Survival of the Sickest

by

Sharon Moalem

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Survival of the Sickest: Chapter 6 Summary & Analysis

Summary
Analysis
At the end of the 18th century, a doctor in Gloucestershire, England named Edward Jenner discovered a pattern: milkmaids who caught cowpox seemed resistant to smallpox. He scraped a cowpox sore from a milkmaid and purposefully infected teenage boys, who as a result were protected from smallpox. This became the first vaccine, and the word actually comes from the Latin name for cowpox, vaccinia.
While the previous chapter illustrated how microbes and other pathogens have learned to evolve adaptations that help them survive and reproduce, this chapter focuses on what humans can do to do the same. Vaccines illustrate how we can use evolutionary information from viruses (i.e., seeking out viruses that will produce antibodies to more harmful diseases) that can then help us  survive deadlier diseases.
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Today, we know more about how vaccination works: modern vaccines introduce a harmless version of the virus into our bodies, stimulating our immune system to produce antibodies tailored to defend against the virus. But for a long time, scientists didn’t understand how our bodies created antibodies to fight against every microbial attacker because we couldn’t have enough genes dedicated to each one—until they recognized that genes could change.
This chapter also introduces the idea that we can develop some adaptations much more rapidly than previously thought. Moalem describes how for a long time, we didn’t fully understand our own immune response, highlighting the ongoing need for research.
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When a sperm and egg cell combine to form a zygote cell, all of the DNA needed to build a human being is already in place—the instructions are carried in 3 billion pairs of nucleotides, which amount to fewer than 30,000 genes. These genes are organized into 23 chromosomes, which carry the same type of instructions in each person but with individualized content (say, for hair color or eye color). Every cell in the body contains the same DNA, except for sperm and egg cells—which contain only one set of 23 chromosomes rather than two sets.
Moalem provides background information on DNA and how we are born with all the genetic information we will ever have. At first, it seems that this emphasizes the fact that DNA is rigid and relatively unchangeable outside of small, random mutations. But given Moalem’s previous point that genes are changeable, it’s likely that our genetic code is actually a lot more mutable than we were once thought.
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Interestingly, less than 3 percent of a person’s DNA contains instructions for building cells; the other 97 percent isn’t active in building anything. Scientists initially called this genetic material “junk DNA,” believing that it didn’t help us in any way and had simply stayed in the gene pool for millions of years. But more recently, scientists have discovered that this genetic information—now called “noncoding DNA”—may be incredibly important in to the evolutionary process. What may be even more surprising is that researchers now believe that as much as a third of our DNA has developed from viruses.
Over the course of the chapter, Moalem illustrates how scientists’ ideas of “junk DNA” have shifted, again emphasizing the need for research in a multitude of fields. He implies that by understanding the evolution and adaptation of viruses, researchers can then recognize how that adaptation has, in turn, helped humans evolve.
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For a long time, the scientific community believed that genetic changes were the product of accidental mutation—errors in copying DNA information from one cell to another that got through our genetic proofreading system. Mutations can also occur when organisms are exposed to radiation or chemicals. Sometimes, a random mutation will give the organism an advantage, which in turn makes its survival and reproduction more likely. This is when natural selection steps in: the mutation increases in successive generations, causing evolution.
Moalem introduces the fact that DNA is relatively unchangeable and that evolution is prompted only by small, random mutation. After all, much of his book has emphasized how the DNA of our ancestors, as much as 10,000 years ago, is still shaping our genome today—giving some credibility to the idea that “biology is destiny.” Yet he articulates this idea as a jumping off point only to show how thinking and research on the topic has progressed and that this belief is actually antiquated.
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More recently, scientists recognized that it would be unlikely for mutations to occur only randomly, because the ability to react to environmental changes and pass on adaptations would be selected for. Additionally, geneticists originally believed that every gene had a single purpose, which would suggest having more than 100,000 genes—but in reality, we only have about 25,000. Thus, genes must interact and shuffle to produce the proteins necessary for human life. Scientists now conceive of genes as “an intricate network of information” that can react to changing circumstances. If one gene fails, another gene can “pick up the slack.” Thus, it is unlikely that small random mutations have led to our evolution, because other genes would simply compensate.
