How a Heart Fails

July 12, 2015 by

July 10, 2015

By Medical Discovery News

A heart

What exactly causes a heart to fail? It may come down to a simple protein, which scientists recently identified as having an important role in how a heart goes from weakening to failing.

Your heart is a strong, muscular pump slightly larger than your fist that pushes blood through your body. Blood delivers the necessary oxygen and nutrients to all cells in all the organs. Every minute, your heart pumps five quarts of blood. Human hearts have four chambers: two atria on top and two ventricles on bottom. Oxygenated blood leaves the lungs, enters the left atrium, moves to the left ventricle, and is then pumped out of the heart to the rest of the body. After it circulates, blood returns to the heart, enters the right atrium, moves to the right ventricle, and is then sent back to the lungs for a fresh dose of oxygen. Although your heart beats 100,000 times each day, the four chambers must go through a series of highly organized contractions to accomplish this.

Any disruption of this process can have serious consequences such as heart failure, which is clinically defined as a chronic, progressive weakening of the heart’s ability to circulate enough blood to meet the body’s demands. To compensate, the heart enlarges, which increases contractions and the volume of blood pumped. Blood vessels elsewhere in the body narrow to keep blood pressure normal. Blood can even be diverted from less important organs, ensuring more vital organs like the brain and heart are satisfied. However, such responses mask the underlying problem: the weakening heart, which continues to worsen. Ultimately, the body can no longer compensate for the heart, which is when it will start to fail.

Scientists at the University of California, San Diego School of Medicine studied the cellular changes in weakened hearts to better understand the transition from the compensatory stage, when it works harder to pump blood, to the decompensation, when it fails to pump blood sufficiently. They were especially interested in a RNA-processing protein called RBFox2 because it is involved in the heart’s early development and its continuing functions. When genes are expressed, DNA is transcribed into RNA, which is then processed and eventually used to make proteins such as RBFox2.

Sure enough, levels of RBFox2 were dramatically reduced in the hearts of mice with a condition similar to heart failure. Then they genetically engineered mice without RBFox2, which developed symptoms of heart failure. Not only are low levels of this protein connected to weakened heart muscle, without enough of it, the body cannot compensate and the heart declines more quickly. However, we still don’t know why levels of RBFox2 decline during the transition to the decompensatory phase of heart failure.

In the future, this research might be used to develop treatments that reverse the decline of RBFox2 and effectively slow or prevent heart failure.

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Bad News for Smokers

June 12, 2015 by

By Medical Discovery News

June 5, 2015

Person smoking a cigarette

Smoking isn’t the only thing that raises your risk of lung cancer. As it turns out, your DNA can have that effect too.

A scientific study scanned the genomes, the entire genetic code, of 11,000 people of European descent in an effort to identify if there was any correlation between gene sequences and a common form of lung cancer, non-small cell carcinoma. They discovered that variants of certain genes increase a person’s susceptibility to developing lung cancer, especially in smokers.

One of the three gene variants they identified, named BRCA2, can double a smoker’s chance for developing lung cancer. BRCA2 is a tumor suppressor gene. It encodes a protein involved in the repair of damaged DNA, which is critical to ensure the stability of cell’s genetic material. When cellular DNA is damaged, there are several ways for the body to detect and repair that damage. If the damage to DNA cannot be repaired, then the cell is programmed to die by a process called apoptosis in order to prevent the damage being passed on to its daughter cells.

Like other tumor suppressor genes, the BRCA2 protein helps to repair breaks in DNA. It also prevents damaged cells from growing and dividing too rapidly. Variants of BRCA2 associated with breast, ovarian, and now lung cancers produce proteins that do not repair DNA damage properly. This causes cells to accumulate additional mutations, which can lead to cells that grow and divide uncontrollably. Such mutations lead to an increased risk of developing cancer.

Scientists have discovered over 800 mutations of BRCA2 that cause disease, including breast, ovarian, lung, prostate, pancreatic, fallopian, and melanoma cancers. Most of the mutations result from the insertion or deletion of a few letters of genetic code into the part of the gene that code for a protein. This disrupts the production of the BRCA2 protein and results in a shortened and nonfunctional form of the BRCA2 protein.

Lung cancer is a leading killer of Americans. Nearly 160,000 Americans will die from lung cancer this year, representing 27 percent of all cancer deaths. Active smoking causes close to 90 percent of lung cancers.

