A finalist for the 2017 Los Angeles Times Book Prize in science and New York Times Book Review Editor’s Choice, science journalist Sonia Shah’s 2016 work Pandemic: Tracking Contagions, from Cholera to Coronaviruses and Beyond interweaves history, firsthand reporting, and personal narrative to explore the origins of epidemics, drawing parallels between cholera—one of history’s deadliest and most disruptive pathogens—and the new diseases that stalk humankind today, from the MRSA bacterium that besieges her own family to the never-before-seen zoonoses that have emerged from China’s wet markets. Delving into the convoluted science, strange politics, and checkered history of the world’s deadliest outbreaks, Pandemic is a work of epidemiological reportage like no other, with urgent lessons for our own time.

 “The most provocative — and sci-fi — part of Ms. Shah’s book is not about the ways humans have altered the evolution of pandemics. It’s about the ways pandemics have altered the evolution of humans.” —The New York Times

Here is an excerpt from Pandemic -

At one time, all life on the planet reproduced asexually (by cloning or other methods). There were no sexually reproducing creatures. But at some point in the history of evolution, sexual reproduction emerged. And yet, from the point of view of our genes, it was a vastly inferior strategy compared to other methods of reproduction. Organisms that clone themselves pass on 100 percent of their genes to their offspring. Sexual reproducers must not only partner up with another individual to reproduce, but both parents lose half of their genes in the bargain, for the resulting child inherits half of its genes from each parent.

To survive, the first sexually reproducing organisms would have had to outcompete the cloners, who dominated the resources and habitats of the planet. But how could they? In the 1970s, the evolutionary biologist William Hamilton created a computer model to simulate what that contest looked like. The simulation set up a population in which half of the individuals practiced cloning and half paired up and had sex. (Imagine a clan of all-female Amazons who replicate themselves without males, alongside a tribe of females who could reproduce only with the help of a male.) Everyone was equally subject to the kind of random deaths that befall populations in the wild, like being attacked by predators or frozen in an ice storm. The model then calculated the reproductive success of the two tribes, counting the number of offspring they each produced.

The cumulative effect of the two different reproductive strategies didn’t take long to reach its logical conclusion. Every time Hamilton ran the model, the sexual reproducers rapidly went extinct. Random deaths in the sexually reproducing tribe resulted in a disproportionate loss to the mating pool (as anyone who has tried to find a date after the age of forty can understand intuitively). Not so for the cloners, who maintained their vigorous rate of replication regardless of random losses. It didn’t matter that the offspring of the sexually reproducing tribe were more genetically diverse and therefore more resilient to long-term changes in the environment. The burden of random deaths was too immediate to allow those benefits to manifest themselves.

Thus sexual reproduction should have been an experiment that failed. And yet it didn’t. Eventually, the reproductive strategy of our most distant ancestors spread throughout the animal kingdom, including in us, many years later, in whom it became a central preoccupation.

It was Hamilton who offered a startling explanation that solved the mystery: sex evolved, he said, because of pathogens.

Sexual reproduction requires a profound genetic sacrifice, he noted, but the payback is that the offspring of sexual reproducers are genetically distinct from their parents. That was no big advantage in surviving hostile weather or predators, Hamilton observed, but it was a huge advantage in surviving pathogens. That’s because pathogens, unlike the weather or predators, refine their attacks upon us.

Imagine a pathogen that first strikes when you’re a baby. As you develop, the pathogen goes through hundreds of thousands of generations. By the time you’re an adult (if you’ve survived the ravages of the pathogen) and are ready to reproduce, the pathogen has become far better at attacking you than you are at defending yourself against it. While your genetic makeup has stayed the same, the pathogen’s has evolved.

But individuals who clone themselves provide pathogens exact replicas of the target they’ve already gotten so good at stalking. They endow their offspring with the worst possible chances of surviving the pathogen’s appetites. Much better, in that case, Hamilton theorized, to produce offspring that are genetically distinct from you, even if that means forsaking half of your own genes.

Scientists have shown how refined pathogens’ attacks become over time by experimentally transferring the pathogens of an old individual into a young one. One study cited by the evolutionary zoologist Matthew Ridley focused on long- lived Douglas fir trees, which are routinely attacked by scale insects. (Although scale insects are not microbes, they are disease-causing organisms just like microbial pathogens.) In the wild, old trees are more heavily infected than young ones. This is not because the old trees are weaker than the young ones, as one might think. The old are more heavily infested because their pathogens have had more time to adapt to them. When scientists transplanted the scale in-sects of an old tree onto a young tree, the young tree suffered the same heavy burden of disease as its elders. It’s easy to see how, with pathogens like that around, sexual reproduction would provide a better chance at survival than cloning.

Since Hamilton first articulated his theory about pathogens and the evolution of sex, a large body of supportive evidence has accumulated. Biologists have found that species that practice both sexual and nonsexual reproduction will switch between the two depending on the presence of pathogens. When raised in a lab devoid of their usual pathogens, or in the presence of pathogens that are altered in such a way that they can-not evolve, the roundworm Caenorhabditis elegans will mostly replicate without sex. But when stalked by pathogens, it will reproduce sexually instead. In other experiments, scientists altered roundworms so that they cannot sexually reproduce. When they reared these worms with pathogens, the nematodes went extinct within twenty generations. In contrast, when they allowed roundworms to practice sexual reproduction, they survived alongside their pathogens indefinitely. Withstanding pathogens seems to require the special benefits provided by sexual reproduction.

To read more, get a copy of Pandemic here: https://www.amazon.in/Pandemic-Tracking-Contagions-Cholera-Beyond/dp/125011800X