Are there any DNA viruses with junk DNA in them?

Are there any DNA viruses with junk DNA in them?

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I know mimiviruses and pandoraviruses have orphan DNA - DNA that is not found in other species - but this is DNA that codes for proteins. I am not able to find out if they contain junk DNA. By junk I mean DNA that does not have ANY function at all. Sort of like the junk DNA in the human genome put there by retroviruses, DNA that just sits there, doing nothing, just going along for the ride.

Viruses typically don't have junk DNA-so to speak because of their tiny size. When the particles (of virus) are so small, there really isn't any space for "junk" or extra DNA.

That being said, while viral DNA replication, there may be some errors that may make the virus DNA unable to code for proteins or "junk". While this is an interesting proposition, the mutations that occur in almost cases do not make non functional proteins but mutated proteins which make the viruses more virulent (more true in case of RNA viruses… which mutate a lot faster).

Regarding virus infecting virus, putting its own code it "kind of happens" but not as you would expect. I am listing 2 such examples here-

  1. There are some viruses called satellite viruses and viroids which depend on "donor" larger viruses for some of the proteins they need for replication. This means a satellite virus can survive in a host only if the donor virus is present.

  2. In animals like pigs, when different strains of Influenza virus infect together, while virus assembly genetic material (RNA) of one strain can enter into the other… creating completely novel strain.

Hope that answers your question. Please feel free to ask for clarification. Thank you and have a nice day.

Mysteries of Epigenetics: There’s More to Genes Than DNA

Biologists at the Universities of Bath and Vienna have discovered 71 new ‘imprinted’ genes in the mouse genome, a finding that takes them a step closer to unraveling some of the mysteries of epigenetics – an area of science that describes how genes are switched on (and off) in different cells at different stages in development and adulthood.

To understand the importance of imprinted genes to inheritance, we need to step back and ask how inheritance works in general. Most of the thirty trillion cells in a person’s body contain genes that come from both their mother and father, with each parent contributing one version of each gene. The unique combination of genes goes part of the way to making an individual unique. Usually, each gene in a pair is equally active or inactive in a given cell. This is not the case for imprinted genes. These genes – which make up less than one percent of the total of 20,000+ genes – tend to be more active (sometimes much more active) in one parental version than the other.

Until now, researchers were aware of around 130 well-documented imprinted genes in the mouse genome – the new additions take this number to over 200. Professor Tony Perry, who led the research from the Department of Biology & Biochemistry at Bath, said: “Imprinting affects an important family of genes, with different implications for health and disease, so the seventy-plus new ones add an important piece of the jigsaw.”

The importance of histones

Close examination of the newly identified genes has allowed Professor Perry and his colleagues to make a second important discovery: the switching on and off of imprinted genes is not always related to DNA methylation, where methyl groups are added to genomic DNA (a process that is known to repress gene activity, switching them off). DNA methylation was the first known type of imprint, and was discovered around thirty years ago. From the results of the new work, it seems that a greater contribution to imprinting is made by histones – structures that are wrapped up with genomic DNA in chromosomes.

A normal 4-day-old mouse embryo (L) and an embryo of the same age that has been manipulated to contain maternal chromosomes only (parthenogenote). At this stage, the embryos (blastocysts) appear similar, but the parthenogenote will soon die, underscoring the importance of inheriting imprinted genes from both parents. Different cell types are stained green or red. Credit: Dr. Maki Asami, University of Bath

Although scientists have known for some time that histones act as ‘dimmer’ switches for genes, fading them off (or back on), until now it was thought that DNA methylation provided the major switch for imprinted gene activity. The findings from the new study cast doubt on this assumption: many of the newly identified genes were found to be associated with changes to the histone 3 lysine 27 (H3K27me3), and only a minority with DNA methylation.

Why imprinting matters

Scientists have yet to work out how one parental version of a given gene can be switched (or faded) on or off and maintained that way while the other is in the opposite state. It is known that much of the on/off switching occurs during the formation of gametes (sperm and egg), but the precise mechanisms remain unclear. This new study points to the intriguing possibility that some imprinted genes may not be marked in gametes, but become active later in development, or even in adulthood.