The good news from this discovery is that since scientists first linked BRCA2 to an increased risk of breast cancer, new therapies have been developed. Current treatments for breast and ovarian cancers could be effective with BRCA2-associated lung cancers, such as PARP inhibition.  PARP1 is another protein involved in repairing DNA damage. When one of two strands of DNA are broken or nicked, PARP1 moves to the region and recruits other proteins to the site to repair the damage. Many chemotherapy agents kill cancer cells by inducing DNA damage in the tumor and inhibiting PARP1. This doesn’t allow cancer cells to repair damage and makes them more susceptible to chemotherapy and radiation therapy. Now that we know this gene is linked to lung cancer, such therapies may be more effective in treating lung cancer and saving lives.

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Biological Fountain of Youth

April 25, 2015 by

March 27, 2015

By Medical Discovery News

The Biological Fountain of Youth

Over 500 years ago, Ponce de Leon landed in Florida as part of his search for the fountain of youth – magical waters that reverse aging, prevent illness, and grant immortality. He never found it, and neither has anyone else. While immortality is still impossible, we have come a long way in understanding the aging process.

We do not know the precise mechanism of aging, but there are some fundamental processes in our bodies that begin to change and this can drive aging. There are several theories of aging under intense scientific investigation.

A widely accepted theory of aging today is called evolutionary senescence, which mainly hinges on the concept of mutation accumulation. As we age, our cells accumulate mutations in our genetic material or DNA, which affects the ability of our cells to replicate and our tissues to regenerate. Also, some of our genes are designed to enhance reproduction early in life, but can cause problems later. Since genes can only be passed on during reproduction, which generally occurs earlier in life, genes that have negative effects later in life are not removed from the population – we are stuck with them! A good example is a gene called p53, which controls the fate of damaged cells by preventing their replication or directing them to die. This is important in preventing cancer in young people, but it may negatively impact our ability to replace aging cells in tissues as we grow older.

Another widely discussed theory centers on the maintenance of our genomes. As we get older, we accumulate damage to our DNA, which affects cellular function and our ability to renew tissues in the body. In a sense, this is a high mileage effect. Take for example the production of free radical molecules. These highly reactive molecules are normally produced in mitochondria, which use oxygen to produce cellular energy, a process that creates free radical molecules as a by-product. These free radical molecules lead to oxidative damage of DNA and other cellular components.

There is also evidence the neuroendocrine system (hormones that affect neurological function) influences aging. For example, a reduction in hormone levels can lead to a lengthening of life, at least in experimental animals. We are beginning to suspect that the insulin-related hormonal pathway may play a significant role in aging, at least in mice. Mutations that reduce the amount of this circulating hormone extend life.

A relatively new model of aging involves the replication of chromosomes as cells divide. When cells replicate, specialized structures at the ends of chromosomes called telomeres are shortened. Shortened telomeres are linked to decreased viability and increased cancer risk. Cells whose telomeres reach a critical length can no longer divide and are described as senescent.

We are expanding our understanding of how aging occurs. The search for a modern-day fountain of youth will require a great deal of dedicated work by biomedical scientists to safely improve and extend human life.

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Vaginal or C-section: Does it matter?

February 22, 2015 by

Feb. 20, 2015

An infant

In the climax of William Shakespeare’s “Macbeth,” the title character is sword fighting and believes himself invincible because he was given a prophesy that said “no man born of woman shall harm thee.” Yet, that is how he was tricked, for his rival, Macduff, was “from his mother’s womb untimely ripped.” This and other historical references show that cesarean sections have been used for centuries, but today the high success rate has made them more common than ever.

The origin of the term Cesarean is popularly and probably falsely attributed to the birth of Julius Caesar. This is unlikely, since C-sections at this time almost always resulted in the death of the mother, and historical records mention Caesar’s mother later in his life. However, the origin may still be linked to Caesar as a law enacted during Caesar’s reign stated that a dead or dying pregnant woman was to be cut open and the child removed from her womb to save the child. Widespread use of this procedure began after anesthetics and antimicrobial therapies became available in the 20th century.

