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Showing posts with label Biology. Show all posts
Showing posts with label Biology. Show all posts

Monday, 23 March 2020

Some Blood Types May Be Slightly More Susceptible to COVID-19, Paper Suggests

As governments take increasingly stringent containment measures to stop the spread of the coronavirus, researchers are still trying to better understand the dynamics of the latter. Recently, a team of Chinese immunologists suggested that not all blood groups were equal in the face of the virus. Indeed, type A would be more likely to contract the infection, while group O would be less. While these results are interesting for a better understanding of SARS-CoV-2, they have not yet been the subject of a peer-review procedure and should therefore be taken with caution.

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The study was undertaken by Chinese researchers and focused on 2,173 patients with COVID-19 from three hospitals in Wuhan and Shenzhen. The team looked at the distribution of blood types in the normal population in each area, and then compared it to their sample of patients with the virus, again in each area.

"Meta-analyses on the pooled data showed that blood group A had a significantly higher risk for COVID-19 compared with non-A blood groups," the researchers write in their paper. "Whereas blood group O had a significantly lower risk for the infectious disease compared with non-O blood groups."

Blood groups potentially affected differently by SARS-CoV-2 coronavirus

But the paper also clearly states that although the results were significant, it's not an all-or-nothing result.

As per the study, the normal population in Wuhan has a blood type distribution of 31 percent type A, 24 percent type B, 9 percent type AB, and 34 percent type O. Those with the virus, by comparison, were distributed as follows: 38 percent type A, 26 percent type B, 10 percent type AB, and 25 percent type O. Similar differences were observed in Shenzhen.

The different blood groups and their antigenic structure. Credits: Maxicours

As you can see, the percentages between the normal population and those with the virus have some differences - but it doesn't mean that people with type O blood type are immune; and not everyone who gets the virus is going to be type A. Far from it.

So, these relatively small differences, if replicated in studies with larger data pools, could lead to slight changes in the way we manage the spread of the disease; but even so, it probably won't change anything about the way we individually should be trying to limit the spread of the virus.

So, that's the low-down on the study. But this raises another fascinating topic - how our blood types can change the way we are affected by certain viruses is interesting in itself.

Norovirus is a stomach flu, and people will usually be infected through the digestive system. Those antigens on our blood cells are also on the surface of cells that line the intestine, and norovirus requires certain antigens to latch on to.

"This difference in susceptibility [to norovirus] has an interesting consequence," microbiologist Patricia Foster writes for The Conversation. "When an outbreak occurs, for example, on a cruise ship, roughly a third of the people may escape infection.

"Because they do not know the underlying reason for their resistance, I think spared people engage in magical thinking – for example, 'I didn't get sick because I drank a lot of grape juice'. Of course, these mythical evasive techniques will not work if the next outbreak is a strain to which the individual is susceptible."

So, how might the new coronavirus exploit our different blood types? At this point, we simply don't know.

The authors of the blood group paper uploaded to medRxiv aren't sure, but they suggest that maybe it has to do with the anti-A antibodies that both type B and type O have. That's just a hypothesis for now, and until we find out more, don't take it as gospel.

But it is a great example of how we are learning new information about the virus every single day. There's currently a vaccine being trialled in humans; many are doing everything they can to flatten the curve; and while the pandemic is stopping the world in its tracks, communities are swapping supplies and helping those in need.


Relationship between the ABO Blood Group and the COVID-19 Susceptibility

Jiao Zhao, Yan Yang, Han-Ping Huang, Dong Li, Dong-Feng Gu, Xiang-Feng Lu, Zheng Zhang, Lei Liu, Ting Liu, Yu-Kun Liu, Yun-Jiao He, Bin Sun, Mei-Lan Wei, Guang-Yu Yang, Xinghuan Wang, Li Zhang, Xiao-Yang Zhou, Ming-Zhao Xing, Peng George Wang


Saturday, 21 March 2020

Study reveals how long COVID-19 remains infectious on cardboard, metal and plastic

The virus that causes COVID-19 remains for several hours to days on surfaces and in aerosols, a new study published in the New England Journal of Medicine found.

The study suggests that people may acquire the coronavirus through the air and after touching contaminated objects. Scientists discovered the virus is detectable for up to three hours in aerosols, up to four hours on copper, up to 24 hours on cardboard and up to two to three days on plastic and stainless steel.

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"This virus is quite transmissible through relatively casual contact, making this pathogen very hard to contain," said James Lloyd-Smith, a co-author of the study and a UCLA professor of ecology and evolutionary biology. "If you're touching items that someone else has recently handled, be aware they could be contaminated and wash your hands."

The study attempted to mimic the virus being deposited onto everyday surfaces in a household or hospital setting by an infected person through coughing or touching objects, for example. The scientists then investigated how long the virus remained infectious on these surfaces.

