplies, especially cake. And so it has been until today. Thank you.

It's time to wake up and smell the Mutating Hash! Signature Based Malware Detection is Dead

The two main problems with signature and heuristic based anti-virus is the mutating hash and the fact that you first need a victim in order to obtain the signature." James Scott, Senior Fellow, Institute for Critical Infrastructure Technology

The potential utility of therapeutic gene editing goes far beyond simply reverting mutated genes back to their healthy states. Some scientists are employing CRISPR in human cells to block viral infections, just like this molecular defense system naturally evolved to do in bacteria. In fact, the first clinical trials to use gene editing are aimed at curing HIV/AIDS by editing a patient’s own immune cells so the virus can’t penetrate them. And in another landmark effort, the first human life was saved by gene editing in combination with another emerging breakthrough in medicine: cancer immunotherapy, in which the body’s own immune system is trained to hunt down and kill cancerous cells.

One was that, as live viruses, the attenuated Sabin poliovirus strains always possessed the potential to revert by mutation to virulence and neurotropism, leading to outbreaks of “vaccine-associated paralytic polio.” This possibility—that the vaccine itself would unleash epidemic disease—is not simply theoretical. Outbreaks of vaccine-associated polio occurred in the Philippines (2001), Madagascar (2002), China (2004), and Indonesia (2005).

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.

Many [Russian] treatment programmes will only treat [patients] for one health problem at a time, forcing them to choose between being treated for their addiction or for their TB. Since drug users' lives are often chaotic anyway, being unable to receive holistic care means that they often move between different treatment programmes, stopping and starting courses of different sorts of medication - exactly the circumstances that cause viruses to mutate. The result is one of the highest rates of multidrug-resistant TB in the world, a hazard to health that extends beyond the users themselves, affecting Russian society at large.

All influenza viruses mutate constantly

Nothing of that kind has happened today, at least not yet. Taking a longer view, perhaps, the scourge of new “plagues” will compound the challenges of technological devolution in the new millennium. The unprecedented bulge in human population in the twentieth century creates a tempting target for rapidly mutating microparasites. Fears about the Ebola virus, or something like it, invading metropolitan populations may be well founded.

Before addressing those questions, we need to understand the commonalities of the few pandemics we have information about: 1889, 1918, 1957, 1968, and 2009. First, all five came in waves. (A few scientists argue that the difference in lethality between 1918’s first and second waves mean that these were caused by different viruses, but evidence showing otherwise seems overwhelming. For one thing, exposure to the first wave provided as high as 94 percent protection against the second wave, far better protection than the best modern vaccine affords, and that’s just one piece of the evidence that the same virus caused both waves.) In fact, some investigators now speculate that the 1918 virus circulated in humans for several years before mutations allowed it to spread easily. If true, this would of course explode the hypothesis that Haskell was the origin. The 1889 pandemic virus did follow this pattern, generating two and a half years of sporadic outbreaks around the world, including

The enemy was a virus. The enemy’s chief weapon was rapid and random mutation. It might well necessitate big changes of strategy, and these were bound to be viewed by the public as signs of ineptitude, and the president would need to seem to be the one to rescue these situations rather than be rescued from them.

The Spanish Flu pandemic of 1918 was a myxovirus. It killed twenty million people. Viruses mutate every few months. The antigens on their surface change so that they’re unrecognizable to the immune system. That’s why seasonals are necessary.

Most current licensed antiviral vaccines utilize live-attenuated or whole-inactivated viruses, although there are now a few examples of effective virus-like particle (VLP) vaccines. In the setting of a new pandemic viral threat and without the advantage of a preexisting understanding of its pathogenesis, growth or attenuating features, it would be difficult to quickly develop traditional live-attenuated or whole-inactivated vaccine approaches due to uncertainty about the safety of attenuating mutations or the production of replication-competent virus in bulk

the COVID virus was related to the common cold and the yearly flu, which always mutated, hence the different formulas for the yearly flu vaccines.

The collapse of the Roman population in many areas obviously contributed to economic and military weakness. Nothing of that kind has happened today, at least not yet. Taking a longer view, perhaps, the scourge of new “plagues” will compound the challenges of technological devolution in the new millennium. The unprecedented bulge in human population in the twentieth century creates a tempting target for rapidly mutating microparasites. Fears about the Ebola virus, or something like it, invading metropolitan populations may be well founded. But

But your genes can also be different from those of your parents just through random mutation, which is the imperfect copying from one strand of DNA to another. It can literally be a cosmic ray from outer space that knocks into one of your genes and changes it. Genes sometimes jump from one place on the DNA molecule to another. These are called transposon genes. It could be that your parent’s eggs or sperm (or a plant’s ova and pollen) got messed with a little by some chemical. It could be radiation from some radioactive elements in Earth’s crust that caused a mutation. Sometimes viruses get into the reproductive cells of an organism and modify its genes. Virus manipulation can also be exploited deliberately—to adjust the genes of corn plants so they are tolerant of aggressive weed killer, for example.