Although it only involves a small proportion of genes, imprinting is important in later life. If it goes wrong, and the imprinted gene copy from one parent is switched on when it should be off (or vice versa), disease or death occur. Faulty imprinted genes are associated with many diseases, including neurological and metabolic disorders, and cancer.

“We may underestimate how important the relationship between imprinting and disease is, as well as the relationship of imprinting to the inheritance of parentally-acquired disease, such as obesity,” said Professor Perry. “Hopefully, this improved picture of imprinting will increase our understanding of disease.”

Reference: “Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3” by Laura Santini, Florian Halbritter, Fabian Titz-Teixeira, Toru Suzuki, Maki Asami, Xiaoyan Ma, Julia Ramesmayer, Andreas Lackner, Nick Warr, Florian Pauler, Simon Hippenmeyer, Ernest Laue, Matthias Farlik, Christoph Bock, Andreas Beyer, Anthony C. F. Perry and Martin Leeb, 21 June 2021, Nature Communications.
DOI: 10.1038/s41467-021-23510-4

Not that Z

Confusingly, there's something else called Z-DNA. The DNA in our cells has a right-handed curve, called B-DNA, to its double helix. But it's also possible to have a double helix with a left-handed curve, called Z-DNA.

But that DNA isn't this DNA. This DNA is distinguished by a base, found nowhere else, that undergoes a different type of base pairing. Diaminopurine, awkwardly abbreviated as Z, is structurally similar to the adenine (A) found in normal DNA. But diaminopurine has an extra nitrogen hanging off one side that lets it form an additional hydrogen bond with A's normal partner, thymidine (T). A Z-T base pair would thus hold DNA's double helix together a bit more than a standard A-T pairing.

DNA incorporating Diaminopurine is called Z-DNA. We've known since 1979 that it exists in nature in the form of a single virus called S-2L, which infects cyanobacteria. But until now, we didn't know if that virus was a one-off oddity or represented the tip of a biological iceberg, with lots of viruses we haven't discovered yet using it. Just as critically, we weren't even sure of how it ended up incorporated in the virus in the first place.

A large team of researchers, largely from China, decided to figure out what's going on here. They started by searching the S-2L virus's genome to figure out whether it encoded anything unusual.

A New Force

The idea that a symbiotic virus or any symbiotic relationship could have such a profound influence on the evolution of a new species is both new and controversial. For more than a century after Charles Darwin published On the Origin of Species , scientists focused on competition as evolution’s chief driving force. Biologist Lynn Margulis wasn’t convinced.

The late University of Massachusetts researcher believed that cooperation also played a role. Her evidence lurked in every cell of every plant and animal. Beginning in the late 1960s, Margulis argued that our cells contained symbiotic bacteria known as mitochondria and chloroplasts, which earned room and board by either supplying energy or producing food from sunlight. Margulis’s idea was ridiculed, and she struggled to find a journal that would publish her hypothesis.

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By the 1990s, however, enough genetic evidence had accumulated to show that Margulis was right. Symbiosis was responsible for some of the most significant evolutionary leaps in the history of the planet. Most scientists, however, viewed this event as an anomaly, a once-off freak occurrence that, although significant, didn’t play a role in the ongoing evolution of most species. Margulis, though, saw symbiosis everywhere and believed that this softer, gentler side of evolution was getting short shrift in research. Although most symbiosis research has focused on the role of the microbiome, the viruses tucked into our DNA can play a similar role in splitting apart two populations, turning one species into two. The first wedge scientists discovered was a protein called syncytin.