In 1965, 4.5 percent of America’s babies were delivered via C-section. Today that figure has risen to almost one in three, and is on the rise worldwide as well. There are plenty of medical and nonmedical reasons for this shift from vaginal childbirth. Both come with side effects and consequences, some lasting longer than others. For example, C-sections have been linked to increased rates of diabetes and obesity, although we’re not sure why. In a recent study, birth by C-section lead to epigenetic changes in the child’s DNA.

Epigenetics are changes in our DNA that don’t result from changes in our genetic code. These changes can come from environmental factors, such as smoking, that alter the ability of a gene to be seen or expressed. What we didn’t understand until relatively recently is that epigenetic changes can be transmitted to offspring. So you are the product of your parents’ DNA and the environmental factors that affected your DNA in your lifetime and their lifetime before you were born. Then your DNA and epigenetic information is passed on to new generations. These changes accrue and could affect your children or grandchildren. So the descendants of a smoker may inherit more than their name, but epigenetic changes in DNA as well.

New research suggests certain epigenetic changes in a baby’s DNA called methylation are different depending on the type of birth. When DNA becomes methylated, it changes whether a gene is used to make a protein and this can then alter the properties of specific cells. In this study, researchers compared the DNA methylation patterns in stem cells of 25 vaginally delivered babies and 18 delivered by C-section. Distinct methylation changes were seen in more than 300 different regions of the genome between the two groups. Interestingly, many of these regions are associated with genes that control the immune system. We don’t know how these epigenetic changes affect the immune system and ability to fight disease, and don’t have sufficient information to link these differences to later health issues. But this remains an intriguing possibility and awaits more research.

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The Irresistible Rise of Genomic Medicine

February 22, 2015 by

Feb. 6, 2015

By Medical Discovery News

Genome

It’s only been 150 years since scientists discovered what we now call DNA. Today, it’s a household word, the basis for the field genomics, and an integral part to multitudes of scientific studies. It’s remarkable how relatively quickly our understanding of genes has progressed.

DNA was first thought to represent the genetic material of living organisms in the 1940s. Doctors Francis Crick and James Watson revealed the double helix structure of DNA in 1953, which is widely considered to be the first revolution in modern biology. In 1977, we first decoded the entire genome of a living organism, a tiny virus that infects bacteria called ФX174. This was the first time we understood all the DNA required to produce a life form. The term genomics was first coined in 1987 to describe the structure and functions of an organism’s entire genetic blueprint.  In 1995, we determined the genome of a free-living organism, a bacterium called Haemophilus influenza, for the first time. The genome of a eukaryotic organism, Baker’s yeast, was first completed in 1996. These early studies provided the novel approaches and advanced technologies that were later used to sequence the human genome, which consists of 3 billion base pairs. The human genome project, the second revolution in modern biology, began in 1990, and was completed in 2003. Since then, the genomes of more than 4,000 other organisms, including the ancient human species Neanderthal and the coffee plant, have been completely determined.

Genomics continues to be a part of the third revolution, convergence, which merges the rigors of computational science and engineering with modern biology. It cost $1 billion and took eight years to complete the sequence of the first human genome. Now, the cost of sequencing a human genome is a fraction of that at $2,000-$4,000 and takes a mere 1-3 days to complete. More than 2,500 human genomes have been sequenced from 26 distinct populations, and 100 million genetic variations have been discovered from these human samples so far. These variations are part of what make us each unique as people, but they can also reveal why we might be experiencing or have susceptibility to disease.

This is where genomic medicine comes in. Dr. Eric Green, the director of the National Human Genome Research Institute at the National Institutes of Health, says there are multiple studies with great promise in this emerging field. For example, cancer genomics has been used to determine the DNA sequence of tumor cells, which can help identify the type of cancer cells in a tumor and the cause of the cancer. That information can then be used to direct the type of treatment that would be the most effective for each individual, creating a personalized approach to medicine. A person’s DNA sequence may also disclose what pharmaceuticals will work most effectively.

The human genome project advanced our understanding of genetics and heredity. Much research is now focused on genomes and their relation to disease. More recently, scientists are using this newfound knowledge to further the science of medicine.

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Quick Diagnosis for Early Treatment

December 19, 2014 by

Dec. 12, 2014

By Medical Discovery News

Quick Diagnosis for Early Treatment

The time it takes to test for the cause of an infection ranges from minutes to weeks. A new generation of biosensors may change that, as they are being developed to identify the viral, bacterial, or fungal origin of an illness within a few hours, allowing physicians to begin the correct treatment sooner.

