DNA mutations in humans are generally bad, but why to they make viruses stronger?

DNA mutations in humans are generally bad, but why to they make viruses stronger?

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When I read about DNA mutations in humans, the mutations are generally bad. When I read about mutations in viruses such as the recent emerging strains of COVID-19, however, it seems to be good for the virus and make it stronger.

Why do mutations seem to be good for viruses, and can we apply that technique to the human body too?

The effects of mutations
As have been already pointed out, mutations are neither good nor bad - they are simply changes in the DNA sequence. The effects of mutations on humans and viruses are rather different, since humans are multicellular organisms - mutations in one cell do not affect the whole organism, but only this cell (except for the germline mutations in sperm and ovum, before these cells start to divide and become an organism with trillions of cells).

A mutation in a human cell may have different effects:

  • if it occurs in a coding region of a protein, this protein may start working better or its functioning may be disrupted (the latter is more statistically probable), leading to cell death.
  • if it occurs in a regulatory region, it may dirupt normal functioning of the cell, e.g., making it divide uncontrollably, and thus creating a cancer tumor.
  • it may also happen in a unimportant region, conferring no special changes. Note also that severe disruptions, such as thsoe leading to cancer, are usually not a result of a single mutation, but an accumulation of many of them.

A mutation in virus may equally have different effects. Most mutations have either negative effect - producing a non-functional virus, or a neutral effect - resulting in no special changes (particularly the so-called synonymous mutations, which do not change the identity of the encoded amino-acid). Some mutations change the proteins in the virus capsid, resulting in viruses which either have different properties vis-à-vis antibodies or can better attach to cellular receptors - these are beneficial for virus survival.

The important difference with the hma, where mutations affect only one cell, is that a single infected cell produces multiple new viruses (from dozens to millions of them,d epending on the virus) - some of them will be disfunctional, some as good as their parents, and some more fit.

Classification of mutations
As could be already conjecture from the discussion above, depending on the effect of the mutation on the new viral particles, they can be classified in deleterious, neutral and beneficial.

Mutations and fitness
A single viral particle being more fit would not pose much problems. However this particle may infect another cell, producing new generation of fit particles, which will replicate again and so on. In other words, what makes a mutation good for a virus is the natural selection among the millions of viral particles.

On the other hand, when we speak about a mutatuion being bad for a huma, we speak about the effect of the mutation on a single individual. In otehr words, we are comparing here appels and oranges. If we were to make an equivalent comparison, we should consider a human population over the course of thousands or even millions of generations. We would see in this case mutations can have similarly different effects: the Neanderthal "human strain" turned out to be less fit and disappeared, whereas the homo sapiens "strain" has survived and populated the whole Earth.


Mutations of the genome are neither bad nor good. They alter. If the product of this alteration is advantagious to the virus or any organism, they may gain some advantage to reproduce better. If the alteration is deleterious, it may be bad for the virus and any organism.

With humans you see bad results with viruses not (they are too small).

FAQ: How viruses mutate

More than 100 people have died in Mexico as a result of an outbreak of swine flu, a strain of the influenza virus that normally targets pigs but has occasionally mutated enough to infect and spread in humans.

This ability to mutate from one host to the next, or one species to the next, is one of the traits that has given the influenza virus a long life and made it both nearly impossible to eradicate and potentially dangerous to animals and humans alike.

Here we explore the reasons why viruses mutate, how they do it, and what impact their environment plays in their ability to cause pandemics.

Why do viruses mutate?

Bird flu vs. swine flu

Almost all human diseases originate from other animals and then adapt to human hosts, says University of Guelph agriculture professor David Waltner-Toews, author of The Chickens Fight Back: Pandemic Panics and Deadly Diseases that Jump from Animals to People.

With influenza, different strains of the virus affect people, birds and pigs. Naturally, human influenza is the easiest for humans to get and to transmit to other humans. Humans can also get bird influenza and pig influenza, but it typically requires very close contact with the animals, Waltner-Toews said .

