Categories
Biology

Ancient DNA reveals the world’s oldest family tree

Analysis of ancient DNA from one of the best-preserved Neolithic tombs in Britain has revealed that most of the people buried there were from five continuous generations of a single extended family.

By analysing DNA extracted from the bones and teeth of 35 individuals entombed at Hazleton North long cairn in the Cotswolds-Severn region, the research team was able to detect that 27 of them were close biological relatives. The group lived approximately 5700 years ago — around 3700-3600 BC — around 100 years after farming had been introduced to Britain.

Published in Nature, it is the first study to reveal in such detail how prehistoric families were structured, and the international team of archaeologists and geneticists say that the results provide new insights into kinship and burial practices in Neolithic times.

The research team — which included archaeologists from Newcastle University, UK, and geneticists from the University of the Basque Country, University of Vienna and Harvard University — show that most of those buried in the tomb were descended from four women who had all had children with the same man.

The cairn at Hazleton North included two L-shaped chambered areas which were located north and south of the main ‘spine’ of the linear structure. After they had died, individuals were buried inside these two chambered areas and the research findings indicate that men were generally buried with their father and brothers, suggesting that descent was patrilineal with later generations buried at the tomb connected to the first generation entirely through male relatives.

While two of the daughters of the lineage who died in childhood were buried in the tomb, the complete absence of adult daughters suggests that their remains were placed either in the tombs of male partners with whom they had children, or elsewhere.

Although the right to use the tomb ran through patrilineal ties, the choice of whether individuals were buried in the north or south chambered area initially depended on the first-generation woman from whom they were descended, suggesting that these first-generation women were socially significant in the memories of this community.

There are also indications that ‘stepsons’ were adopted into the lineage, the researchers say — males whose mother was buried in the tomb but not their biological father, and whose mother had also had children with a male from the patriline. Additionally, the team found no evidence that another eight individuals were biological relatives of those in the family tree, which might further suggest that biological relatedness was not the only criterion for inclusion. However, three of these were women and it is possible that they could have had a partner in the tomb but either did not have any children or had daughters who reached adulthood and left the community so are absent from the tomb.

Dr Chris Fowler of Newcastle University, the first author and lead archaeologist of the study, said: “This study gives us an unprecedented insight into kinship in a Neolithic community. The tomb at Hazleton North has two separate chambered areas, one accessed via a northern entrance and the other from a southern entrance, and just one extraordinary finding is that initially each of the two halves of the tomb were used to place the remains of the dead from one of two branches of the same family. This is of wider importance because it suggests that the architectural layout of other Neolithic tombs might tell us about how kinship operated at those tombs.”

Iñigo Olalde of the University of the Basque Country and Ikerbasque, the lead geneticist for the study and co-first author, said: “The excellent DNA preservation at the tomb and the use of the latest technologies in ancient DNA recovery and analysis allowed us to uncover the oldest family tree ever reconstructed and analyse it to understand something profound about the social structure of these ancient groups.”

David Reich at Harvard University, whose laboratory led the ancient DNA generation, added: “This study reflects what I think is the future of ancient DNA: one in which archaeologists are able to apply ancient DNA analysis at sufficiently high resolution to address the questions that truly matter to archaeologists.”

Ron Pinhasi, of the University of Vienna, said: “It was difficult to imagine just a few years ago that we would ever know about Neolithic kinship structures. But this is just the beginning and no doubt there is a lot more to be discovered from other sites in Britain, Atlantic France, and other regions.”

The project was an international collaboration between archaeologists from the Universities of Newcastle, York, Exeter and Central Lancashire, and geneticists at the University of Vienna, University of the Basque Country and Harvard University. Corinium Museum, Cirencester, provided permission to sample the remains in their collection.

The work received primary funding from a Ramón y Cajal grant from the Ministerio de Ciencia e Innovación of the Spanish Government (RYC2019-027909-I), Ikerbasque — Basque Foundation of Science, the US National Institutes of Health (grant GM100233), the John Templeton Foundation (grant 61220), a private gift from Jean-François Clin, the Allen Discovery Center program, a Paul G. Allen Frontiers Group advised program of the Paul G. Allen Family Foundation, and the Howard Hughes Medical Institute

DNA sequencing illustration (stock image).
Categories
Biology human body

Second HIV patient to have recovered naturally!!!