Such then is the nature of quasispecies : the density of the sequence cloud at any point in sequence space is determined by the relative fitness of the sequence; regions of the cloud representing sequences of lesser fitness will be less densely populated and those with higher fitness, most populated. Here lies the most powerful quality of viral quasispecies: the density distribution of fitness variants dictates that sequences are represented at frequencies in relation to their relative fitness. Genomes with lower fitness will replicate poorly, or not at all, and the fittest genomes will replicate most efficiently. It therefore follows that there is a large bias toward the production of well-adapted genotypes: there are more of them, and they undergo most replicative cycles. This can permit viruses to experience evolutionary adaptation at rates that are orders of magnitude higher than those that could be achieved by truly random unbiased mutation. Sequences rapidly condense around the fittest area of the sequence space. Should the environment change, and, therefore, selective pressures change, a quasispecies can opportunistically exploits its inherent adaptive potential. Genotypes rapidly and ever-faster gravitate toward the cloud's new notational center of gravity. Changes in the fitness landscape of the sequence space that is occupied by a quasispecies are the natural consequence of altered selective pressures operating on the virus population. Such alterations may be the consequence of changed immunologic pressures exerted by the host, the application of antiviral drug therapy, or even cross-species transmission requiring the virus to adapt to a new host. Genotypes that once occupied the 'central' space, reserved for the fittest genotypes, are reduced in frequency and now occupy the more sparsely populated fringes of the fitness landscape; the very edge of the sequence cloud if you will. Here too lies an advantage for a quasispecies: it has a memory. The once best-adapted genotypes, now at a fitness disadvantage, can persist in the quasispecies as minor sequence variants. Under circumstances of fluctuating selective pressures, the ability of the population to recall an 'old' genome variant is a great asset. The quasispecies can rapidly respond and adapt by plucking out a preexisting variant and quickly coalescing around it to recreate an optimal fitness landscape.

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.

Collectively, the veritable zoo of mobile genetic elements comprises a remarkable 40 percent of our genome. The retroviral sequences littered across all vertebrate genomes are termed endogenous retroviral elements (ERVs). Endogenous retroviral sequences themselves are so plentiful that they take up more space in our genomes than genes encoding human proteins. Their existence is evidence of waves of retroviral infection and germline infiltration throughout vertebrate evolution. We have only recently begun to realize the powerful influence that retroviruses wielded over the evolution of vertebrate genomes and the identity of our species. They were catalysts of genetic instability that fueled evolutionary change; today they are vestiges of their former selves, fossils of viruses that once preyed on vertebrate hosts. Their remains are evidence of pyrrhic victories of sorts in many wars and arms races that have taken place between retroviruses and hosts. Most endogenous retroviruses have long been silenced by host cell restriction mechanisms. Associated with no phenotype, and under no selective pressure they become nonviable after millions of years of mutational drift, resulting in the accumulation of mutations and deletions in their coding sequences and control elements.

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.

The litter of ERVs across vertebrate genomes, mainly in the form of defective and deleted proviruses, mutationally inactivated proteins coding sequences, and isolated LTRs, confirms that the vast majority of endogenized retroviral genones decay to nonfunctional sequences. If they have been silenced by cellular regulatory mechanisms or if their gene products are not under purifying or positive selective pressures, their DNA sequences will be under no selective pressure to retain their functionality. Over time, they accumulate random mutations and their sequences drift without consequence to the host. That ERVs mostly become such inconsequential DNA is a topic of hot debate; it is, however, an easy matter to pick several examples that illustrate how hosts can benefit from their ERVs. As for all matters of evolution, we bear witness only to the successful events that are now fixed in genomes. Evolutionary failures, no matter they far outnumber the successes, go unrecorded, rapidly purged from the gene pool.

Dan Quayle, mutating the memes in the United Negro College Fund’s motto, “A mind is a terrible thing to waste.” There is some good news in this book. So before I get into how mind viruses are spreading wildly throughout the world—infecting people with unwanted programming like the Michelangelo computer virus infects computers with self-destruct instructions—I’ll start with the good news. . . .

Now we fight back," she said. "We know how to hurt them. Now we are the virus, and we will spread from here." Her eyes glittered with intent. "Let's go make some noise.