Many infections have symptoms that resemble the flu, such as HIV, the fungal infection coccidioidomycosis, Ebola, and even anthrax. This makes it very difficult to make a diagnosis. The emergence of new microbial pathogens such as SARS and MERS and bacterial resistance to antibiotics only adds to the fight against infectious agents. Scientists like Louis Pasteur and Robert Koch developed the traditional method for diagnosing infectious disease about 150 years ago, and modern methods have improved their discoveries.

Viruses, bacteria, and fungi have genetic information contained in DNA, RNA, or both. Each strand of DNA or RNA is made of four kinds of building blocks called nucleotides: adenine (A), cytosine (C), guanine (G), and thymine (T) in DNA or uracil (U) in RNA. Every species has a unique genetic code as seen in its arrangement of nucleotides, and by unlocking that code scientists can determine their identity. Each of the nucleotides has a different molecular weight, so the number of each nucleotide in a strand of DNA or RNA can be determined by measuring it on a device called a mass spectrometer. This can identify a microbial pathogen faster than the traditional culturing method, and can also identify those that can’t be grown in a lab.

However, the massive amount of DNA and RNA in a patient’s own cells complicates things. To tackle this problem, inventors of the new biosensor have coupled a mass spectrometer with polymerase chain reaction (PCR) to amplify any piece of genetic information that matches a known sequence from a pathogen. The sensor can then detect a very broad array of potential pathogens simultaneously.

Scientists have been very careful in selecting the unique genetic regions of various pathogens for this test. Once the PCR is used to amplify pieces of potential pathogens in the sample, the mass spectrometer spits out a series of numbers that can be cross-referenced to a database of over 1,000 pathogens that cause human disease in just a few hours.

For example, two children were hospitalized with flu-like symptoms in Southern California in 2009. They tested positive for the flu virus, but doctors did not know which strain of the flu they had. The new sensor analyzed their samples and revealed that both children were infected with H1N1, otherwise known as swine flu, which was not circulating at that time. H1N1 became a pandemic strain with cases all around the world.

This new technology represents a universal pathogen detector, capable of identifying the organism responsible for a person’s illness in just a few hours. Networking the detectors between hospitals and health departments would quickly identify outbreaks and possibly save lives.

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More Bad News for Smokers

October 27, 2014 by

Oct. 24, 2014

By Medical Discovery News

Lung X-ray

Smoking isn’t the only thing that raises your risk of lung cancer. As it turns out, your DNA can have that effect too.

A scientific study scanned the genomes, the entire genetic code, of 11,000 people of European descent in an effort to identify if there was any correlation between gene sequences and a common form of lung cancer, non-small cell carcinoma. They discovered that variants of certain genes increase a person’s susceptibility to developing lung cancer, especially in smokers.

One of the three gene variants they identified, named BRCA2, can double a smoker’s chance for developing lung cancer. BRCA2 is a tumor suppressor gene. It encodes a protein involved in the repair of damaged DNA, which is critical to ensure the stability of cell’s genetic material. When cellular DNA is damaged, there are several ways for the body to detect and repair that damage. If the damage to DNA cannot be repaired, then the cell is programmed to die by a process called apoptosis in order to prevent the damage being passed on to its daughter cells.

Like other tumor suppressor genes, the BRCA2 protein helps to repair breaks in DNA. It also prevents damaged cells from growing and dividing too rapidly. Variants of BRCA2 associated with breast, ovarian, and now lung cancers produce proteins that do not repair DNA damage properly. This causes cells to accumulate additional mutations, which can lead to cells that grow and divide uncontrollably. Such mutations lead to an increased risk of developing cancer.

Scientists have discovered over 800 mutations of BRCA2 that cause disease, including breast, ovarian, lung, prostate, pancreatic, fallopian, and melanoma cancers. Most of the mutations result from the insertion or deletion of a few letters of genetic code into the part of the gene that code for a protein. This disrupts the production of the BRCA2 protein and results in a shortened and nonfunctional form of the BRCA2 protein.

Lung cancer is a leading killer of Americans. Nearly 160,000 Americans will die from lung cancer this year, representing 27 percent of all cancer deaths. Active smoking causes close to 90 percent of lung cancers.