History of giants in the gene: Scientists use DNA to trace the origins of giant viruses

Scientists investigate the evolution of Mimivirus, one of the world's largest viruses, through how they replicate DNA. Researchers from the Indian Institute of Technology Bombay shed light on the origins of Mimivirus and other giant viruses, helping us better understand a group of unique biological forms that shaped life on earth. Credit: Indian Institute of Technology Bombay

Researchers from the Indian Institute of Technology Bombay shed light on the origins of Mimivirus and other giant viruses to better understand a group of unique biological forms that shaped life on Earth. In their latest study, published in Molecular Biology and Evolution, the researchers show that giant viruses may have come from a complex single-cell ancestor, keeping DNA replication machinery but shedding genes that code for other vital processes like metabolism.

2003 was a big year for virologists. The first giant virus was discovered that year, which shook the virology scene, revising what was thought to be an established understanding of this elusive group and expanding the virus world from simple, small agents to forms that are as complex as some bacteria. Because of their link to disease and the difficulties in defining them—they are biological entities but do not fit comfortably in the existing tree of life—viruses incite the curiosity of researchers.

Scientists have long been interested in how viruses evolved, especially when it comes to giant viruses that can produce new viruses with very little help from the host—in contrast to most small viruses, which use the host's machinery to replicate.

Even though giant viruses are not what most people would think of when it comes to viruses, they are actually very common in oceans and other water bodies. They infect single-celled aquatic organisms and have major effects on their population. Dr. Kiran Kondabagil, molecular virologist at the Indian Institute of Technology (IIT) Bombay, says, "Because these single-celled organisms greatly influence the carbon turnover in the ocean, the viruses have an important role in our world's ecology. So, it is just as important to study them and their evolution, as it is to study the disease-causing viruses."

In a recent study, the findings of which have been published in Molecular Biology and Evolution, Dr. Kondabagil and co-researcher Dr. Supriya Patil performed a series of analyses on major genes and proteins involved in the DNA replication machinery of Mimivirus, the first group of giant viruses to be identified. They aimed to determine which of two major suggestions regarding Mimivirus evolution—the reduction and the virus-first hypotheses—were more supported by their results. The reduction hypothesis suggests that the giant viruses emerged from unicellular organisms and shed genes over time the virus-first hypothesis suggests that they were around before single-celled organisms and instead gained genes.

Scientists investigate the evolution of Mimivirus, one of the world's largest viruses, through how they replicate DNA. Researchers from the Indian Institute of Technology Bombay shed light on the origins of Mimivirus and other giant viruses, helping us better understand a group of unique biological forms that shaped life on earth. Credit: Indian Institute of Technology Bombay

Dr. Kondabagil and Dr. Patil created phylogenetic trees with replication proteins and found that those from Mimivirus were more closely related to eukaryotes than to bacteria or small viruses. Additionally, they used a technique called multidimensional scaling to determine how similar the Mimiviral proteins are. A greater similarity would indicate that the proteins co-evolved, which means that they are linked together in a larger protein complex with coordinated function. And indeed, their findings showed greater similarity. Finally, the researchers showed that genes related to DNA replication are similar to and fall under purifying selection, which is natural selection that removes harmful gene variants, constraining the genes and preventing their sequences from varying. Such a phenomenon typically occurs when the genes are involved in essential functions (like DNA replication) in an organism.

Taken together, these results imply that Mimiviral DNA replication machinery is ancient and evolved over a long period of time. This narrows us down to the reduction hypothesis, which suggests that the DNA replication machinery already existed in a unicellular ancestor, and the giant viruses were formed after getting rid of other structures in the ancestor, leaving only replication-related parts of the genome.

"Our findings are very exciting because they inform how life on earth has evolved," Dr. Kondabagil says. "Because these giant viruses probably predate the diversification of the unicellular ancestor into bacteria, archaea, and eukaryotes, they should have had major influence on the subsequent evolutionary trajectory of eukaryotes, which are their hosts."

In terms of applications beyond this contribution to basic scientific knowledge, Dr. Kondabagil feels that their work could lay the groundwork for translational research into technology like genetic engineering and nanotechnology. He says, "An increased understanding of the mechanisms by which viruses copy themselves and self-assemble means we could potentially modify these viruses to replicate genes we want or create nanobots based on how the viruses function. The possibilities are far-reaching."