Bird or avian influenza is particularly hard to get, but humans who do get it experience very severe symptoms. That is why people were worried about a deadly pandemic if avian influenza were to mutate in such a way as to become easily transmissible between humans. Swine influenza is somewhat easier to transmit to humans but its symptoms tend to be milder than bird influenza.

Most flus contracted by humans are made up of predominately human influenza, but contain small pieces of avian or swine influenza. Swine flu is unusual because it is made up mostly of swine influenza but contains small amounts of avian and human influenza.

The movement of a virus between species opens up more opportunities for mutations in the virus, said Dr. Ruben Donis, head of the molecular genetics branch of the influenza division at the U.S. Centers for Disease Control.

The mutations would not necessarily make the virus cause more severe disease, but it cannot be ruled out, Donis said.

Mutations could also perhaps make the virus stronger at beating the immune system or resistant to drugs, said Stephen Drews, a clinical microbiologist at Ontario's Public Health Laboratories.

To survive: unlike plants, animals and other organisms, the only way a virus can reproduce is through a host cell, which it does by attaching its surface proteins to the cell's membrane and injecting its genetic material into the cell. This genetic material, either DNA or RNA, then carries with it the instructions to the cell's machinery to make more viruses. These new viruses then leave the cell and spread to other parts of the host organism.

But host organisms are not passive observers to this process, and over time a human's or pig's immune system can learn from these encounters and develop strategies to prevent reinfection. The next time the same virus comes to a host cell, it may find that it is no longer able to attach to the cell's surface membrane. So to survive, viruses must adapt or evolve, changing its surface proteins enough to trick the host cell into allowing it to attach.

What makes one virus mutate quickly while others change more slowly?

The genetic material inside the virus plays an enormous role in how quickly a virus mutates, which in turn can impact how the illness can spread in the population.

Viruses that replicate through DNA use the same mechanisms the host cell uses to create its own DNA, a process that includes a kind of "proof-reading" of the genetic material being copied. This means mutations occur more slowly.

Examples of DNA viruses such as smallpox. These viruses spread through human populations and were often fatal. But once vaccinations were developed viruses like smallpox were contained and all but eradicated. RNA viruses, on the other hand, replicate without a similar proofreading activity, and as a result, errors in the genetic coding occur. Its these errors that allow RNA viruses, such as influenza and HIV, to mutate rapidly from host cell to host cell, and make it difficult for vaccines and natural immunities to keep up and prepare for new strains of the virus.

How does a virus travel from an animal like a pig to a human?

Viruses spread from one animal to another through close contact, in whatever manner it normally spreads, such as coughing or sneezing in the case of a respiratory virus. Normally, these infections have no impact on the new host since they were not built to infect them. But when one host is infected by two or more strains of a virus like influenza, new combinations can result.

Influenza, for example, has eight distinct segments to its genome, increasing its ability to form new combinations that can include elements of avian flu, swine flu and human flu. It's these recombined versions of the flu that have the potential to cross over and actually spread through a new host.

Pigs are a particularly good incubator as they have receptors for influenza from all three species, said University of Guelph agriculture professor David Waltner-Toews, author of The Chickens Fight Back: Pandemic Panics and Deadly Diseases that Jump from Animals to People.

"So, if they happen to be around people or birds that have influenza, they will pick them up, and the viruses will mix up inside them."

And as the flu spreads, its list of available hosts spreads as well. Until five years ago, for example, dogs were not susceptible to influenza, said Dr. Earl Brown, a professor of microbiology at the University of Ottawa Faculty of Medicine. But the flu has since spread to canines through horses.

What role does the environment play in mutation?

One of the big factors in the mutation rate of viruses is population density, said Brown.

"When you have high density conditions and overcrowding, like you would see in a pig farm, then the mutation occurs much more quickly as it passes from one snout to the next," he said. The kind of virus likely to thrive is also a function of its environment, he said.