A 30-year-old woman from the city of Esperanza, Argentina — the so-called Esperanza Patient — appears to be the second person whose immune system cleared the HIV-1 virus without antiretroviral therapy.

“During infection, HIV places copies of its genome into the DNA of cells, creating what is known as a viral reservoir,” said senior co-author Dr. Xu Yu, a researcher at Ragon Institute of MGH, MIT and Harvard Brigham and Women’s Hospital, and her colleagues.

“In this state, the virus effectively hides from anti-HIV drugs and the body’s immune response.”

“In most people, new viral particles are constantly made from this reservoir.”

“Antiretroviral therapy can prevent the new viruses from being made but cannot eliminate the reservoir, necessitating daily treatment to suppress the virus.”

“Some people, known as elite controllers, have immune systems that are able to suppress HIV without the need for medication.”

“Though they still have viral reservoirs that can produce more HIV virus, a type of immune cell called a killer T cell keeps the virus suppressed without the need for medication.”

In 2020, Dr. Yu and co-authors identified the first elite controller who had no intact HIV-1 viral sequence in her genome, indicating that her immune system may have eliminated the HIV-1 reservoir — what the scientists call a sterilizing cure.

The researchers sequenced billions of cells from that patient — known as the San Francisco Patient — searching for any HIV-1 sequence that could be used to create new virus, and found none.

The newly-identified patient, like the San Francisco Patient, has no intact HIV-1 genomes in a total of 1.188 billion peripheral blood mononuclear cells and 503 million mononuclear cells from placental tissues.

“These findings, especially with the identification of a second case, indicate there may be an actionable path to a sterilizing cure for people who are not able to do this on their own,” Dr. Yu said.

“The results may suggest a specific killer T cell response common to both patients driving this response, with the possibility that other people with HIV have also achieved a sterilizing cure.”

“If the immune mechanisms underlying this response can be understood by researchers, they may be able to develop treatments that teach others’ immune systems to mimic these responses in cases of HIV infection.”

“We are now looking toward the possibility of inducing this kind of immunity in persons on antiretroviral therapy through vaccination, with the goal of educating their immune systems to be able to control the virus without antiretroviral therapy,” she said.

Hope this seemingly magical recovery opens the doors to the ultimate cure/prevention for HIV infection!

HIV Virus
Categories
Biology environment human body

Why do Mosquitoes Bite Some More Than Others?

Monsoon can take a toll on human health. From manageable disease like cold and flu, to fatal diseases like dengue, malaria and chikungunya, monsoon brings along with it health complications that can put us at risk. While it might not be possible to avoid mosquito bites, as despite using ways like using mosquito repellents and avoiding mosquito-breeding, the vector succeeds in transmitting these diseases.

In a group, you must have noticed there is always someone who will complain about mosquitoes attacking them the most. That’s because, according to a report by Huff Post mosquitoes are selective insects, and some people are more likely to get bites than others.

There are certain factors which contribute to this effect. In one controlled study by the Journal of Medical Entomology, the bugs landed on people with blood Type O nearly twice as frequently as those with Type A. The researchers noted this has to do with secretions we produce, which tips mosquitoes off on a person’s blood type.

Entomology professor at the University of Florida, Jonathan F. Day said that more research needs to be conducted on mosquitoes’ potential preference for certain blood types over others. However, he agreed that mosquitoes do pick up on some cues we give off that make the bugs more likely to land on certain people.

“These cues let them know they are going to a blood source,” Day said. “Perhaps CO2 is the most important. The amount of CO2 you produce, like people with high metabolic rates ― genetic, other factors ― increases the amount of carbon dioxide you give off. The more you give off, the more attractive you are to these arthropods.”

The next question which pops up is what separates us from the nonliving entities that give off carbon dioxide, like cars? Mosquitoes look for primary cues in conjunction with what Day calls “secondary cues.”

Lactic acid — the stuff that causes our muscles to cramp during exercise — is one of those secondary cues, for example. Lactic acid is released through the skin, signaling to mosquitoes that we are a target, Day said.

Mosquitoes also have other qualities that help them pick up on secondary cues. “Mosquitoes have excellent vision, but they fly close to the ground to stay out of the wind,” Day said. “They are able to contrast you with the horizon, so how you’re dressed matters. If you have on dark clothes, you are going to attract more because you’ll stand out from the horizon, whereas those wearing light colors won’t as much.”