Words Without Meaning

Nature has a peculiar way of writing. Our genetic script uses only four letters: A, G, C, and T. Long combinations of these letters make up our genes, which inform the construction of proteins. But the protein-making process is not as straightforward as reading a cooking recipe. Before putting proteins together, DNA gets transcribed into threads of RNA that are chopped and reassembled into smaller pieces.

During the chopping, the non-coding stretches — the junk — are discarded, meaning they never even get used to make proteins. Why nature carries so much seemingly unnecessary material in its guidebook is a question that researchers continue to ponder. The most logical explanation is that this “junk DNA” might not be so useless after all.

Study finds clues to aging in 'junk' DNA

Fluorescence microscopy images of the Charlie5 transcript in young versus old human skin cells. Credit: Aging Cell

For decades, greater than 60% of the human genome was believed to be "junk DNA" that served little or no purpose in the course of human development. Recent research by Colorado State University is challenging this notion to show that junk DNA might be important after all.

A new study, published on June 5 in Aging Cell, found that a portion of noncoding genetic material, called repetitive element transcripts, might be an important biomarker of the aging process.

Tom LaRocca, an assistant professor in the Department of Health and Exercise Science and faculty member in the Columbine Heath Systems Center for Healthy Aging at CSU, led the study to investigate a growing body of evidence that repetitive elements—transposons and other sequences that occur in multiple copies in the human genome—may become active over time as we age.

LaRocca, graduate student Alyssa Cavalier, and postdoctoral researcher Devin Wahl centered specifically on RNA transcripts, molecules that are transcribed from the DNA of repetitive elements, to test whether they increase in number with age.

"The biomarker angle is important here," LaRocca said. "Ten to 20 years from now, we might be able to take samples or certain measurements from people in the doctor's office and get some insight into what's going on with them biologically, so that we can know how to best treat them and maximize their healthspan. If these repetitive element RNAs are a biomarker of aging, then maybe someday you can get a measurement like this done to see how your repetitive elements are being expressed. Are there too many of them? Is that a problem?"

To carry out the study, the researchers began by analyzing an existing RNA sequencing dataset gathered from skin cells in healthy human subjects aged 1-94 years old. Just as the Human Genome Project of the 1990s sought to sequence and map the approximately 20,500 genes in human DNA, RNA sequencing can provide a map of the entire transcriptome in the cells under study. From that analysis, which was all computational, the researchers found that transcripts from most major types of repetitive elements were increased in older subjects.

In a second wave of study, the researchers verified their initial findings by performing their own lab analyses on skin cells from a biobank. Using fluorescent microscopy, the researchers tagged the transcript of a specific transposon, Charlie5, to see how it fluctuates with the age of cells: the brighter the tag appears under the microscope, the more Charlie5 transcript is detectable.

As hypothesized, skin cells from older adults revealed a marked accumulation of Charlie5 transcript compared to cells from younger individuals, showing that repetitive element RNAs appear to accumulate with age.

While an important observation, the grander outcome of this study is that repetitive RNA transcripts might be linked with biological age, or the health of a person's cells, as opposed to chronological age in years.

"If you find something that changes progressively with aging, that finding alone is not necessarily interesting, because lots of things increase or decrease with age. What you really want to find is something that reflects biological aging," LaRocca said. "For example, let's say you're a smoker and you're under a lot of chronic stress. Then, perhaps even if you're only 45, your biological age—the health of your cells—could actually be 60 or 65. We think that repetitive element transcripts could be a marker of this."

To study biological age, Cavalier performed an analysis that compared sun-exposed skin cells to skin cells that had not been exposed to sunlight—the theory being that the more damaging UV rays a skin cell is exposed to, the older the cell will be biologically. Consistent with her hypothesis, Cavalier noted higher levels of repetitive element RNAs in the sun-exposed cells.

A link between repetitive element transcripts and biological age was further confirmed by studying skin cells from patients with Hutchinson-Gilford progeria syndrome (HGPS), a premature aging syndrome, and by studying an RNA-sequencing dataset from the roundworm Caenorhabditis elegans.