The study's authors are from UCLA, the National Institutes of Health's National Institute of Allergy and Infectious Diseases, the Centers for Disease Control and Prevention, and Princeton University. They include Amandine Gamble, a UCLA postdoctoral researcher in Lloyd-Smith's laboratory.

As shown in Panel A, the titer of aerosolized viable virus is expressed in 50% tissue-culture infectious dose (TCID50) per liter of air. Viruses were applied to copper, cardboard, stainless steel, and plastic maintained at 21 to 23°C and 40% relative humidity over 7 days. The titer of viable virus is expressed as TCID50 per milliliter of collection medium. All samples were quantified by end-point titration on Vero E6 cells. Plots show the means and standard errors ( bars) across three replicates. As shown in Panel B, regression plots indicate the predicted decay of virus titer over time; the titer is plotted on a logarithmic scale. Points show measured titers and are slightly jittered (i.e., they show small rapid variations in the amplitude or timing of a waveform arising from fluctuations) along the time axis to avoid overplotting. Lines are random draws from the joint posterior distribution of the exponential decay rate (negative of the slope) and intercept (initial virus titer) to show the range of possible decay patterns for each experimental condition. There were 150 lines per panel, including 50 lines from each plotted replicate. As shown in Panel C, violin plots indicate posterior distribution for the half-life of viable virus based on the estimated exponential decay rates of the virus titer. The dots indicate the posterior median estimates, and the black lines indicate a 95% credible interval. Experimental conditions are ordered according to the posterior median half-life of SARS-CoV-2. The dashed lines indicate the limit of detection, which was 3.33×100.5 TCID50 per liter of air for aerosols, 100.5 TCID50 per milliliter of medium for plastic, steel, and cardboard, and 101.5 TCID50 per milliliter of medium for copper.

In February, Lloyd-Smith and colleagues reported in the journal eLife that screening travelers for COVID-19 is not very effective. People infected with the virus -- officially named SARS-CoV-2 -- may be spreading the virus without knowing they have it or before symptoms appear. Lloyd-Smith said the biology and epidemiology of the virus make infection extremely difficult to detect in its early stages because the majority of cases show no symptoms for five days or longer after exposure.

"Many people won't have developed symptoms yet," Lloyd-Smith said. "Based on our earlier analysis of flu pandemic data, many people may not choose to disclose if they do know."

The new study supports guidance from public health professionals to slow the spread of COVID-19:

  • Avoid close contact with people who are sick.

  • Avoid touching your eyes, nose and mouth.

  • Stay home when you are sick.

  • Cover coughs or sneezes with a tissue, and dispose of the tissue in the trash.

  • Clean and disinfect frequently touched objects and surfaces using a household cleaning spray or wipe.


Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1.

Neeltje van Doremalen, Trenton Bushmaker, Dylan H. Morris, Myndi G. Holbrook, Amandine Gamble, Brandi N. Williamson, Azaibi Tamin, Jennifer L. Harcourt, Natalie J. Thornburg, Susan I. Gerber, James O. Lloyd-Smith, Emmie de Wit, Vincent J. Munster.

New England Journal of Medicine, 2020;

DOI: 10.1056/NEJMc2004973

Friday, 13 March 2020

In obese people, bacteria escape from the intestine to spread throughout the body

Overweight and obesity are growing health issues across many developed and developing countries. Considered as a simple “handicap” in the eyes of some, in France, obesity is defined as being a real chronic disease. Recently, a team of researchers identified traces of bacterial DNA in the blood, liver and adipose tissue of obese people, revealing that fragments of bacteria (or whole living bacteria) infiltrate their bodies from the intestines.

Bacteria may be involved in the development of type 2 diabetes, according to a study published today in Nature Metabolism by researchers from Université Laval, the Québec Heart and Lung Institute (IUCPQ), and McMaster University.

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The authors found that the blood, liver, and certain abdominal fat deposits in diabetics have a different bacterial signature than in non-diabetics.

The researchers demonstrated this using blood and tissue samples from 40 patients suffering from severe obesity taken during bariatric surgery. Half of the participants suffered from type 2 diabetes, while the other subjects showed insulin resistance without being diabetic.

The researchers identified the bacterial genetic material in each of the tissues sampled, which came from the liver and three abdominal fat deposits. Based on the type of bacteria present and their relative abundance, the researchers were able to determine the bacterial signature for each tissue.

Their analysis revealed that the bacterial signature in diabetics was not the same as in non-diabetics. It also showed that the total number of bacteria varied from one tissue to another, and was highest in the liver and the greater omentum (a fatty tissue connecting the stomach and the transverse colon), two areas that play an important role in metabolic regulation.