A mosquito also takes in “tactile cues” once it has landed on you.

“Body heat is a really important tactile cue,” Day said. “That comes into play with genetic differences or physiological differences. Some people tend to run a little warmer — when they land, they’re looking for a place where blood is close to the skin.” That means those whose temperatures are a little higher are more likely to get the bite.

Lifestyle or other health factors may also play a role, said Melissa Piliang, a dermatologist at Cleveland Clinic. “If body temperature is higher, you’re exercising and moving around a lot, or if you’re drinking alcohol, you are more attractive to mosquitoes,” Piliang said. “Being pregnant or being overweight also increases metabolic rate.”

Huff Post also said that one study showed that people who consumed just one can of beer were more at risk of attracting mosquitoes than those who didn’t. Of course, drinking outside is a popular summer and fall activity. “If you’ve been moving around all day doing yardwork and then you stop around dusk and drink a beer on your patio, you’re definitely at risk of bites,” Piliang said.

mosquitoes biting a person
Categories
Biology human body

Can body’s own immune system fight cancer?-turns out- YES!!

I was watching Netflix series- “Alexa & Katie” which is about the high school journey two best friends one of whom suffers from leukemia (blood cancer). Watching it really motivated me to find out more about the life threatening disease- cancer which kills many people every year.

While surfing I came across this article about a novel research that optimizes that our body’s own immune system can fight cancer.

Before jumping on to the article, first, let’s look at what is cancer?

Cancer is a disease in which some of the body’s cells grow uncontrollably and spread to other parts of the body. 

Cancer can start almost anywhere in the human body, which is made up of trillions of cells. Normally, human cells grow and multiply (through a process called cell division) to form new cells as the body needs them. When cells grow old or become damaged, they die, and new cells take their place.

Sometimes this orderly process breaks down, and abnormal or damaged cells grow and multiply when they shouldn’t. These cells may form tumors, which are lumps of tissue. Tumors can be cancerous.

Cancerous tumors spread into, or invade, nearby tissues and can travel to distant places in the body to form new tumors (a process called metastasis). Cancerous tumors may also be called malignant tumors. Many cancers form solid tumors, but cancers of the blood, such as leukemias, generally do not.

Armed with the basics of cancer let’s move on to the research article,

A groundbreaking study led by engineering and medical researchers at the University of Minnesota Twin Cities shows how engineered immune cells used in new cancer therapies can overcome physical barriers to allow a patient’s own immune system to fight tumors. The research could improve cancer therapies in the future for millions of people worldwide.

The research is published in Nature Communications, a peer-reviewed, open access, scientific journal published by Nature Research.

Instead of using chemicals or radiation, immunotherapy is a type of cancer treatment that helps the patient’s immune system fight cancer. T cells are a type of white blood cell that are of key importance to the immune system. Cytotoxic T cells are like soldiers who search out and destroy the targeted invader cells.

While there has been success in using immunotherapy for some types of cancer in the blood or blood-producing organs, a T cell’s job is much more difficult in solid tumors.

“The tumor is sort of like an obstacle course, and the T cell has to run the gauntlet to reach the cancer cells,” said Paolo Provenzano, the senior author of the study and a biomedical engineering associate professor in the University of Minnesota College of Science and Engineering. “These T cells get into tumors, but they just can’t move around well, and they can’t go where they need to go before they run out of gas and are exhausted.”

In this first-of-its-kind study, the researchers are working to engineer the T cells and develop engineering design criteria to mechanically optimize the cells or make them more “fit” to overcome the barriers. If these immune cells can recognize and get to the cancer cells, then they can destroy the tumor.

In a fibrous mass of a tumor, the stiffness of the tumor causes immune cells to slow down about two-fold — almost like they are running in quicksand.

“This study is our first publication where we have identified some structural and signaling elements where we can tune these T cells to make them more effective cancer fighters,” said Provenzano, a researcher in the University of Minnesota Masonic Cancer Center. “Every ‘obstacle course’ within a tumor is slightly different, but there are some similarities. After engineering these immune cells, we found that they moved through the tumor almost twice as fast no matter what obstacles were in their way.”