A virus that quickly kills its host as it spreads is more likely to thrive in densely populated areas where it can out-compete other viruses, but would die out when the supply of new hosts is in short supply, he said. Conversely, a virus that incubates in the host for weeks and spreads slowly is more likely to thrive in animals like migratory birds, he said.

How much do farming practices contribute?

Human populations have grown over the past few centuries, and in recent decades, the demand for pork and chicken has soared. That has led to the proliferation of large, dense farms with thousands of animals. Waltner-Toews said those result in a number of factors that boost transmission of viruses such as influenza:

  • Many genetically similar animals are kept in one place, and their similarity leaves them susceptible to the same diseases.
  • The stress of crowded conditions increases the chance that infected animals will show disease symptoms that help the disease spread, such as coughing and sneezing.
  • The animals are shipped all over the world.
  • People are traveling all over the world, including migrant farm workers brought in from other countries as cheap agricultural labour.

Waltner-Toews suggested that two changes would reduce the spread of new strains of influenza:

The Future Of Everything

This piece is part of's series The Future Of Everything.

From OBEs to CEOs, professors to futurologists, economists to social theorists, politicians to multi-award winning academics, we think we had the future covered, away from the doom-mongering or easy Minority Report references.

2 Комментариев

Tamashunas, Mitchell B

When reading this I was wondering why Neanderthals had an increased immunity to diseases. I would think that modern humans would have a greater immunity because their population was so much larger. I thought it would be this way because they most likely interacted with other humans more often, which would introduce them to more diseases. I thought that as these humans were introduced to more diseases, their immune systems would strengthen, as they learned how to handle different types of viruses and diseases. I believe this would be similar to the way using hand sanitizer too often is bad because it prevents your system from encountering germs, so it doesn't know how to defend itself.

The main reason I could see Neanderthals having stronger immune systems is if they lived in harsher climates so their body had to adapt to change. But I would not think this would have a greater impact than what the modern humans experienced because a harsh climate does not necessarily mean their immune systems need to strengthen. It may have just been that they needed to create clothing and shelter than was better equipped to deal with their particular situation.

Sailor, Emma

When I read an earlier post on the topic of Neanderthal DNA in the modern human genome, I wondered what the evolutionary advantages were to keeping a small percentage of Neanderthal DNA, so it's interesting to see a post that addresses that question! It's not surprising that the genes cause lighter skin tone are among the genes retained from Neanderthals as these genes probably lent a substantial advantage to homo sapiens as they migrated into regions with less daylight. But, as Mitchell observed, the connection between Neanderthal DNA and increased immunity is far less obvious. I wonder what this information suggests about the differences between early homo sapiens' and Neanderthals' respective environments.

Genetic Echoes

The DNA used to construct the new genome came from an individual dubbed Vindija 33.19, named for the cave where her bone fragments were found.

Though partial genomes have been sequenced from at least five other individuals, the Vindija bone fragments preserved enough intact DNA for Prüfer and his colleagues to parse out a highly detailed genome.

From there, they were able to distinguish between the two sets of genes the Vindija female inherited from her parents. That’s only been accomplished once before, from a 122,000-year-old sample from the so-called Altai Neanderthal found in Siberia.

By effectively doubling the amount of detailed Neanderthal genetic information, researchers are starting to more accurately home in on just how much Neanderthal DNA persists in modern humans and where, exactly, it comes from. (Find out about the last of the Neanderthals in National Geographic magazine.)

“The Neanderthals who mixed with our ancestors seem to be more closely related to the Vindija Neanderthals, the ones from Europe,” Prüfer says. “And it doesn’t matter where you look in the world—even people in Asia are also more closely related to that Neanderthal,” despite the fact that the Altai Neanderthal bones are geographically closer.

In a separate study released today in the American Journal of Human Genetics, two of Prüfer’s colleagues, Michael Dannemann and Janet Kelso, took a slightly different tack. Rather than look at disease-related genes, they looked at how ancient genes might account for physical appearance and even some behaviors.