“Our findings suggest that in people suffering from severe obesity, bacteria or fragments of bacteria are associated with the development of type 2 diabetes,” said the lead author, André Marette, professor at Université Laval’s Faculty of Medicine and researcher at the IUCPQ research centre.
According to the study, the bacterial genetic material detected in the tissues most likely comes from the intestine.

“We know that the intestinal barrier is more permeable in obese patients,” said Professor Marette. “Our hypothesis is that living bacteria and bacterial fragments cross this barrier and set off an inflammatory process that ultimately prevents insulin from doing its job, which is to regulate blood glucose levels by acting on metabolic tissues.”

Fernando Forato Anhê, an author on the paper and a postdoctoral research fellow at McMaster, added: “Location, location location...Beyond knowing the names of bacteria, their location is key to understanding how gut microbes influence host metabolism."

Professor Marette and his collaborators will be able to pursue their research further thanks to a $2 million grant they were recently awarded by the Canadian Institutes of Health Research.

“Our next objective is to determine if the bacteria found in the liver and fat deposits of people suffering from severe obesity are also present in those who are overweight or moderately obese,” said André Marette.

“We also want to see if certain pathogenic bacteria found in the tissues can trigger type 2 diabetes in an animal model. And lastly, we want to find out if certain beneficial bacteria found in these tissues can be used to prevent the development of the disease. If so, they might lead us to a new family of probiotic bacteria or a source of bacteria-based treatments to help fight diabetes,” concluded the researcher who is also a member of Université Laval’s Institute of Nutrition and Functional Foods (INAF).


Type 2 diabetes influences bacterial tissue compartmentalisation in human obesity

Fernando F. Anhê, Benjamin Anderschou Holbech Jensen, Thibault V. Varin, Florence Servant, Sebastian Van Blerk, Denis Richard, Simon Marceau, Michael Surette, Laurent Biertho, Benjamin Lelouvier, Jonathan D. Schertzer, André Tchernof & André Marette.

Nat Metab (2020).

Tuesday, 10 March 2020

Researchers Discover New Stem Cells That Can Generate New Bone

Many areas of the body are home to niches of stem cells that differentiate into tissue progenitors. For several years, biologists have known that bone stem cells are present in two particular places: bone marrow and periosteum. Previous research has also shown that there are vascular channels for cell transfer between the bone marrow and the outside of the bone. And recently, scientists have discovered that these channels themselves harbor bone progenitor stem cells.

A population of stem cells with the ability to generate new bone has been newly discovered by a group of researchers at the UConn School of Dental Medicine.

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In the journal STEM CELLS, lead investigator Dr. Ivo Kalajzic, professor of reconstructive sciences, postdoctoral fellows Dr. Sierra Root and Dr. Natalie Wee, and collaborators at Harvard, Maine Medical Research Center, and the University of Auckland present a new population of cells that reside along the vascular channels that stretch across the bone and connect the inner and outer parts of the bone.

“This is a new discovery of perivascular cells residing within the bone itself that can generate new bone forming cells,” said Kalajzic. “These cells likely regulate bone formation or participate in bone mass maintenance and repair.”

Stem cells present in the intraosseous canals

Stem cells for bone have long been thought to be present within bone marrow and the outer surface of bone, serving as reserve cells that constantly generate new bone or participate in bone repair. Recent studies have described the existence of a network of vascular channels that helped distribute blood cells out of the bone marrow, but no research has proved the existence of cells within these channels that have the ability to form new bones.

In the intraosseous vascular channels, in addition to the immune and bone blood cells, the researchers discovered bone stem cells capable of repairing the structure. Credits: Christopher Ritchlin & Iannis E. Adamopoulos

In this study, Kalajzic and his team are the first to report the existence of these progenitor cells within cortical bone that can generate new bone-forming cells – osteoblasts – that can be used to help remodel a bone.

To reach this conclusion, the researchers observed the stem cells within an ex vivo bone transplantation model. These cells migrated out of the transplant, and began to reconstruct the bone marrow cavity and form new bone.

While this study shows there is a population of cells that can help aid bone formation, more research needs to be done to determine the cells’ potential to regulate bone formation and resorption.

This study was funded by the Regenerative Medicine Research Fund (RMRF; 16-RMB-UCHC-10) by CT Innovations and by National Institute of Arthritis and Musculoskeletal and Skin.


Perivascular osteoprogenitors are associated with transcortical channels of long bones.

Sierra H. Root, Natalie K. Y. Wee, Sanja Novak, Clifford J. Rosen, Roland Baron, Brya G. Matthews, Ivo Kalajzic.