To engineer cytotoxic T cells, the authors used advanced gene editing technologies (also called genome editing) to change the DNA of the T cells so they are better able to overcome the tumor’s barriers. The ultimate goal is to slow down the cancer cells and speed up the engineered immune cells. The researchers are working to create cells that are good at overcoming different kinds of barriers. When these cells are mixed together, the goal is for groups of immune cells to overcome all the different types of barriers to reach the cancer cells.

Provenzano said the next steps are to continue studying the mechanical properties of the cells to better understand how the immune cells and cancer cells interact. The researchers are currently studying engineered immune cells in rodents and in the future are planning clinical trials in humans.

While initial research has been focused on pancreatic cancer, Provenzano said the techniques they are developing could be used on many types of cancers.

“Using a cell engineering approach to fight cancer is a relatively new field,” Provenzano said. “It allows for a very personalized approach with applications for a wide array of cancers. We feel we are expanding a new line of research to look at how our own bodies can fight cancer. This could have a big impact in the future.”

Honestly, let’s hope that this approach of treating cancer is able to save lives of millions of people affected with cancer

Categories
Biology

WOO-HOO!! WE CAN NOW REVERSE CELL AGING!

Turning off a newly identified enzyme could reverse a natural aging process in cells.

Research findings by a KAIST team provide insight into the complex mechanism of cellular senescence and present a potential therapeutic strategy for reducing age-related diseases associated with the accumulation of senescent cells.

Simulations that model molecular interactions have identified an enzyme that could be targeted to reverse a natural aging process called cellular senescence. The findings were validated with laboratory experiments on skin cells and skin equivalent tissues, and published in the Proceedings of the National Academy of Sciences (PNAS). 

“Our research opens the door for a new generation that perceives aging as a reversible biological phenomenon,” says Professor Kwang-Hyun Cho of the Department of Bio and Brain engineering at the Korea Advanced Institute of Science and Technology (KAIST), who led the research with colleagues from KAIST and Amorepacific Corporation in Korea. 

Cells respond to a variety of factors, such as oxidative stress, DNA damage, and shortening of the telomeres capping the ends of chromosomes, by entering a stable and persistent exit from the cell cycle. This process, called cellular senescence, is important, as it prevents damaged cells from proliferating and turning into cancer cells. But it is also a natural process that contributes to aging and age-related diseases. Recent research has shown that cellular senescence can be reversed. But the laboratory approaches used thus far also impair tissue regeneration or have the potential to trigger malignant transformations. 

Professor Cho and his colleagues used an innovative strategy to identify molecules that could be targeted for reversing cellular senescence. The team pooled together information from the literature and databases about the molecular processes involved in cellular senescence. To this, they added results from their own research on the molecular processes involved in the proliferation, quiescence (a non-dividing cell that can re-enter the cell cycle) and senescence of skin fibroblasts, a cell type well known for repairing wounds. Using algorithms, they developed a model that simulates the interactions between these molecules. Their analyses allowed them to predict which molecules could be targeted to reverse cell senescence.

They then investigated one of the molecules, an enzyme called PDK1, in incubated senescent skin fibroblasts and three-dimensional skin equivalent tissue models. They found that blocking PDK1 led to the inhibition of two downstream signaling molecules, which in turn restored the cells’ ability to enter back into the cell cycle. Notably, the cells retained their capacity to regenerate wounded skin without proliferating in a way that could lead to malignant transformation.

The scientists recommend investigations are next done in organs and organisms to determine the full effect of PDK1 inhibition. Since the gene that codes for PDK1 is overexpressed in some cancers, the scientists expect that inhibiting it will have both anti-aging and anti-cancer effects.

THE SCIENTISTS CONDUCTED WHAT IS KNOWN AS AN ENSEMBLE MODEL SIMULATION TO IDENTIFY MOLECULES THAT COULD BE TARGETED TO REVERSE CELL SENESCENCE. THEY THEN USED THE MODEL TO PREDICT THE EFFECTS OF INHIBITING PDK1 IN SENESCENT CELLS, AND CONFIRMED THE RESULTS IN LAB-CULTURED CELLS AND SKIN EQUIVALENT TISSUE MODELS.
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Biology Evolution human body

New microevolutinary change :Median artery in the human forearm

The median artery is the main vessel that supplies blood to the forearm and hand, when first formed in the mother’s womb, but it disappears once two arteries seen in adults develop.

The radial and ulnar arteries usually replace the median artery during developmental stages in the womb, so most adults obviously don’t have a median artery, but increasing numbers of cases retain it, so a person can have all three arteries.