This team compared the Altai Neanderthal’s genes with genetic and—for the first time—physiological data from 112,000 individuals of northern European descent who contributed their information to the UK Biobank. (Also read about a Neanderthal child who grew up just like a modern human.)

Dannemann and Kelso found 15 regions in the Altai Neanderthal genome that frequently overlap with sections of the Biobank group’s genomes. These genes determine hair and eye color, how badly you sunburn, and even sleep time preference, or whether you’re a morning person or a night owl.

Again, just having the gene isn’t a guarantee for anything—the Neanderthal genes are just as likely as modern genes to have an effect. But it’s intriguing to know that they remain firmly lodged in our makeup.

Dannemann says he and Kelso plan on repeating the research using the new Vindija genome and an expanded Biobank cohort of 500,000 people, hoping to reveal even more hidden associations.

“The data are still pretty sparse, but hopefully it will not take as long to double the Neanderthal genome again,” Dannemann says. “Having more references will help us understand if certain gene variations were common in Neanderthals.”

Miguel Vilar, lead scientist for National Geographic’s Genographic Project, says Vindija is a great advance in building a more complete picture of Neanderthal history, as well as understanding how their ancestry affects us still. He expects even more genetic information to flow from labs around the world, rapidly compounding what we know.

“The fact that we’re now able to pinpoint specific traits is a huge step ahead of what we knew before,” Vilar says. The new research is also a step toward solving the mystery of why Neanderthal genes have persisted in our genome over the last 40,000 to 50,000 years.

“We’ve known there was a mixing already now for 10 to 12 years. Now we’re getting to the meat of why these genes survived,” Vilar adds. “Trying to explain why those traits were important in the context of human evolution, that’s where the greater truths will come.”

Chromosomal Abnormalities

Different Number of Chromosomes

People usually have 23 pairs of chromosomes. But, sometimes a person is born with a different number. Having an extra chromosome is called trisomy. Missing a chromosome is called monosomy.

For example, people with Down syndrome have an extra copy of chromosome 21. This extra copy changes the body&rsquos and brain&rsquos normal development and causes intellectual and physical problems for the person. Some disorders are caused by having a different number of sex chromosomes. For example, people with Turner syndrome external icon usually have only one sex chromosome, an X. Women with Turner syndrome can have problems with growth and heart defects.

Changes in Chromosomes

Sometimes chromosomes are incomplete or shaped differently than usual. Missing a small part of a chromosome is called a deletion. A translocation is when part of one chromosome has moved to another chromosome. An inversion is when part of a chromosome has been flipped over.

For example, people with Williams syndrome external icon are missing a small part of chromosome 7. This deletion can result in intellectual disability and a distinctive facial appearance and personality.

Why do viruses mutate?

Stephen Goldstein is an evolutionary virologist who studies coronaviruses at Utah University Health. He tells Inverse there's no evidence that any variants of SARS-CoV-2 are more contagious or lethal than others. (SARS-CoV-2 is the virus that causes Covid-19.)

“To say that this single mutation is going to make people able to get reinfected or make a vaccine ineffective is getting way out ahead of where the data is,” Goldstein says.

The idea that certain mutant strains will drastically affect the course of the pandemic isn’t supported by current data, Goldstein says. He also describes that claim made in the study as "unwarranted and irresponsible."

Lucy van Dorp, a researcher at the University College London Genetics Institute, argues the term “mutant strain” has misleading connotations. On Tuesday, van Dorp and her team published a peer-reviewed study in the journal Infection, Genetics, and Evolution which analyzed how SARS-CoV-2 is mutating.

Van Dorp's team found 198 recurrent mutations after studying the genomes of 7,500 people infected with Covid-19.

“All viruses mutate,” van Dorp tells Inverse. “It is important to keep track of changes in the genome of the virus, but detection of a single change at high frequency is not sufficient alone to say a strain has become more contagious, transmissible or virulent.”

While a number of studies suggest SARS-CoV-2 is mutating, mutations are simply a feature of viruses, Goldstein explains. The fact that the virus' genetic sequences are changing is expected.