DOI: 10.1002/stem.3159

Sunday, 8 March 2020

Research: Social isolation could cause physical inflammation

Social isolation not only affects mood, it also affects the body. As a meta-analysis now shows, a lack of social contacts seems to go hand in hand with increased inflammatory reactions. Feeling loneliness also affects the inflammatory process in the organism - but differently than the actual isolation from other people.

Those who live isolated from other people or feel lonely do not only suffer psychologically. The perceived or actual social isolation can also have tangible physical effects. Studies have shown that lonely people sleep less, feel more stress and perceive pain and symptoms of illness as worse . In addition, loneliness weakens the immune system - as a result, those affected get sick more easily and may even age prematurely.

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Social isolation could be associated with increased inflammation in the body new research from the University of Surrey and Brunel University London has found.

Relation to inflammation markers

In the largest study of its kind researchers investigated the link between social isolation and loneliness with inflammation in the body.  Analysing 30 previous studies in this area researchers found that social isolation could be linked to increased inflammation in the body. Inflammation is the body's way of signalling the immune system to heal and repair damaged tissue, as well as defending itself against viruses and bacteria. Inflammation can eventually start damaging healthy cells, tissues and organs and lead to an increased risk of developing non-communicable diseases such as cardiovascular disease.

Researchers found that social isolation, the objective state of being isolated from other people, was associated with the presence of C-reactive protein, a protein substance released into the bloodstream within hours of a tissue injury, and increased levels of the glycoprotein fibrinogen, which is converted into fibrin-based blood clots.

Interestingly, researchers also identified that the link between social isolation and physical inflammation was more likely to be observed in males than females. Further work is needed to clarify why this might be, but previous work suggests that males and females might respond differently to social stressors.

Feeling loneliness works differently

The link between loneliness and inflammation was less clear-cut with results indicating a possible link between loneliness and the pro inflammatory cytokine IL-6. However, this finding was not consistent across the studies examined. Taken in combination with previous knowledge the researchers propose that it is likely that loneliness changes how the inflammatory system responds to stress rather than directly impacting inflammatory response.

Dr Kimberley Smith, Lecturer in Health Psychology at the University of Surrey, said: “Loneliness and social isolation have been shown to increase our risk of poorer health. Many researchers propose that part of the reason for this is because they influence the body’s inflammatory response.

“The evidence we examined suggests that social isolation may be linked with inflammation, but the results for a direct link between loneliness and inflammation were less convincing. We believe these results are an important first step in helping us to better understand how loneliness and social isolation may be linked with health outcomes.”

Christina Victor, Professor of Gerontology and Public Health at Brunel, added: “Our results suggest loneliness and social isolation are linked with different inflammatory markers. This shows how important it is to distinguish between loneliness and isolation, and that these terms should neither be used interchangeably nor grouped together.”


The association between loneliness, social isolation and inflammation: A systematic review and meta-analysis

Kimberley J.Smith, Shannon Gavey, Natalie E.RIddell, Panagiot Kontari, Christina Victor

Neuroscience & Biobehavioral Reviews

Monday, 24 February 2020

Superresolution provides unexpected insights into the dynamic structure of mitochondria

Researchers have discovered an exciting property of mitochondria - the power plants of our cells. Their experiments show that the inner membranes of these cell power plants change their structure every few seconds. In this way, the team apparently can dynamically adapt to the energy requirements in the cell.

As power plants and energy stores, mitochondria are essential components of almost all cells in plants, fungi and animals. Until now, it has been assumed that these functions underlie a static structure of mitochondrial membranes. Researchers at the Heinrich Heine University Düsseldorf (HHU) and the University of California Los Angeles (UCLA) have now discovered that the inner membranes of mitochondria are by no means static, but rather constantly change their structure every few seconds in living cells.

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This dynamic adaptation process further increases the performance of our cellular power plants. "In our opinion, this finding fundamentally changes the way our cellular power plants work and will probably change the textbooks," says Prof. Dr. Andreas Reichert, Institute of Biochemistry and Molecular Biology I at the HHU. The results are described in a publication in EMBO Reports.

Mitochondria are extremely important components in cells performing vital functions including the regulated conversion of energy from food into chemical energy in the form of ATP. ATP is the energy currency of cells and an adult human being produces (and consumes) approximately 75 kilograms of ATP per day. One molecule of ATP is produced about 20,000 times a day and then consumed again for energy utilization.

This immense synthesis capacity takes place in the inner membrane of the mitochondria, which has numerous folds called cristae. It was previously assumed that a specific static structure of the cristae ensured the synthesis of ATP. Whether and to what extent cristae membranes are able to dynamically adapt or alter their structure in living cells and which proteins are required to do so, was unknown.