The median artery is now present in about 35% of people and researchers predict that people born 80 years from now will all carry a median artery if the trend continues.

“The median artery offers benefits because it increases overall blood supply and can be used as a replacement in surgical procedures in other parts of the human body,” said senior author Professor Maciej Henneberg, a researcher in the Biological Anthropology and Comparative Anatomy Research Unit at the University of Adelaide and the Institute of Evolutionary Medicine at the University of Zurich.

“This is microevolution in modern humans and the median artery is a perfect example of how we’re still evolving because people born more recently have a higher prevalence of this artery when compared to humans from previous generations.”

In the study, Professor Henneberg and colleagues aimed to investigate the prevalence of persistent median arteries in postnatal humans over the last 250 years and to test the hypothesis that a secular trend of increase in its prevalence has occurred.

They found a total of 26 median arteries in 78 upper limbs (a prevalence rate of 33.3%) obtained from Australians aged 51 to 101 years.

“Our study into the prevalence of the artery over generations shows that modern humans are evolving at a faster rate than at any point in the past 250 years,” said lead author Dr. Teghan Lucas, a researcher in the Department of Archaeology at Flinders University and the School of Medical Sciences at the University of New South Wales.

“Since the 18th century, anatomists have been studying the prevalence of this artery in adults and our study shows it’s clearly increasing.”

“The prevalence was around 10% in people born in the mid-1880s compared to 30% in those born in the late 20th century, so that’s a significant increase in a fairly short period of time, when it comes to evolution.”

“This increase could have resulted from mutations of genes involved in median artery development or health problems in mothers during pregnancy, or both actually,” he added.

“If this trend continues, a majority of people will have median artery of the forearm by 2100.”

“When the median artery prevalence reaches 50% or more, it should not be considered as a variant, but as a normal human structure,” the authors said.

Lucas.et al. find that the prevalence of the persistent median artery in postnatal life approximately tripled over the last 125 years.

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Biology Covid-19 human body

Covid 19’s lingering problem : Heart damage

Massachusetts General Hospital pathologist James Stone can tell that most of the hearts he’s examined from COVID-19 patients are damaged from the first moment he holds them. They’re enlarged. They’re heavy. They’re uneven.

What he can’t tell—at least until he starts looking at samples of the tissue under a microscope—is exactly how those hearts were damaged, and whether it is a direct result of SARS-CoV-2 infection.

Early in the pandemic, other clinicians noted that even some patients who didn’t have preexisting heart conditions experienced cardiovascular damage while fighting COVID-19 infections, pointing to a possible causative link. Researchers had found, for example, that 8–12 percent of hospitalized COVID-19 patients had elevated levels of muscle contraction–regulating proteins called troponins—a sign of heart damage—and that these patients had an increased risk of mortality compared with those who didn’t have excess troponins. And early observations of patients in China who suffered reduced ejection fraction—the amount of blood getting pumped out of the heart each time it contracts—led researchers to suggest that these individuals were likely experiencing myocarditis, a severe form of inflammation that can weaken the heart and is commonly associated with infections.

But Stone and his collaborators’ analysis of heart tissue from 21 patients who died of COVID-19, published today (September 24) in the European Heart Journal, shows that while 86 percent of the patients did have inflammation in their hearts, only three had myocarditis. Several had other forms of heart injury, such as right ventricular strain injuries.

“The problem we identified in this study is that there’s other types of myocardial injury in these patients that is also causing elevated troponins,” says Stone. His international team sought to determine the mechanisms through which the disease damaged the heart and found that some conditions “really haven’t been talked about at all in the [COVID-19] papers that have previously been published.”

The pathologists observed a median of 20 slides from each heart, which is more than are included in most other studies regarding COVID-19’s cardiac effects. George Abela, a cardiologist at Michigan State University who was not involved in the study, tells The Scientist in an email, “This provides a more in-depth view of the extent of injury.”

The researchers expected to find some macrophages, a type of white blood cell that indicates inflammation, as pathologists had observed macrophages in the hearts of SARS patients during the 2003 outbreak. But Stone says he was surprised to see just how common these were—18 out of 21 COVID-19 patients’ hearts harbored macrophages that exhibited this type of inflammation. “It was really quite extensive,” he says.