Mutations can happen each time a virus's genetic sequence is copied. Coronaviruses (which depend on an enzyme called RNA polymerase to replicate) tend to mutate more rapidly and are more error-prone than other viruses that use DNA polymerase, Goldstein says.

"They make mistakes they're sloppy but there's a benefit to that for the virus," he says. Replicating quickly gives the virus genetic diversity, which can help it spread farther within a population.

Importantly, mutations don't necessarily increase the potential harm of a virus or have clear downstream effects on infected people.

Scientists make first attempt to permanently change a person’s DNA to cure a disease

On Monday, 44-year-old Brian Madeux – who has a metabolic disease called Hunter syndrome – received billions of copies of a corrective gene through an IV, along with a tool to cut his DNA in the relevant location.

Signs of whether it's working may come in a month, and tests will show for sure in three months.

If the treatment is successful, it could give a major boost to the fledgling field of gene therapy. Prior to this, scientists have altered cells in the lab that are then returned to patients, but never before has it been attempted in someone’s body.

There also are gene therapies that don't involve editing DNA.

But these methods can only be used for a few types of diseases, and some give results that may not last or could cause a new problem like cancer.

This time, the gene tinkering is happening in a precise way inside the body. It's like sending a mini surgeon along to place the new gene in exactly the right location.

"We cut your DNA, open it up, insert a gene, stitch it back up. Invisible mending," said Dr Sandy Macrae, president of Sangamo Therapeutics, the California company testing this strategy for two metabolic diseases and haemophilia. "It becomes part of your DNA and is there for the rest of your life."

That also means there's no going back, no way to erase any mistakes the editing might cause.

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"You're really toying with Mother Nature," said one independent expert, Dr Eric Topol of the Scripps Translational Science Institute in San Diego, adding that the risks can't be fully known, but the studies should move forward because these are incurable diseases,

"It's kind of humbling," said Mr Madeux. "I'm willing to take that risk. Hopefully it will help me and other people."

Protections are in place to help ensure safety, and animal tests were very encouraging, said Dr Howard Kaufman, a Boston scientist on the National Institutes of Health panel that approved the studies.

He said gene editing's promise is too great to ignore. "So far there's been no evidence that this is going to be dangerous," he said. "Now is not the time to get scared."

Fewer than 10,000 people worldwide have these metabolic diseases, partly because many die very young. Those with Mr Madeux's condition, Hunter syndrome, lack a gene that makes an enzyme that breaks down certain carbohydrates. These build up in cells and cause havoc throughout the body.

Patients may have frequent colds and ear infections, distorted facial features, hearing loss, heart problems, breathing trouble, skin and eye problems, bone and joint flaws, bowel issues and brain and thinking problems.

"Many are in wheelchairs . dependent on their parents until they die," said Dr Chester Whitley, a University of Minnesota genetics expert who plans to enroll patients in the studies.

Weekly IV doses of the missing enzyme can ease some symptoms, but cost $100,000 to $400,000 a year and don't prevent brain damage.

Mr Madeux, who now lives near Phoenix is engaged to a nurse, Marcie Humphrey, who he met 15 years ago in a study that tested this enzyme therapy at UCSF Benioff Children's Hospital Oakland, where the gene editing experiment took place.

He has had 26 operations for hernias, bunions, bones pinching his spinal column, and ear, eye and gall bladder problems.

"It seems like I had a surgery every other year of my life," Mr Madeux said. Last year he nearly died from a bronchitis and pneumonia attack. The disease had warped his airway.

"I was drowning in my secretions, I couldn't cough it out," he said.

Mr Madeux has a chef's degree and was part owner of two restaurants in Utah, cooking for US ski teams and celebrities, but now can't work in a kitchen or ride horses as he used to.

Gene editing won't fix damage he's already suffered, but he hopes it will stop the need for weekly enzyme treatments.

Initial studies will involve up to 30 adults to test safety, but the ultimate goal is to treat children very young, before much damage occurs.