Here, Moalem provides a series of points to argue why it would be advantageous for genes to be more adaptable. Even though not all mutations are good, the mere ability to spur those mutations for a chance of adapting more quickly in the face of environmental pressure would be very helpful in enabling our survival. Additionally, he gives some evidence that genes are  already capable of adapting to new circumstances because they are able to respond to changes in the environment— or, as Moalem has noted before, of developing antibodies for new pathogens.
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Jean-Baptiste Lamarck, according to popular accounts, was the chief proponent of a theory called inherited acquired traits. The theory holds that traits acquired by a parent during their lifetime could be passed on to their offspring—like giraffes’ necks stretching further and further with each generation to reach leaves on higher branches. According to history, Charles Darwin then proved Lamarck’s theory incorrect with his theory of natural selection. Moalem writes that little of this story is true: Lamarck promoted inherited acquired traits, but he also believed in natural selection—and Darwin believed in both as well. The irony is that the theory of inherited acquired traits isn’t completely wrong.
The theory of inherited acquired traits is often contrasted with Darwin’s theory of natural selection, but Moalem makes a point of illustrating the ways in which the theory may not have been so off—genes might be more mutable than Darwin’s theory supposes.
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Barbara McClintock was a revolutionary thinker who was largely ignored by her peers. She received her Ph.D. in 1927 at age 25, and she focused the next 50 years of her career on research on corn genetics. McClintock discovered that in certain circumstances, particularly when the corn was stressed, whole sequences of DNA moved from one place to another and triggered significant changes in the genome. These were often caused by changes in the environment, and the “jumping genes” relocated to certain parts of the genome more often than to other parts. It seemed as though the corn was mutating intentionally rather than randomly.
McClintock’s research provides the first tangible example of how an organism’s genes can adapt at a much more rapid pace than previously thought. Not only that, but they can adapt during an organism’s lifetime. This proves how organisms can be immediately impacted on a genetic level by changes in their environment—a concept vastly different from the idea that a change in environment can make certain adaptations more advantageous and passed down due to that fact. This implies, as indicated by the use of the words “active” and “intentional,” that these adaptations are not passively selected for but are actively mutated.
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Barbara McClintock’s findings were largely faced with skepticism until 1983, at age 81, when she received the Nobel Prize. Her discoveries opened the door to the possibility of intentional mutation and much faster evolution. Scientists are still only beginning to understand how these jumping genes (transposons) work—sometimes they copy themselves and insert new material elsewhere, or sometimes they cut themselves out of their starting place and insert somewhere else. One study showed the enormity of the effect they can have: a jumping gene in one line of fruit flies gave them the ability to resist starvation, withstand high temperature, and have a 35 percent longer life expectancy.
The example of the fleas suggests that not only are jumping genes able to respond to environmental pressure (for example, a lack of food), but that these genes can also be passed down from one generation to the next. This gives credence to the inherited acquired traits theory for which Lamarck has historically been lambasted, and it also provides some evidence for the idea that adaptation can occur at a much more rapid rate than previously believed.
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McClintock believed that these responses were caused by internal or environmental stress, spurring jumping genes to take a chance on mutating in hopes that they would get a mutation that might help. When that occurs, the proofreading mechanism is suppressed and adaptations are allowed. Today, scientists believe this notion that the genome is not as rigid as once thought, and that mutation is not simply random.
Moalem sums up McClintock’s findings of jumping genes, suggesting that genes are not necessarily set in stone even after an organism is born, and that the immediate environment of an organism can have an effect on its genes and spur it to advantageous mutation.
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In the 1980s and 1990s, researchers studied other organisms that exhibited the same jumping genes: E. coli, which appeared to target specific areas of its genome where mutations were likely to be advantageous—a process researchers called “hypermutation.” When E. coli was placed in an environment with only lactose (which it could not digest),  studies showed increased mutation in the bacteria’s genome, and not just in an attempt to overcome lactose intolerance.
The example of E. coli demonstrates that organisms are not simply spurring mutations that might help them overcome a particular environmental stress; rather, the jumping genes are shifting in a way that might allow them to develop any helpful mutation, providing evidence for the idea that jumping genes can lead to any number of adaptations. Additionally, the study of the E. coli illustrates how environmental factors are important in spurring those adaptations.