As they analyzed the hearts further, the pathologists noted that only three patients had myocarditis, while four showed signs of heart injury due to right ventricular strain and another four had small blood clots in the vessels in the heart. It’s not clear why patients experience such inconsistent cardiac issues.

Abela says these findings have implications for treatment. For example, if the patient has right heart failure, a condition where the right side of a patient’s heart is not pumping enough blood to the lungs, a device that mechanically helps the heart pump blood might help, rather than drugs that target the inflammation or infection, which could be used to treat myocarditis.

Because so many of the hearts were infiltrated by macrophages, the researchers say that it may be difficult to discern who is experiencing myocarditis, which is characterized by different inflammatory cells—lymphocytes—while patients are alive. The two cell types would appear similar on tests that image the hearts of living patients. So, the team looked back at the patients’ medical records to see if they could find patterns in clinical tests that would reveal the type of heart damage when it still might be treatable. The three patients with myocarditis all had both troponin levels above 60 ng/mL and abnormal ECG readings while in the hospital. Only 15 percent of the patients without myocarditis had this combination.

The findings need to be replicated in larger groups of patients but could help doctors determine the best course of treatment for heart damage due to COVID-19, Stone says. The study is “giving the cardiologists and the ICU doctors that are taking care of these patients a roadmap of the changes that are going on in the heart.”

“Novel disease entities like SARS-CoV-2 reinforce the tremendous importance of continuing our efforts at continuing to facilitate autopsy evaluations,” says Allan Jaffe, a cardiologist at the Mayo Clinic, in an email. “This consortium of hospitals have added substantially to our knowledge of Covid disease.”

Categories
Biology

“THE KILLER MUTATIONS”

Scientists have discovered a handful of ultrarare mutations present in our cells from birth that likely shave years off a person’s life. Each of these DNA variants, most likely inherited from our parents, can reduce life span by as much as 6 months, the researchers estimate. And different combinations can dictate how long people live before developing age-related diseases such as cancer, diabetes, and dementia.

A person’s genes don’t set a specific natural life span—diet and many other factors play large roles, too—but studies have shown that DNA variants can influence the aging process. Biologists chalk up less than one-third of that influence to the genes we inherit. The source of other age-influencing DNA variation is environmental: Sun damage, chemical exposure, and other insults that create thousands of random mutations. Each cell’s collection of these environmental mutations differs, and most don’t greatly impact a person’s life span.

Hunting for these rare mutations, which are found in less than one in every 10,000 people, required a group effort. Harvard University geneticist Vadim Gladyshev, a senior co-author in the new study, partnered with academic colleagues and a biotech company called Gero LLC to scour the UK Biobank, a public database containing the genotypes of about 500,000 volunteers.

Using more than 40,000 of these genotypes, the team looked for correlations between small changes in DNA and health conditions, a so-called genomewide association study. Specifically, the variants they were targeting knock out genes entirely, depriving all the cells in the body of certain proteins.

On average, each person is born with six ultrarare variants that can decrease life span and “health span,” the amount of time people live before developing serious diseases, the team reports this month in eLife. The more mutations, the more likely a person was to develop an age-related illness at a younger age or die. “The exact combination matters,” Gladyshev says, but in general, each mutation decreases life span by 6 months and health span by 2 months.

The results build on what is already known about aging: “Family genes” matter. But rather than studying the common mutations found in especially long-lived people, researchers can now target rarer variants present in everyone. Gladyshev hopes this information can be used in clinical trials to categorize participants by their mutations in addition to things like gender and actual age.

He admits the findings are potentially controversial, as they minimize the perceived contribution to

aging of environmental “somatic” mutations acquired throughout life. Somatic mutations “live in a larger universe of age-related changes” influenced by lifestyle, he says, adding that changes to hormone and gene expression also come with age. “They [all] contribute to the aging process, but on their own they do not cause it.”

Jan Vijg, a geneticist at the Albert Einstein College of Medicine who studies the role of somatic mutations in aging, agrees, though he adds that somatic mutations can still cause diseases such as skin cancer that decrease life span.

Alexis Battle, a biomedical engineer at the Johns Hopkins University School of Medicine, points to an important caveat, however: The new research only looked at the “exome,” the 1% of the genome that actively builds the proteins that direct our cells. The rest is largely a black box, although growing evidence shows it can affect gene expression. Both Battle and Vijg agree that this DNA could be even more important in aging than the regions targeted by Gladyshev and his colleagues.