Why might repetitive element transcripts increase with age? The researchers suspect that chromatin—the complex of DNA and protein in cells that typically represses repetitive elements from being expressed—might become disrupted, allowing for the transcription of repetitive elements.

All in all, for a portion of the genome that scientists used to ignore, evidence is growing that noncoding RNAs and repetitive elements play vital roles in regulating the rest of the human genome, and in this case, as potentially targetable biomarkers of aging.

"This is a really big chunk of the genome that, for the longest time, no one really knew what it did, so they just kind of assumed it was junk. But we're finding more and more that these noncoding regions might not only be doing something, but they might have actual health implications," Cavalier said.

Future studies in LaRocca's Healthspan Biology Lab will compare chromatin structure in people who exercise routinely with those who don't to understand how exercise impacts repetitive element levels. Other studies will investigate the possibility of using a drug to inhibit repetitive element RNAs from being transcribed.

Ancient Viruses Are Buried in Your DNA

In July, scientists reported that a strange protein courses through the veins of pregnant women. No one is sure what it’s there for.

What makes this protein, called Hemo, so unusual is that it’s not made by the mother. Instead, it is made in her fetus and in the placenta, by a gene that originally came from a virus that infected our mammalian ancestors more than 100 million years ago.

Hemo is not the only protein with such an alien origin: Our DNA contains roughly 100,000 pieces of viral DNA. Altogether, they make up about 8 percent of the human genome. And scientists are only starting to figure out what this viral DNA is doing to us.

Aris Katzourakis, a virologist at the University of Oxford, and his colleagues recently published a commentary in the journal Trends in Microbiology in which they explored the possibility that viral genes that produce proteins like Hemo are affecting our health in a variety of unexpected ways.

Some of our ancient viruses may be protecting us from disease others may be raising our risks for cancer, among other conditions. “It’s not an either-or — are these things good or bad? It’s a lot more complicated than that,” Dr. Katzourakis said in an interview. “We’re barely at the beginning of this research.”

Most of our viral DNA comes from one group in particular: retroviruses, a group that includes HIV.

A retrovirus invades a host cell and inserts its genes into that cell’s DNA. These viral genes co-opt the cell’s machinery, using it to make new viruses that escape to infect more cells.

If a retrovirus happens to infect an egg or sperm, its DNA can potentially be passed to the next generation and the generation after that. Once retroviruses become inherited stowaways, scientists refer to them as endogenous retroviruses.

At first, endogenous retroviruses coax cells to make more retroviruses that can infect other cells. But over the generations, the viral DNA mutates, and endogenous retroviruses eventually lose the ability to infect new cells.

Even after being hobbled, these endogenous retroviruses can still sometimes make their proteins. And they can also reproduce, after a fashion. They can force cells to make copies of their DNA, which are inserted back in the cell’s own genome.

After a single infection, an endogenous retrovirus may build up hundreds of copies of itself in its host’s DNA.

Some endogenous retroviruses are unique to humans, but others are found in a variety of species. In January, Dr. Katzourakis was a co-author on a study showing that one retrovirus common in mammals also is present in fish like cod and tuna. Retroviruses, that study indicated, were invading our marine ancestors 450 million years ago — or even earlier.

Just as we have defenses against free-living viruses, we have also developed defenses against endogenous retroviruses. Our cells can coat their DNA with molecules that suppress viral genes, for example.

But sometimes these viral genes manage to switch on anyway. In many kinds of tumor cells, for instance, scientists find proteins produced by endogenous retroviruses. That discovery has fueled a long-running debate: Do endogenous retroviruses help cause cancer?

Recent studies suggest they can. A team of French researchers engineered healthy human cells to make a viral protein found in many tumors and watched the cells grow in a petri dish.

The protein caused the cells to behave in some suspiciously cancer-like ways. They changed shape, as cancer cells do, becoming long and skinny. And they also started to move across the dish.