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Moalem transitions to how jumping genes can play into human evolution. In the 19th century, biologist August Weissman divided the body’s cells into two categories: germ cells (egg and sperm cells) and somatic cells (all other kinds of cells). Weissman’s theory, now known as the Weissman barrier, holds that information in somatic cells is never passed on to germ cells. Thus, a mutation in one’s red blood cells would not be passed on to one’s children—only a mutation in the germ line would be passed on. But new research suggests that this might not necessarily the case.
Again, Moalem introduces long-held scientific concepts so that he can illustrate how research and accepted science have progressed. Since the 19th century, conventional wisdom dictated that mutations that occurred during a person’s life would not then be inherited by that person’s offspring. However, as with the discovery of jumping genes, it’s likely that there may be exceptions to the Weissman barrier theory.
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Jumping genes are very active in the early stages of brain development, and Moalem posits that this may help create the variety and individuality that make every brain unique. This activity is only found in the brain because it benefits from individuality—the heart, by contrast, does not. The immune system also welcomes diversity, and scientists from Johns Hopkins have found that jumping genes may help us produce antibodies to develop protection against invaders. However, even if we develop antibodies, we can’t pass them on to our children because of the Weissman barrier. Babies are born with a small number of antibodies, which is why breast milk (which contains some of the mother’s antibodies) is important for babies.
The fact that jumping genes have helped us develop the individuality in our brains is significant, as it again suggests that our DNA (and even our intelligence) is not totally set in stone. Further, the diversity that jumping genes create in our immune system is evidence for why we can adapt so many antibodies, a puzzle that Moalem brought up at the beginning of the chapter.
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There is now evidence that one-quarter of active (coding) human genes have incorporated DNA from jumping genes. The more we understand about how they work, “the more they may reveal about how our immune systems protect us against disease.” Moalem also notes that as much as half of the “junk DNA” that was previously believed to be unhelpful is actually made up of jumping genes.
The fact that so much of our noncoding DNA is made up of jumping genes illustrates how important it may have been to evolution. Jumping genes would presumably have conferred an advantage to humans that adapted them because those humans were more likely to develop helpful mutations, and they were therefore better equipped to survive and reproduce.
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Additionally, the jumping genes discovered in human DNA look a lot like virus DNA. A virus is essentially a small portion of genetic code that can’t reproduce on its own—instead, viruses reproduce by infecting a host and using the hosts’ cellular machinery to replicate. Retroviruses are a subset of viruses that are made of RNA (which usually acts as a messenger, copying instructions from DNA to create specific proteins). Retroviruses are able to reverse the process of DNA being copied to RNA, and they can write themselves into a person’s DNA.
Retroviruses reinforce one of the ideas from Moalem’s earlier chapters: that we are evolving alongside viruses, not independent of them. More than that, viruses may be helping us to evolve from the inside, not only spurring our evolution from the outside, because jumping genes might have once been viral DNA and now enables us to adapt more rapidly.
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Retroviruses can thus write themselves into the DNA of cells in the germ line of an organism, and that organism’s offspring is then born with the virus encoded in  its DNA. If the virus is harmful, it is unlikely that offspring will survive. But if the virus is not harmful, the offspring can survive and reproduce, and the virus becomes a permanent part of the gene pool. Scientists know that at least 8 percent of the human genome is composed of helpful retroviruses. Viruses can help us because they are “master mutators” which can evolve incredibly fast and help us adapt.
Moalem demonstrates how viruses—and jumping genes—not only provide us with acquired mutations but can then enable us to pass on those mutations. Viruses have a vested interest in our survival,  because that is how those viruses then continue to be passed on. Thus, this interspecies adaptation is mutually beneficial, because it might allow us to overcome all kinds of different environmental obstacles.
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Moalem reiterates that jumping genes are probably descended from viruses, and these genes have helped us evolve into complex organisms much faster than we could have otherwise. Humans and African primates also share an interesting genetic trait: our genomes have been modified by a retrovirus in a way that makes it easier for us to be infected by other retroviruses. This capacity to support infection may have enabled us to evolve at a much faster rate, as exposure to other retroviruses could have facilitated more rapid mutation.
Again, Moalem emphasizes how having viruses and jumping genes as a part of our DNA has actually been incredibly beneficial to us—even suggesting that their involvement in our genome is what allowed us to evolve into humans in the first place. Thus, while Moalem has demonstrated how viruses can be harmful, they can clearly also help us adapt and survive.
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