Going forward, Gladyshev would like to repeat his analysis on DNA from centenarians: those that live to be older than 100. “Most of the previous research focused on what these people have that makes them long-lived,” he says. “But [we want to look at] the opposite—it’s what they don’t have.”

Illustration of a damaged ribonucleic acid or dna strand
Categories
Biology

Ebola virus : A deadly havoc in people and not bats!!! Why???

The Ebola virus causes a devastating, often fatal, infectious disease in people. Within the past decade, Ebola has caused two large and difficult to control outbreaks, one of which recently ended in the Democratic Republic of the Congo.

When a virus brings serious disease to people, it means that humans are not good hosts for the virus. Viruses depend on a living host for their survival and have natural reservoirs — a hosting animal species in which a virus naturally lives and reproduces without causing disease. Bats are likely a natural reservoir for the Ebola virus, but little is known about how the virus evolves in bats.

Like most other RNA viruses, Ebola’s molecules are structured in a way that makes them more prone to genomic errors and mutations than other types of viruses. Because of this, Ebola and similar viruses have a remarkable ability to adapt to and replicate in new environments.

In the study, the research team, led by Alex Bukreyev, a UTMB virologist in the departments of pathology and microbiology and immunology, working with the team of Raul Andino, University of California, San Francisco, investigated how the Ebola virus adapts to both bat and human cells. They assessed changes in mutation rates and the structure of Ebola virus populations repeatedly in both bat and human cell lines using an ultra-deep genetic sequencing.

“We identified a number of meaningful differences in how the Ebola virus evolves when placed in a human cell line relative to a bat cell line,” Bukreyev said. “For instance, the RNA editing enzyme called ADAR within bat cells play a greater role in the replication and evolution of the Ebola virus than do such enzymes in human cells. We found that the envelope protein of Ebola virus undergoes a drastic increase in certain mutations within bat cells, but this was not found in human cells. This study identifies a novel mechanism by which Ebola virus is likely to evolve in bats.”

The study suggests that the Ebola virus and bats can live together harmoniously because of the bat cell’s ability to induce changes in the virus that make it less capable of harm. Bukreyev said that the study’s findings validate the ultra-deep genetic sequencing used in this study as a predictive tool that can identify viral mutations associated with more adaptive evolution. This technology can be very useful in studying, and perhaps shaping, the evolution of emerging viruses, like SARS-CoV-2, the virus responsible for COVID-19.

EBOLA VIRUS – A DANGER TO HUMANS

Categories
Biology Evolution

New insight into the evolution of complex life on Earth

A novel connection between primordial organisms and complex life has been discovered, as new evidence sheds light on the evolutionary origins of the cell division process that is fundamental to complex life on Earth.

The discovery was made by a cross-disciplinary team of scientists led by Professor Buzz Baum of University College London and Dr Nick Robinson of Lancaster University.

Their research, published in Science, sheds light on the cell division of the microbe Sulfolobus acidocaldarius, which thrives in acidic hot springs at temperatures of around 75?C. This microbe is classed among the unicellular organisms called archaea that evolved 3.5 billion years ago together with bacteria.

Eukaryotes evolved about 1 billion years later — likely arising from an endosymbiotic event in which an archaeal and bacterial cell merged. The resulting complex cells became a new division of life that now includes the protozoa, fungi, plants and animals.

Now a common regulatory mechanism has been discovered in the cell division of both archaea and eukaryotes after the researchers demonstrated for the first time that the proteasome — sometimes referred to as the waste disposal system of the cell — regulates the cell division in Sulfolobus acidocaldarius by selectively breaking down a specific set of proteins.

The authors report: “This is important because the proteasome has not previously been shown to control the cell division process of archaea.”

The proteasome is evolutionarily conserved in both archaea and eukaryotes and it is already well established that selective proteasome-mediated protein degradation plays a key role in the cell cycle regulation of eukaryotes.

These findings therefore shed new light on the evolutionary history of the eukaryotes.

The authors summarise: “It has become increasingly apparent that the complex eukaryotic cells arose following an endosymbiotic event between an ancestral archaeal cell and an alpha-proteobacterium, which subsequently became the mitochondria within the resulting eukaryotic cell. Our study suggests that the vital role of the proteasome in the cell cycle of all eukaryotic life today has its evolutionary origins in archaea.”