In addition, the viral protein caused the cells to switch on other genes that have been linked to cancer.

But John M. Coffin, a virologist at Tufts University, suspects there’s less to these viral proteins than meets the eyes. He speculates that in many cases, cancer cells make viral proteins only because they are switching on genes willy-nilly — both human and viral genes alike.

“Our starting position is that this is largely a chance event,” Dr. Coffin said.

But in certain cases, Dr. Coffin said, we have domesticated our viruses. We make proteins from endogenous retroviruses to carry out functions we depend on. Some endogenous retroviruses offer protection against other viruses, for example.

And some viral proteins are important for reproduction. Placentas make viral proteins, and scientists have found that some types, known as syncytins, fuse together placental cells, a crucial step in fetal development.

“My speculation is that without syncytins, mammal evolution would have looked very different,” Dr. Coffin said.

Five years ago, the French biologist Odile Heidmann and her colleagues went on a search for more endogenous retroviruses in the human genome.

Dr. Heidmann, who works at Gustave Roussy, a cancer research institute in Paris, discovered a stretch of viral DNA that had gone overlooked. She and her colleagues named it Hemo.

Dr. Heidmann was surprised to find versions of Hemo in other species. Among primates, the gene that makes this protein has barely changed over the ages.

Its consistency across many species shows that the gene and its protein must have an important job to do: “It isn’t simply a relic,” Dr. Heidmann said. Mutations to Hemo must have been harmful or even fatal to the unfortunate animals who had them.

The placenta produces Hemo, and so do cells in the early embryo itself. But so far Dr. Heidmann and her colleagues have not been able to figure out why.

“It’s very, very old, so it has to do something,” she said. It’s possible, she said, that Hemo proteins are a message from fetus to mother, dampening the mother’s immune system so that it doesn’t attack the fetus.

But there are other possibilities, too.

The early embryo is a hotbed of activity for endogenous retroviruses, recent studies have shown. To understand why embryonic cells make viral proteins, scientists have run experiments to see what happens when viral genes are silenced.

These experiments suggest that viral proteins help the embryo develop a variety of tissues.

Early on, the cells in an embryo can turn into any tissue. As these stem cells divide, they can lose this flexibility, committing to becoming one kind of cell or another. After that, cells typically shut down their viral genes.

Viral proteins appear to help keep stem cells from losing this potential. And Gkikas Magiorkinis of the University of Athens has speculated that this feature might have a sinister origin.

Viruses might have exploited embryos to make more copies of themselves. By keeping their hosts as stem cells for longer, the viruses were able to invade more parts of the embryo’s body.

“When the host grows, it will have copies in the retrovirus in most of its cells,” Dr. Magiorkinis said.

This strategy may do more than create more viruses. Stem cells can produce eggs and sperm in embryos. The viruses may be raising their odds of getting into the next generation.

In other words, early embryos may have come to depend on the tricks viruses use to manipulate them. “We’re exploiting a property that has evolved for the virus’s benefit,” Dr. Katzourakis said.

Could DNA editing help stop viruses that are slowly killing the world’s koalas?

The marsupials are dying from cancer at curiously high rates, writes James Gorman. Scientists have now discovered that a retrovirus that built itself into their DNA is to blame – and it’s causing a fascinating hyper-evolution too

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K oalas have been running into hard times. They have suffered for years from habitat destruction, dog attacks and car accidents. But that’s only the beginning.

They are also plagued by chlamydia and cancers such as leukaemia and lymphoma, and in researching those problems, scientists have found a natural laboratory in which to study one of the hottest topics in biology: how viruses can insert themselves into an animal’s DNA and sometimes change the course of evolution.

The target of this research is Koala retrovirus, or KoRV, a bit of protein and genetic material in the same family as HIV that began inserting itself into the koala genome about 40,000 years ago and is now passed on from generation to generation, like genes. It is also still passed between animals, like typical viral infections.

In recent years, scientists have found that the insertion of viruses into the genomes of animals has occurred over and over again. An estimated 8 per cent of the human genome is made up of viruses left over from ancient infections, ancient as in millions of years ago, many of them in primate ancestors before humans existed.