The good news from this discovery is that since scientists first linked BRCA2 to an increased risk of breast cancer, new therapies have been developed. Current treatments for breast and ovarian cancers could be effective with BRCA2-associated lung cancers, such as PARP inhibition.  PARP1 is another protein involved in repairing DNA damage. When one of two strands of DNA are broken or nicked, PARP1 moves to the region and recruits other proteins to the site to repair the damage. Many chemotherapy agents kill cancer cells by inducing DNA damage in the tumor and inhibiting PARP1. This doesn’t allow cancer cells to repair damage and makes them more susceptible to chemotherapy and radiation therapy. Now that we know this gene is linked to lung cancer, such therapies may be more effective in treating lung cancer and saving lives.

For a link to this story, click here.

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A One-Letter Blond

October 17, 2014 by

Oct. 10, 2014

By Medical Discovery News

Blond hair

Out of the 3 billion letters contained in the human genetic code, all it takes to be born a blond is a single change in a certain place from an A to a G. With the sheer complexity of the human genome, this new discovery shows how remarkably simple it is to be a natural blond. Especially when you consider the lengths people go to become one artificially.

This discovery actually came from research on the evolution of Sticklebacks, small fish that emerged from the oceans and colonized streams, rivers, and lakes at the end of the last Ice Age. Scientists at Stanford University have been studying how Sticklebacks have adapted to different habitats around the world, and particularly how different populations acquired their skin colors. They discovered that changes in a single gene determined the pigmentation of fish throughout the world. The gene responsible, the Kit ligand gene, is also in the human genome. Different versions of it have evolved around the world and are associated with differences in skin color.

The protein encoded in the Kit ligand gene aids in the development of pigment-producing cells, so its role in skin and hair color makes sense. However, the Kit ligand protein plays other important roles elsewhere in the body, such as developing stem cells into blood cells and producing sperm. Therefore, changes to this gene are not simple and could have detrimental consequences. This caused scientists to wonder how such an important gene could evolve while still preserving its essential roles. Both in fish and humans, the changes that lead to differences in pigmentation were not in the genetic region that encodes the Kit ligand protein, but rather at sites in the genome quite distant from here, where elements responsible for regulating that gene are located.

To find the regions that regulate the Kit ligand gene and therefore influence hair color, scientists cut out various regions at a time and linked them to a gene that produces a color when activated. Done in mice, only one of the regions activated in developing hair follicles. Comparing the DNA sequence of that region between brunettes and blonds, they then identified the single A to G change unique to blonds. This change reduced the amount of Kit ligand protein by 20 percent compared to brunettes. Even in mice, when scientists made this genetic alteration, their hair was lighter too. This means that changing a single letter only affects the utilization of the Kit ligand gene in one part of the body – the hair follicles. This region contributes to the diversity of hair color in humans while maintaining the same roles in other parts of the body. As it turns out, being blond is only skin deep.

This work further proves that large regions of our genetic information once thought of as “junk” DNA actually play critical roles. Subtle changes like this reveal how intricately genes are controlled and how even simple alterations are responsible for human diversity. This information can also help us understand how other gene variations may be associated with disease or resistance.

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Warning: Third-hand Smoke

September 13, 2014 by

Sept. 5, 2014

By Medical Discovery News

Smoke

Science has long proven that smoking is bad for you and those around you, with 90 percent of lung cancer cases caused by smoking. Even second-hand smoke is dangerous enough to warrant banning smoking in public places. The idea of third-hand smoke premiered in 2009, and scientific evidence shows that it too can harm human health.

Third-hand smoke is the many toxic compounds from tobacco smoke that settle onto surfaces (particularly fabrics) such as carpet, furniture, and the inside of a car. Researchers have identified chemicals in third-hand cigarette smoke called NNA and NNK that can bind to DNA, a person’s genetic information, and cause damage and mutations that could lead to cancer.

There are 4,000 known pollutants in cigarette smoke including a large number that cause DNA damage. Many of them have been found in the carpets, walls, furniture, dust, clothing, hair, and skin of smokers long after they’ve smoked a cigarette. The pollutants from smoke can accumulate over time, making the environment increasingly toxic. Mainstream smoke has more than 60 known carcinogens, which cause cancer, and other toxins, many of which are present in second- and third-hand smoke. Nonsmokers are exposed to these toxic compounds when they inhale, touch, or ingest them off of surfaces containing third-hand smoke. To make matters worse, some of the smoke residue can undergo a chemical transformation into secondary compounds when it interacts with other indoor pollutants, like ozone and nitrous acid. For example, nicotine reacts with ozone in the atmosphere to produce byproducts and ultrafine particles that can trigger asthma attacks.

