The Bible also predicts the problem of disease at the end of history. Jesus himself says, “There will be great earthquakes, and in various places plagues and famines” (Lk. 21:11). John writes, “I looked, and there before me was a pale horse! Its rider was named Death, and Hades was following close behind him. They were given power over a fourth of the earth to kill by sword, famine and plague, and by the wild beasts of the earth” (Rev. 6:8 NIV).
Skeptics in the early modern era believed that the fear of disease was an ancient problem—not a modern one. After the advent of modern medicine, it seemed that plagues were obsolete. However, in recent years, we have begun to see how all too vulnerable we are to disease. Joshua Lederberg (the Nobel Prize winner for medicine in 1958) writes,
The single biggest threat to man’s continued dominance on the planet is a virus.
We have unprecedented mixing of people; a million passengers a day cross national boundaries by air, not to mention the movement of armies, refugees, and road transport as well-documented vehicles for the rapid spread of disease. One could hardly have concocted a better—calculated recipe for a tinderbox, as AIDS already harshly teaches. From this perspective, we have never been more vulnerable.
In his book The Fate of the Species, Fred Guterl (the executive editor of Scientific American) writes,
We are surrounded by influenza viruses that live in birds, and this reservoir poses a constant existential threat to humans. The prospect of eradicating this threat is essentially zero. From the history of bird flu in the last few decades, you might get the impression that influenza has a demonic intention to wreak havoc. The virus seems to be straining to evolve into a new form that targets the world’s human population.
Influenza is the master of change—its survival as a species hinges on its ability to alter its genetic makeup. Each nucleotide of the influenza genome is subject to mutations—sometimes these occur randomly, sometimes they involve swapping whole genes with other viruses. This is true of nucleotides in all organisms, of course. But flu viruses are particularly swift at this evolutionary roulette, which gives the virus an alarming ability to target itself as a human pathogen. It is influenza’s way of probing for a new pathogenic niche. It’s like playing a slot machine. Each season we pull on the handle and wait to see if we’ve won a jackpot. Usually we get mixed fruit, and a mild outbreak. Once in a while, we get a small jackpot (a mild pandemic, say, such as the 2009 outbreak). The slot machine could also come up all bananas—some combination of nucleotides that turn a mild human pathogen into a killer on a scale that nobody has known before. The virus, by recombining with other viruses, swapping genes, and taking on random mutations in its genetic code, keeps trying to find this jackpot combination—a bug that spreads easily and quickly, but strikes with deadly virulence. It’s possible that the genetic slot machine hasn’t yet produced is worst—and that the deadliest human influenza virus awaits us.
The difference between the April 1983 virus and the November one—between a nuisance and a death sentence—came down to a single protein.
In 1918, the H1N1 virus burned through the world in less than two years, despite the lack of air travel, leaving 50 million to 100 million people dead in its wake. (Nobody knows precisely how many died. Information about influenza deaths was hard to come by back then, and in many ways it still is.) At the time, the world held 1.6 billion people. By simple extrapolation to the current population of more than 7 billion, a similar disaster today would leave 180 million to 375 million dead.
[Regarding the H1N1 pandemic virus; quoting Dr. Robert Webster of St. Jude Children’s hospital] This time we got damn lucky the virus was only mildly pathogenic. If H1N1 had truly killed as effectively as the 1918 flu, it would have been total disaster… You wouldn’t get the gasoline for your car, you wouldn’t get the electricity for your power, you wouldn’t get the medicines you need. Society as we know it would fall apart. There wouldn’t be a hell of a lot scientists could do for you in the first wave.
The Black Death struck a very different planet than the one we now inhabit. News traveled slowly back then, and so did people—the trip from Crimea to China, where the disease first emerged, took about twelve months over the mountains and along the hardscrabble roads. The strain of bacteria that caused the plague took several years to make its way across the Eurasian continent, hitchhiking on rats and their fleas. When it arrived, though, it seemed like Armageddon to those who lived through it. In Europe, it killed about a third of the population—as much as 60 percent in some places. The population of China dropped 50 percent.
As these experts in the field argue, disease is still a daunting prospect for humanity—exactly as the Bible foresaw for the end of human history.
Go back to article: “Predictions of the End of Human History”
 Crawford, D. The Invisible Enemy: A Natural History of Viruses. New York, NY: Oxford University Press. 2003. 2.
 Journal of the American Medical Association (JAMA), January 17. 1996 Vol. 275, No. 3
 Guterl, Fred. The Fate of the Species: Why the Human Race May Cause Its Own Extinction and How We Can Stop It. New York: Bloomsbury, 2012. 13.
 Guterl, Fred. The Fate of the Species: Why the Human Race May Cause Its Own Extinction and How We Can Stop It. New York: Bloomsbury, 2012. 16.
 Guterl, Fred. The Fate of the Species: Why the Human Race May Cause Its Own Extinction and How We Can Stop It. New York: Bloomsbury, 2012. 17.
 Guterl, Fred. The Fate of the Species: Why the Human Race May Cause Its Own Extinction and How We Can Stop It. New York: Bloomsbury, 2012. 19.
 Guterl, Fred. The Fate of the Species: Why the Human Race May Cause Its Own Extinction and How We Can Stop It. New York: Bloomsbury, 2012. 17-18.
 Guterl, Fred. The Fate of the Species: Why the Human Race May Cause Its Own Extinction and How We Can Stop It. New York: Bloomsbury, 2012. 25-26.