The koala retrovirus is unusual because 40,000 years is an evolutionary blink of an eye and because the process appears to be continuing. Scientists last week reported in Cell that they observed a genome immune system fighting to render the virus inactive now that it has established itself in koala DNA. They also reported that koala retrovirus may have activated other ancient viral DNA. All of this activity stirs the pot of mutation and variation that is the raw material for natural selection.

The koala retrovirus is unusual because 40,000 years is an evolutionary blink of an eye and because the process appears to be continuing

Koala genetics are a gold mine, says report author William Theurkauf, a professor in molecular medicine at the University of Massachusetts Medical School. “What they are going through is the process of what’s driven the evolution of every animal on the planet.”

Past viral infections have led to major evolutionary changes, he says. For example: “A gene that is absolutely essential for the placenta was derived from the shell of a virus millions of years ago.” Humans would not exist without that retroviral infection.


Retroviruses are made of RNA, a single strand of genetic information. When they infect a cell, they translate themselves into DNA, the two-stranded molecule that carries all the information for making humans, koalas and other animals. The retroviruses take over the DNA machinery to make more of themselves, which keeps the process going.

That process makes us and other animals sick. Aids is probably the best known retroviral disease. But when the insertion of a retrovirus occurs in a sperm or an egg cell, the change can become permanent, passed on forever. When retroviruses become part of an animal’s inherited DNA, they are called endogenous and eventually they no longer cause the kind of original infection they once did. But they can still be used by the animal’s genetic machinery for other purposes, like making a placenta.

“It was long thought they were just junk DNA,” says Shawn Chavez, a molecular biologist at the Oregon Health and Science University School of Medicine in Portland, who wrote a review of research on endogenous retroviruses in mammals. Now it is clear that some of them have changed the course of evolution. Exactly how is what scientists are trying to find out. “It seems like there’s a new publication every day,” she says.

Consequently, koalas are drawing a lot of attention from scientists who did not start out with an interest in the animal or its conservation. “I’m a fruit fly guy,” Theurkauf says. He became interested after a report in 2006 by Rachael Tarlinton of the University of Nottingham and other scientists about the invasion of the koala genome by the retrovirus.

Ancient virus, its effects on DNA found in study

Researchers have found evidence that a coronavirus epidemic swept East Asia some 20,000 years ago and was devastating enough to leave an evolutionary imprint on the DNA of people alive today.

The new study suggests that an ancient coronavirus plagued the region for many years, researchers say. The finding could have dire implications for the covid-19 pandemic if it is not brought under control soon through vaccination.

"It should make us worry," said David Enard, an evolutionary biologist at the University of Arizona who led the study, which was published last week in the journal Current Biology. "What is going on right now might be going on for generations and generations."

Until now, researchers could not look back very far into the history of this family of pathogens. Over the past 20 years, three coronaviruses have adapted to infect humans and cause severe respiratory disease: Covid-19, SARS and MERS. Studies on each of these coronaviruses indicate that they jumped into our species from bats or other mammals.

Four other coronaviruses can also infect people, but they usually cause only mild colds. Scientists did not directly observe these coronaviruses becoming human pathogens, so they have relied on indirect clues to estimate when the jumps happened. Coronaviruses gain new mutations at a roughly regular rate, and so comparing their genetic variation makes it possible to determine when they diverged from a common ancestor.

The most recent of these mild coronaviruses, called HCoV-HKU1, crossed the species barrier in the 1950s. The oldest, called HCoV-NL63, may date as far back as 820 years.

But before that point, the coronavirus trail went cold -- until Enard and his colleagues applied a new method to the search. Instead of looking at the genes of the coronaviruses, the researchers looked at the effects on the DNA of their human hosts.

Over generations, viruses drive enormous amounts of change in the human genome. A mutation that protects against a viral infection may well mean the difference between life and death, and it will be passed down to offspring. A lifesaving mutation, for example, might allow people to chop apart a virus's proteins.