MIC13‐SNAP shows that CJs and cristae undergo remodelling at a timescale of seconds

The research team of Prof. Dr. Andreas Reichert with Dr. Arun Kondadi and Dr. Ruchika Anand from the Institute of Biochemistry and Molecular Biology I of the HHU in collaboration with the research team of Prof. Dr. Orian Shirihai and Prof. Dr. Marc Liesa from UCLA (USA), also supported by the Center for Advanced Imaging (CAi) of HHU, succeeded for the first time in showing that cristae membranes in living cells continuously change their structure dynamically within seconds within mitochondria.

This showed that the cristae membrane dynamics requires a recently identified protein complex, the MICOS complex. Malfunctions of the MICOS complex can lead to various serious diseases, such as Parkinson's disease and a form of mitochondrial encephalopathy with liver damage. After the identification of the first protein component of this complex (Fcj1/Mic60) about ten years ago by Prof. Andreas Reichert and his research group, this is another important step to elucidate the function of the MICOS complex.

"Our now published observations lead to the model that cristae, after membrane fission, can exist for a short time as isolated vesicles within mitochondria and then re-fuse with the inner membrane. This enables an optimal and extremely rapid adaptation to the energetic requirements in a cell," said Prof. Andreas Reichert.


Cristae undergo continuous cycles of membrane remodelling in a MICOS ‐dependent manner

Arun Kumar Kondadi, Ruchika Anand, Sebastian Hänsch, Jennifer Urbach, Thomas Zobel, Dane M Wolf, Mayuko Segawa, Marc Liesa, Orian S Shirihai, Stefanie Weidtkamp‐Peters, Andreas S Reichert.

EMBO reports, 2020;

DOI: 10.15252/embr.201949776

Monday, 17 February 2020

Unique recordings provide insight into the sexual activity of the arthropods

Millipedes during sex - the structures of their genitals are clearly visible in UV light. © Stephanie Ware, Field Museum

Researchers have observed millipedes during sex - and looked very closely. Her recordings of the sexual act reveal for the first time in detail how the genitals of males and females of the genus pseudopolydesmus interact with each other. It also turned out: After sex, the millipede lady apparently seals her vulva with a sticky secretion - maybe this way she protects the sperm, the team suspects.

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Whether foreplay-loving tardigrade, the underwater act of the dolphins or snow monkeys with extraordinary erotic preferences: The diverse genital organs and sex practices in the animal kingdom always amaze researchers. Even males who mutilate their partner's genitals after mating and species in which the female sex has the penis have already discovered biologists.

At the same time, there are many animals that have not yet been observed during lovemaking. How they do it is therefore largely a mystery - this also applies to the millipedes. These multi-legged arthropods have produced thousands of species in the course of evolution, and each of them is likely to reproduce in its own way, as Xavier Zahnle from the University of California at Davis and his colleagues explain.

Love game in the petri dish

In order to find out more about the genitals and sex practices of the millipedes, the team of scientists has now devoted itself to representatives from the genus Pseudopolydesmus. “The problem with millipedes is that they do many things underground. If you take them out, you disturb them and then they stop,” says co-author Petra Sierwald of the Field Museum in Chicago. Not so pseudopolydesmus millipedes: "These animals have sex even in bright light in the petri dish."

This exhibitionistic disposition was just right for the researchers: they observed the arthropods during reproduction and took a large number of photos of the act. They used UV light, among other things, because the genital organs of the arthropods shine under the influence of this radiation and the individual tissues can be better distinguished. Computed tomography (CT) studies provided additional insights into the structure of the genitals.

View of the female genital organs on the second pair of legs © Stephanie Ware, Field Museum

Ejaculation and mating members separated

The recordings of the millipede genitals - both individually and combined in the sexual act - now reveal for the first time how sex works in the genus pseudopolydesmus. Specifically, it turned out that, as already known from other millipedes, the testicles of the males are not directly connected to the mating extremities. "The male must therefore ejaculate and immerse his so-called gonopods in the bluish ejaculate," reports Sierwald.

For the actual sexual act, the female then turns her vulva outwards, as the scientists found. "She has two openings between her second pair of legs," says the researcher. When the male penetrates, tiny pliers hook it into the end of his gonopods in the female genitals. Gonopods and vulva fit together like a key to the lock - this is the only way the mating act works, as the team suspects.

Sealing of Vulva after sex

Also interesting: After sex, the vulva is sealed with a sticky secretion and the sperm is enclosed in the female's body. If the millipede later lays eggs, they come into contact with the stored sperm on the way out. But who actually closes the external female genital organs?

"Before the study, I thought that the secretion came from the male, who wants to use this method to prevent the female from mating again," reports Sierwald. “But our CT images revealed glands inside the vulva. This suggests that much of the secretion could come from the female. Whether it wants to protect his genitals or the sperm, it is an exciting question for further research."