Sequences of base pairs, called genes, code for and produce gene products such as proteins. If just one of the base pairs is altered by mutation, say from ultraviolet damage, a virus, or cigarette smoke, the resulting protein will be aberrant, and usually faulty. Some of these mutations are not fatal and are actually kept by the cells and the population. These are called single nucleotide polymorphisms, or SNPs. If the incidence of the change is found in less than 1 percent of the population of humans, it is called a mutation; if more than 1 percent, it is typically called an SNP. There are about twenty million SNPs found in humans, and they account for many differences in the appearance and behavior of people, from curly hair to obesity to drug addiction. It is these SNPs where the hunt for genetic “causes” of traits and diseases has focused since the 1990s.

There’s a curious correlation between these sunspot peaks and flu epidemics. In the twentieth century, six of the nine sunspot peaks occurred in tandem with massive flu outbreaks. In fact, the worst outbreaks of the century, killing millions in 1918 and 1919, followed a sunspot peak in 1917. This might just be coincidence, of course. Or it might not. Outbreaks and pandemics are thought to be caused by antigenic drift, when a mutation occurs in the DNA of a virus, or antigenic shift, when a virus acquires new genes from a related strain. When the antigenic drift or shift in a virus is significant enough, our bodies don’t recognize it and have no antibodies to fight it—and that spells trouble. It’s like a criminal on the run taking on a whole new identity so his pursuers can’t recognize him. What causes antigenic drift? Mutations, which can be caused by radiation. Which is what the sun spews forth in significantly greater than normal amounts every eleven years.

The virus of modern anti-Semitism started here in Europe, but after the war it spread to the Arab world, where it mutated and grew stronger. Now Europe and the radical Muslims are passing it back and forth, infecting one another. -Eli Lavon

Public health experts monitor this drift and each year adjust the flu vaccine to try to keep pace. But they will never be able to match up perfectly, because even if they predict the direction of mutation, the fact that influenza viruses exist as mutating swarms means some will always be different enough to evade both the vaccine and the immune system.

But the 1918 virus, like all influenza viruses, like all viruses that form mutant swarms, mutated rapidly. There is a mathematical concept called “reversion to the mean”; this states simply that an extreme event is likely to be followed by a less extreme event. This is not a law, only a probability. The 1918 virus stood at an extreme; any mutations were more likely to make it less lethal than more lethal. In general, that is what happened. So just as it seemed that the virus would bring civilization to its knees, would do what the plagues of the Middle Ages had done, would remake the world, the virus mutated toward its mean, toward the behavior of most influenza viruses. As time went on, it became less lethal.

But the virus, even as it lost some of its virulence, was not yet finished. Only weeks after the disease seemed to have dissipated, when town after town had congratulated itself on surviving it—and in some places where people had had the hubris to believe they had defeated it—after health boards and emergency councils had canceled orders to close theaters, schools, and churches and to wear masks, a third wave broke over the earth. The virus had mutated again. It had not become radically different. People who had gotten sick in the second wave had a fair amount of immunity to another attack, just as people sickened in the first wave had fared better than others in the second wave. But it mutated enough, its antigens drifted enough, to rekindle the epidemic. Some places were not touched by the third wave at all. But many—in fact most—were.

As I write in 2015, scientists are looking at the next potential pandemics. It may take only a few mutations for a strain of bird flu to evolve into a new strain of human influenza virus. Reassortment could accelerate the change. No one can say when, or if, any particular strain will make the jump. But we are not helpless as we wait to see what evolution has in store for us. We can do things to slow the spread of the flu, such as washing our hands. And scientists are learning how to make more effective vaccines by tracking the evolution of the flu virus so they can do a better job of predicting which strains will be most dangerous in flu seasons to come.

But the virus can adapt to man. It can do so directly, with an entire animal virus jumping to humans and adapting with a simple mutation. It can also happen indirectly. For one final and unusual attribute of the influenza virus makes it particularly adept at moving from species to species.

When people in the Near East first domesticated cattle from a type of wild ox called an aurochs, a mutation in the cowpox virus allowed it to jump into humans—and smallpox was born. Rinderpest in cattle migrated to people and became measles. Tuberculosis probably originated in cattle, influenza in birds and pigs, whooping cough in pigs or dogs, and malaria in chickens and ducks. The same process goes on today: Ebola probably jumped to humans from bats, while HIV crashed into our species from monkeys and chimpanzees.

Hello Corona Virus, goodbye world.

virus emerged through a background of seasonal flu sometime in the winter of 1917–18, and was already circulating at low levels the following spring. Whether it came directly from a bird, or passed via a pig, he can’t yet say. In the summer of 1918, it mutated, becoming highly contagious between humans. This new, more virulent form spread through the viral population that summer, and in the autumn the disease erupted. By then, the seasonal background had receded, and there was nothing to dilute the ‘pure’ pandemic variety.