But viruses can evolve, too. Their proteins can change shape to overcome a host's defenses. And those changes might spur the host to evolve even more counteroffensives, leading to more mutations.

When a random new mutation happens to provide resistance to a virus, it can swiftly become more common from one generation to the next. And other versions of that gene, in turn, become rarer. So if one version of a gene dominates all others in large groups of people, scientists know that is most likely a signature of rapid evolution in the past.

In recent years, Enard and his colleagues have searched the human genome for these patterns of genetic variation in order to reconstruct the history of an array of viruses. When the pandemic struck, he wondered whether ancient coronaviruses had left a distinctive mark of their own.

He and his colleagues compared the DNA of thousands of people across 26 different populations around the world, looking at a combination of genes known to be crucial for coronaviruses but not other kinds of pathogens. In East Asian populations, the scientists found that 42 of these genes had a dominant version. That was a strong signal that people in East Asia had adapted to an ancient coronavirus.

But whatever happened in East Asia seemed to have been limited to that region. "When we compared them to populations around the world, we couldn't find the signal," said Yassine Souilmi, a postdoctoral researcher at the University of Adelaide in Australia and a co-author of the new study.

The scientists then tried to estimate how long ago East Asians had adapted to a coronavirus. They took advantage of the fact that once a dominant version of a gene starts being passed down through the generations, it can gain harmless random mutations. As more time passes, more of those mutations accumulate.

Enard and his colleagues found that the 42 genes all had about the same number of mutations. That meant that they had all rapidly evolved about the same time. "This is a signal we should absolutely not expect by chance," Enard said.

They estimated that all of those genes evolved their antiviral mutations sometime between 20,000 and 25,000 years ago, most likely over the course of a few centuries. It's a surprising finding, since East Asians at the time were not living in dense communities but instead formed small bands of hunter-gatherers.

Aida Andres, an evolutionary geneticist at the University College London who was not involved in the new study, said she found the work compelling. "I'm quite convinced there's something there," she said.

Still, she didn't think it was possible yet to make a firm estimate of how long ago the ancient epidemic took place. "The timing is a complicated thing," she said. "Whether that happened a few thousand years before or after -- I personally think it's something that we cannot be as confident of."

Scientists looking for drugs to fight the new coronavirus might want to scrutinize the 42 genes that evolved in response to the ancient epidemic, Souilmi said. "It's actually pointing us to molecular knobs to adjust the immune response to the virus," he said.

Anders agreed, saying that the genes identified in the new study should get special attention as targets for drugs.

Print Headline: Ancient virus, its effects on DNA found in study

DNA previously written off as 'junk' actually determines genitals at birth

A small snippet of “junk” DNA which was previously thought not to play any essential role in humans may be the difference between being born male or female, UK researchers have found.

In 1991 scientists made a female mouse develop as a male by inserting the Sry gene - short for sex-determining region Y - into the developing embryo. Showing a single gene change could determine our sex.

Now, research published in leading journal Science, shows there is another equally important instruction located in a seemingly unrelated part of our DNA manual which, if removed, results in a genetically male mouse develop female genitals and ovaries.


This newly discovered section, called enhancer 13, massively boosts the signal from Sry to the gonads, which start off as neither male nor female, and ensures they become testes and trigger other male traits.

It also has an equivalent in the human genetic code and may help explain why people missing genes in this area may be born with partially-formed genitals ones that do not conform to their gender, the researchers said.

“It’s finely balanced, it needs to go one way or the other,” Professor Robin Lovell-Badge, who heads the research team at London’s Francis Crick Institute and first identified Sry 27 years ago, told The Independent.

“Sry is there and it starts the process, then you immediately get all these mechanisms that reinforce it, like enhancer 13."

Once the testes have developed they can release testosterone, the male sex hormone, which floods the other bodily tissues and directs them to form the penis and underpins further changes in puberty.

If this process isn’t followed all the way through it could mean the outward genitals don’t fully form, or the foetus begins to develop as female.