In addition to giving us a better understanding of the mechanics of millipede sex, Sierwald hopes the project will enable scientists to better understand the relationships between different millipede species, which could shed light on how they evolved.

"This study will be important for understanding how millipedes in this genus are related and how they're distributed," says Sierwald. "They can tell us about the geologic history of North America. As mountain ranges and rivers formed, groups of millipedes would get cut off from each other and develop into new species." And, she notes, Pseuopolydesmus is just the tip of the iceberg.

"There are 16 orders of millipedes in the world, and for most of them, we have only faint ideas what the vulvae look like."


Genital morphology and the mechanics of copulation in the millipede genus Pseudopolydesmus (Diplopoda: Polydesmida: Polydesmidae).

Xavier J. Zahnle, Petra Sierwald, Stephanie Ware, Jason E. Bond

Arthropod Structure & Development, 2020; 54: 100913

DOI: 10.1016/j.asd.2020.100913

Research: Prenatal exposure to cosmetic ingredients promote childhood overweight

If unborn babies in the womb increasingly come into contact with butylparaben, their risk of later being overweight obviously increases. © Janulla / thinkstock

Consequential stress in the womb: If pregnant women use paraben-containing cosmetics, this could harm their offspring. As a study shows, prenatal exposure to butyl paraben increases the risk of being overweight in childhood. This could be due to epigenetic changes triggered by the environmental hormone. Butyl paraben is often used in skin creams, make-up and the like as a preservative.

Parabens are mainly used as preservatives in numerous everyday products. Recently, however, these connections have come under increasing criticism. Because studies suggest that certain parabens act as so-called endocrine disruptors. This means that they behave like hormones and can therefore intervene in the hormonal balance of humans and animals . As a result, developmental and reproductive disorders or other health problems may occur.

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The butyl paraben often found in cosmetic products such as skin creams, make-up and sun milk was considered to be comparatively harmless for a long time. But then studies indicated that this paraben variant also acts more like a hormone than assumed.

Stress in pregnancy

For this reason, Beate Leppert from the Helmholtz Center for Environmental Research in Leipzig and her colleagues have now devoted more attention to this paraben. You wanted to know: Does prenatal exposure to butyl paraben affect the later risk of being overweight? After all, environmental hormones like bisphenol A are already known to be able to set the course for extra pounds in the womb.

For their study, the scientists first evaluated data from 629 mother-child pairs. The mothers were asked about their cosmetic use during pregnancy and their urine was checked for parabens. After the birth, the focus was on the children: How would their body weight develop over the years?

From the skin to the body

The evaluations showed that many women used at least one cosmetic product that contained parabens during pregnancy. This was also evident in her urine: compared to subjects who only used paraben-free cosmetics, they had increased concentrations of these chemicals in their urine. As the research team explains, parabens can enter the body through the skin and can then also be detected in blood and excretions.

But this also means that if substances such as butyl paraben penetrate the organism, they may strain the unborn child in the event of pregnancy. But with what consequences? In their investigations, Leppert and her colleagues actually found a connection between the concentration of butyl paraben in the mother's urine and the later body weight of the children.

Increased risk of being overweight

Specifically, it became clear that the greater the exposure to butyl paraben during pregnancy, the more the offspring tended to be overweight in the first eight years of life. This relationship was more pronounced in girls than in boys, as the scientists found.

Looking for a possible explanation, the researchers then carried out experiments with mice. It also became apparent in the rodents: exposure to butyl paraben during pregnancy and lactation, especially in the offspring of female mice, led to the animals eating more and getting fatter. However, increased contact with this paraben in adulthood did not appear to affect weight gain.

Changes in appetite regulators

The exciting thing: paraben exposure in the young mice was not only associated with an increased risk of being overweight, but also with a striking epigenetic change in the hypothalamus. For example, the genes for the leptin receptor and prohormone proopiomelanocortin (POMC) were less active than normal, as studies revealed. Leptin is known as a satiety hormone and POMC also plays an important role in regulating appetite - this regulation could therefore be disrupted by paraben exposure.

“Childhood obesity has now reached epidemic-like dimensions worldwide. Endocrine disruptors are an example of environmental factors that can contribute to programming for overweight and obesity - especially in the sensitive phase around childbirth,” stated Leppert and her colleagues. "Our results suggest that prenatal exposure to butyl paraben also promotes the development of obesity in children."

Gender differences in view

As the scientists emphasize, other influencing factors such as nutrition or physical activity are of course also decisive for body weight in childhood. In her view, however, prenatal stress and its consequences play a significant role in the susceptibility to excess pounds. In the future, Leppert and her colleagues want to get to the bottom of the effects of butyl paraben. They also want to find out why girls are apparently more sensitive to this environmental hormone than boys - a possible explanation could be, for example, the different concentrations of sex hormones such as estrogen.