Other secondary products such as NNA and a related compound called NNK are also formed. A recent study aimed to discover what level of third-hand smoke mutagens and carcinogens a nonsmoker might be exposed to in realistic scenarios, and whether these levels would be high enough to cause damage to DNA or other adverse effects. Unrepaired DNA damage can lead to mutations and increase the risk of developing cancer. They concluded that human cells exposed to third-hand smoke or secondary compounds had increased DNA damage within 24 hours. These results provide evidence that third-hand smoke does include carcinogens from cigarette smoke and the environment. The study also showed that NNA and NNK have damaging effects on developing lungs, making them particularly harmful to infants.

Smokers themselves are giving off third-hand smoke toxins, so going outside to smoke helps but is no solution. It is unclear how long toxic third-hand smoke compounds continue to be a risk. Depending on the compound, they may linger for hours, days, weeks, or longer. When smokers quit they should take steps to rid their homes and vehicles of third-hand smoke. This is potentially a time-consuming and expensive proposition but it is worth doing.

In 2011, 44 million American adults smoked cigarettes and 34 million of them smoked every day. Smoking causes one in five deaths, killing nearly 500,000 people in the U.S. every year. That is more deaths than HIV, illegal drugs, alcohol, motor vehicle accidents, and firearms combined. Is it really worth it?

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A Real Ice Monster

July 4, 2014 by

July 4, 2014

By Medical Discovery News

From the ice, scientists hauled a monster of unimaginable size. It was larger than any of its kind, and it was alive. Luckily, it wasn’t the Yeti, but Pithovirus sibericum, an abominable snow virus of sorts.

P. sibericum is the largest virus ever discovered. It’s about 1.5 micrometers, larger than some bacterium (a single-celled organism). All things considered though, it’s still microscopic – 1,333 copies of P. sibericum would fit on top of a pin. Luckily, this gigantic virus only infects amoebas, single-celled protozoans that live in bodies of water including lakes, ponds, streams, rivers, and even puddles. Some amoebas are associated with diseases such as dysentery.

This newly discovered virus was named P. sibericumbecause it was found in a sample of permafrost from Siberia, hence the word sibericum. The scientists who discovered it were French, and they were inspired by its shape to call it a Pithovirus from the ancient Greek word pithos, which were large containers used to store wine. They estimate the virus had been in the deep freeze for at least 30,000 years before they resurrected it this year. In 2012, the French scientists also resurrected an ancient plant from fruits buried in the same Siberian permafrost, which led them to search for the virus.

P. sibericum is unique in many ways beyond its record-breaking size. It is oval-shaped with a thick wall and a hole in one end. It has a distinctive honeycomb structure that caps the opening. Most viruses tightly pack their genetic information inside, but P. sibericum has a surprisingly small genome for a virus that big. Viruses one-third its size store two to three times more gene bases. Only about one-third of its proteins have any similarity to those of other viruses.

It is not, however, the first giant virus. Mimivirus was the first large virus ever found, reported in 2003. Previously, the record for largest virus went to Megavirus chilensis, which was found in water samples from Chile.

Just like Mimiviruses and Megaviruses, Pithoviruses are taken up by their amoebic hosts and once inside, they release their proteins and their genetic information. They then commandeer the host cell to produce hundreds of new viral particles, which are released when the host cell ruptures.

Interestingly, another giant virus called Marseillevirus also infects amoebas. Its genome contains a collection of genes found in similar viruses, bacteriophage viruses that infect bacteria, amoebas, and cells from the animal, plant, and fungus kingdoms. This suggests that amoebas may be acting as vessels for mixing genetic information from multiple forms of life. An amoeba could simultaneously be infected with Marseillevirus and bacteria, making it possible to produce complex genomes such as those of the giant viruses.

The resurrection of P. sibericum, a DNA virus long frozen in the now-thawing permafrost, has scientists wondering about undiscovered viruses that might be future threats to human or animal health.

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