A gene-editing tool called CRISPR has gotten a lot of recent attention, but this study used a different one called zinc finger nucleases. They're like molecular scissors that seek and cut a specific piece of DNA.

The therapy has three parts: The new gene and two zinc finger proteins. DNA instructions for each part are placed in a virus that's been altered to not cause infection but to ferry them into cells. Billions of copies of these are given through a vein.

They travel to the liver, where cells use the instructions to make the zinc fingers and prepare the corrective gene. The fingers cut the DNA, allowing the new gene to slip in. The new gene then directs the cell to make the enzyme the patient lacked.

Only 1 per cent of liver cells would have to be corrected to successfully treat the disease, said Mr Madeux's physician and study leader, Dr Paul Harmatz at the Oakland hospital.

"How bulletproof is the technology? We're just learning," but safety tests have been very good, said Dr Carl June, a University of Pennsylvania scientist who has done other gene therapy work but was not involved in this study.

Safety issues plagued some earlier gene therapies. One worry is that the virus might provoke an immune system attack. In 1999, 18-year-old Jesse Gelsinger died in a gene therapy study from that problem, but the new studies use a different virus that's proved much safer in other experiments.

Another worry is that inserting a new gene might have unforeseen effects on other genes. That happened years ago, when researchers used gene therapy to cure some cases of the immune system disorder called ‘bubble boy’ disease. Several patients later developed leukaemia because the new gene inserted into a place in the native DNA where it unintentionally activated a cancer gene.

"When you stick a chunk of DNA in randomly, sometimes it works well, sometimes it does nothing and sometimes it causes harm," said Hank Greely, a Stanford University bioethicist. "The advantage with gene editing is you can put the gene in where you want it."


Finally, some fear that the virus could get into other places like the heart, or eggs and sperm where it could affect future generations. Doctors say built-in genetic safeguards prevent the therapy from working anywhere but the liver, like a seed that only germinates in certain conditions.

This experiment is not connected to other, more controversial work being debated to try to edit genes in human embryos to prevent diseases before birth — changes that would be passed down from generation to generation.

Mr Madeux's treatment was to have happened a week earlier, but a small glitch prevented it.

He and his fiancee returned to Arizona, but nearly didn't make it back to Oakland in time for the second attempt because their Sunday flight was canceled and no others were available until Monday, after the treatment was to take place.

Scrambling, they finally got a flight to Monterey, California, and a car service took them just over 100 miles north to Oakland.

On Monday he had the three-hour infusion, surrounded by half a dozen doctors, nurses and others wearing head-to-toe protective garb to lower the risk of giving him any germs. His doctor, Harmatz, spent the night at the hospital to help ensure his patient stayed well.

"I'm nervous and excited," Mr Madeux said as he prepared to leave the hospital. "I've been waiting for this my whole life, something that can potentially cure me."

Additional reporting by AP.

Why Do Genetic Mutations Occur And How Can We Stop Them?

How do genetic mutations occur, and what can be done to prevent them? originally appeared on Quora: the place to gain and share knowledge, empowering people to learn from others and better understand the world.

Mutations happen in our cells all the time. It's actually how all humans grow and change. The vast majority of mutations are harmless. Some are even beneficial. If you think about evolution, mutations helped humanity transform — increased our brain size and even got us out of the oceans.

Sometimes mutations are influenced by environmental factors — like smoking and lung cancer — and other times it is a misprint that happens when a cell divides.

We have seen the weakening of some genes that can lead to mutations in cases of inbreeding . Some groups including island nations like Iceland and Scotland, historically experienced genetic problems thanks to small populations and tiny gene pools. The Ashkenazi Jewish population also has an increased risk of genetic disease thanks to historic socio-political isolation and a shared cultural attitude among numerous cultures, that intermarriage between cousins and other members of the family was socially advantageous. Although, today attitudes have changed and groups are far less isolated than they ever have been, the takeaway remains: We are stronger when we mix up our gene pools.