In view of their results to date, the researchers are already making a clear recommendation: "Expectant mothers should definitely use paraben-free products during the sensitive phases of pregnancy and lactation with a view to future health," says co-author Irina Lehmann. "Many cosmetics have already been declared paraben-free, otherwise take a look at the list of ingredients or, for example, using the ToxFox app helps," she concluded.


Maternal paraben exposure triggers childhood overweight development.

Beate Leppert, Sandra Strunz, Bettina Seiwert, Linda Schlittenbauer, Rita Schlichting, Christiane Pfeiffer, Stefan Röder, Mario Bauer, Michael Borte, Gabriele I. Stangl, Torsten Schöneberg, Angela Schulz, Isabell Karkossa, Ulrike E. Rolle-Kampczyk, Loreen Thürmann, Martin von Bergen, Beate I. Escher, Kristin M. Junge, Thorsten Reemtsma, Irina Lehmann, Tobias Polte.

Nature Communications, 2020;

DOI: 10.1038/s41467-019-14202-1

Saturday, 15 February 2020

Researchers make human organs transparent to enable 3D mapping down at cellular level

This image shows details of a human kidney that has been made transparent. © Helmholtz Zentrum München / Ertürk Lab

A look inside the organ: For the first time, researchers have succeeded in making human organs completely transparent. Thanks to their process, the complex structure of these tissues can be visualized and analyzed down to the cellular level. This enables accurate mapping of the organs - and could one day help create functional artificial replicas.

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Whether brain , heart or kidney: human organs are incredibly complex. Doctors now know the basic structure and function of these tissues. Deciphering its structure in every detail has always been a challenge. Because technologies to make organ structures visible down to the cellular level were missing.

That should change with so-called tissue clearing. This process makes organs transparent and thus enables complex 3D images of them to be generated. So far, however, this was only possible with tissues from mice. The problem: In the course of time, insoluble molecules such as collagen accumulate in human organ tissue and make it stiff. Common cleaning agents can therefore make mouse organs transparent - but they fail to work on human organs, especially to human tissue in adults.

A look into the brain, kidney and co

Shan Zhao from Helmholtz Zentrum München and her colleagues have now succeeded in making the apparently impossible: They have made intact human organs transparent. "We had to take a completely new path and start all over again to find a chemical that could also make human organs transparent," reports the researcher.

After a series of experiments, the scientists came up with the solution: They found that a detergent called CHAPS can create small holes in the stiff organs. This makes them more permeable to other solutions, which then penetrate the fabric a centimeter deep and convert it into transparent structures. In this way, Zhao's team managed, among other things, a unique look into a human brain and kidney.

For example, SHANEL provides insight into the cellular structures of an intact human eye.© Helmholtz Zentrum München / Ertürk Lab

"Key for mapping"

In order to be able to examine the transparent organs in detail, the researchers developed a new laser scanning microscope with a particularly large recording capacity and a self-learning algorithm. As they report, the microscope can take pictures of entire human organs up to the size of a kidney. The algorithm is then used to analyze the millions of cells imaged.

Zhao and her colleagues summarize their entire method under the name SHANEL (Small-micelle-mediated human organ efficient clearing and labeling). “SHANEL could become a key technology for mapping intact human organs in the near future. This would enable us to quickly understand much better how organs such as our brain develop and how they function in a healthy and diseased state,” explains Zhao's colleague Ali Ertürk.

Alternative to donor organs?

According to the scientists, this will result in exciting new possibilities for 3D printing of organs. Because cellular three-dimensional maps of human organs could in future serve as templates for such artificially produced tissues. To achieve this goal, the team is already working on mapping the most important human organs, starting with the pancreas, heart and kidney.

If one day the detailed replication of human organs succeeds, patients who depend on a donor organ in particular could benefit. "There is a huge shortage of organ donors for hundreds of thousands of people," says Ertürk. "The waiting time for patients and the transplantation costs are a real burden. Detailed knowledge about the cellular structure of human organs brings us an important step closer to creating functional organs artificially on demand." emphasizes the researcher.


Cellular and Molecular Probing of Intact Human Organs

Shan Zhao, Mihail Ivilinov Todorov, Ruiyao Cai, Hanno Steinke, Elisabeth Kemter, Eckhard Wolf, Jan Lipfert, Ingo Bechmann, Ali Ertürk

Published:February 13, 2020


Wednesday, 12 February 2020

Discovery of a mysterious virus in Brazil whose genome is almost completely unknown

Paulo VM Boratto et al. 2020

With almost 5000 species currently described, viruses are ubiquitous on Earth. From the bottom of the oceans to the human blood via the atmosphere, these acaryotic infectious agents can adopt extremely simple as well as extremely complex structures; as such, virologists have been studying them for many years, focusing more and more on viral genomes. And recently, a team of researchers discovered a virus whose genome is unlike any other known viral genome.