When it comes to genetic conditions, mutations or variants sometimes happen spontaneously. A form of dwarfism called achondroplasia is an example of a variant that spontaneously occurs in an individual, then passes down the family tree of that person. There are multiple achondroplasia-gene “founders” - or people who experienced the same spontaneous mutation at different times that led to the achondroplasia variant in multiple family trees.

My gene variant, in a similar style to the gene variants for cystic fibrosis (CF) and cycle cell anemia, is believed to have started with a spontaneous mutation in one individual, then passed down the family tree of that person until it spread out among multiple families. I think it's amazing to think that cystic fibrosis, one of the oldest existing genetic conditions, is believed to have started with a person in Europe 52,000 years ago, 3600 generations ago. Today, hundreds of thousands of people carry or experience symptoms from the CF gene. My family gene is only 137 years and 6 generations old. Only 14 of us have ever had our gene. But if left to its own devices, over time our gene could spread to hundreds of thousands of people. It could become another genetic scourge.

When you think about what genes you can and can’t pass to offspring, it’s pretty fascinating. My family gene likely began with a spontaneous mutation in my great-great grandmother. If it did, either the egg or the sperm that made her already contained the variant gene, and it existed in all of her cells when she was born, or when she was one cell old, the misprint happened during cell division - so that gene variant existed in 50% or 10% or 1% of her cells’ DNA, and as bad luck would have it, when she passed genetic information on to her daughter Mae, she gave her that bad information which then occurred in every one of Mae’s cells.

Our family gene is on the X-chromosome. A man who is XY always passes daughters an X and sons a Y. Both children inherit X’s from their mothers who - like all females (basically) — are XX. So if my father had daughters, which he did, he passed us his X, marked by this variant. My father’s brother also inherited this bad X from his mother. But he had two sons (he adopted a daughter). So neither boy inherited his bad gene.

My family is trying to stop our gene in the fifth generation. Because we know where our gene is — on the X-chromosome, we are able to breed it out. My sister used a process called in vitro fertilization with a preimplantation genetic diagnosis to weed out the family in her twins.

But in all cases the way a mutation happens is basically the same: A misprint occurs during cell division.

This question originally appeared on Quora - the place to gain and share knowledge, empowering people to learn from others and better understand the world. You can follow Quora on Twitter, Facebook, and Google+. More questions:

Our complicated relationship with viruses

When viruses infect us, they can embed small chunks of their genetic material in our DNA. Although infrequent, the incorporation of this material into the human genome has been occurring for millions of years. As a result of this ongoing process, viral genetic material comprises nearly 10 percent of the modern human genome. Over time, the vast majority of viral invaders populating our genome have mutated to the point that they no longer lead to active infections. But, as scientists funded by the National Institutes of Health have demonstrated, they are not entirely dormant.

Sometimes, these stowaway sequences of viral genes, called "endogenous retroviruses" (ERVs), can contribute to the onset of diseases such as cancer. They can also make their hosts susceptible to infections from other viruses. However, scientists have identified numerous cases of viral hitchhikers bestowing crucial benefits to their human hosts -- from protection against disease to shaping important aspects of human evolution, such as the ability to digest starch.

Protecting Against Disease

Geneticists Cedric Feschotte, Edward Chuong and Nels Elde at the University of Utah have discovered that ERVs lodged in the human genome can jump start the immune system.

For a virus to successfully make copies of itself inside a host cell, it needs molecular tools similar to the ones its host normally uses to translate genes into proteins. As a result, viruses have tools meticulously shaped by evolution to commandeer the protein-producing machinery of human cells.

Feschotte and his team recognized that because viruses tend to attack the immune system, they may be particularly adept at manipulating immune system genes. Ancient human genomes may have evolved in response. Feschotte believes it is possible that the genomes of humans (or our ancient ancestors) repurposed viral DNA for their own defense, using it to spur the immune system into action against viruses and other foreign invaders.

"We hypothesized that these ERVs were likely to be primary players in regulating immune activity because viruses themselves evolved to hijack the machinery to control immune cells," says Feschotte.

To investigate their hypothesis, Feschotte and his team used a gene-editing technique called CRISPR to systematically eliminate individual ERV sequences in human cells. After removing one of the sequences, the researchers observed a notable weakening of immune function when the cells were challenged by viral infection. The removal of three other ERV sequences also compromised the immune response.

These findings suggest that each of these ERV elements can activate different gene components of the immune system. The team believes there are thousands more ERV sequences with similar regulatory activities, and it hopes to explore them systematically in future studies.

"We think we've only scratched the surface here on the regulatory potential of ERVs," says Feschotte.

Underscoring the complicated relationship humans have with viruses, strong evidence also exists that in some cases ERVs cause cancer but in other cases they protect against cancer. For example, an ERV called ERV9 can detect cancer-related damage in the DNA of cells in the testis. ERV9 then prompts a neighboring gene to induce the damaged cells to commit suicide. This protective mechanism ensures that the cancer cells will not spread.

Shaping Human Evolution

Scientists have also discovered that viral intruders have driven the evolution of human physiological functions ranging from early development to digestion.

Nearly 20 years ago, scientists identified an ERV-derived gene called syncytin that appears to play a key role in the development of the human placenta. Syncytin originated from a retroviral gene encoding a protein that is embedded in the outer surface of a virus. This protein mediates the fusion of the virions with the host cell membrane, thereby facilitating viral infection. In a remarkable turn of events, the human body has repurposed the viral protein's cell-fusing activities to promote the formation of the layer of cells that merge the placenta and the uterus.

Scientists have also found that viral invaders are critical to humans' ability to digest starch. The insertion of an ERV near the human pancreatic gene for making amylase -- a protein that helps humans digest carbohydrates -- led to the expression of amylase in saliva. The consequent ability to digest starch in the mouth has had profound effects on the human diet, notably a shift toward eating foods like rice and wheat. By helping to kick start digestion in the mouth, amylase relieves some of the burden of breaking down food faced by the small intestine. If this critical enzyme were not excreted in saliva, the small intestine would have more difficulty metabolizing sugars and starches.

More recently, in 2016, a team of U.S. and Israeli researchers reported that a common strategy that host organisms use for nullifying viruses -- bombarding them with mutations -- has helped shape human evolution.

The researchers, led by computational biologist Alon Keinan of Cornell University, in collaboration with Erez Levanon from Bar-Ilan University, study a virus-fighting family of human enzymes called APOBECs. During periods when DNA unzips into two single strands -- when it has been damaged, is in the process of being copied, or is being transcribed into RNA -- the APOBEC enzymes seek out bits of viral DNA. They then systematically strafe the viral DNA -- typically swapping many instances of one DNA base for another -- in order to neutralize pathogens lurking within the host genome.

It's likely that this APOBEC mechanism has also mutated non-viral portions of the human genome. Keinan says the majority of these genetic changes would have done enough damage to cause disease. For the most part, such mutations have been weeded out of the population because they were harmful to survival and reproduction. However, researchers have increasingly linked APOBECs to various cancers.

Keinan's team has shown that these mutations are also occurring in cells that develop into sperm and eggs and so they are inherited by future generations. And not all of the mutations have been detrimental. The genetic changes that survived through evolutionary time -- the ones that did not lead to disease -- are more likely to be beneficial. This insight suggests that the APOBEC anti-viral mechanism has helped shape primate evolution through a variety of yet-to-be-identified beneficial mutations. Keinan's team has reported tens of thousands of such mutations in hominid genomes and is now searching for specific examples that led to changes in function that have contributed to human evolution.

While the search for additional examples of beneficial ERVs and antiviral mechanisms continues, scientists are learning more about viral trespassers with the help of large databases of genomic information from numerous species. They're trying to figure out how viral DNA integrates into host genomes, how ERVs can jump from one host species to another and how to protect people in the case of these rare, but occasionally deadly, events.