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The Yaravirus , named after Yara - or Iara, a figure of water queen in Brazilian mythology -, was recovered from Lake Pampulha, an artificial lake in the Brazilian city of Belo Horizonte. The Yaravirus ( Yaravirus brasiliensis ) constitutes a new line of amoebic viruses with a confusing origin and phylogeny, according to the research team.

Virologists Bernard La Scola from the University of Aix-Marseille in France and Jônatas S. Abrahão from the Federal University of Brazil Minas Gerais, however, are not beginners. Two years ago, the duo helped discover another aquatic viral novelty: the Tupanvirus, a potentially giant virus found in extreme aquatic habitats.

Giant viruses: that can perform complex biological tasks

Giant viruses, unlike the regular variety, are so called because of their huge capsids (protein shells that encapsulate virions). These much larger viral forms were only discovered this century, but they are not only remarkable for their size. They also have more complex genomes, giving them the ability to synthesize proteins, and therefore to perform complex tasks such as DNA repair, as well as DNA replication, transcription and translation.

Before their discovery, it was thought that viruses could not do such things, being considered as relatively inert and non-living entities, only capable of infecting their hosts. We now know that viruses are much more complex than previously believed, and in recent years scientists have discovered other types of viral forms that also challenge our thinking about how viruses can spread. and operate. The new discovery, the Yaravirus, does not appear to be a giant virus, made up of small 80 nm particles.

Transmission electron microscopy images of the Yaravirus (A) and its infection cycle (B, C, D, E). Credits: Paulo VM Boratto et al. 2020

Yaravirus: an almost completely new genome virus

But what is remarkable is how unique its genome is. “Most of the known amoeba viruses have been seen to share many features that ultimately prompted the authors to classify them into common evolving groups. Contrary to what is observed in other viruses isolated from the amoeba, the Yaravirus is not represented by a giant size and a complex genome, but at the same time carries a significant number of genes not previously described", write the authors.

Circular representation of the Yaravirus genome. Only six genes (red arrows) in total are identical to known viral genes. Credits: Paulo VM Boratto et al. 2020

In their investigations, the researchers discovered that more than 90% of the genes of Yaravirus had never been described before, constituting what are called orphan genes (ORFans). Only six genes found by far resembled known viral genes documented in public scientific databases, and a search among more than 8,500 metagenomes available to the public gave no clue as to what the Yaravirus could be closely linked to.

Giant viruses with more reduced viral forms?

“Using standard protocols, our very first genetic analysis could not find any recognizable capsid or other conventional viral genes sequences in the Yaravirus. According to current metagenomic protocols for viral detection, the Yaravirus would not even be recognized as a viral agent”.

As for what Yaravirus really is , the researchers can only speculate for the moment, but suggest that it could be the first isolated case of an unknown group of amoebic viruses, or potentially of a distant type giant virus that could have evolved into a reduced form.


A mysterious 80 nm amoeba virus with a near-complete “ORFan genome” challenges the classification of DNA viruses

Paulo V. M. Boratto, Graziele P. Oliveira, Talita B. Machado, Ana Cláudia S. P. Andrade, Jean-Pierre Baudoin, Thomas Klose, Frederik Schulz, Saïd Azza, Philippe Decloquement, Eric Chabrière, Philippe Colson, Anthony Levasseur, Bernard La Scola, Jônatas S. Abrahão


Wednesday, 29 January 2020

Organoids developed in the laboratory produced real snake venom

In some countries or regions of the world, poisonous snakes pose a constant threat. Each year, these animals permanently kill or injure more than half a million people. Yet researchers still know surprisingly little about the biology of venom, which complicates efforts to develop treatments. But a new breakthrough made by researchers at the Hubrecht Institute in the Netherlands is very promising in this area: they have succeeded in developing miniature organs from snake stem cells in the laboratory. Cultured organoids work just like the snake's venom glands, and produce real venom.

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"It's a breakthrough," says José María Gutiérrez, toxicologist specializing in snake venom at the University of Costa Rica (San José), who did not participate in the study. "This work offers the possibility of studying the cell biology of cells secreting venom at a very fine level, which has not been possible in the past".

The breakthrough could also help researchers study the venom of rare snakes, which are difficult to keep in captivity, paving the way for new treatments for a variety of venoms.

Researchers have been creating mini-organs (or organoids) for years from adult human and mouse stem cells. These so-called pluripotent cells are able to divide and develop into new types of tissue throughout the body. Recently, scientists have used them to produce tiny livers and even rudimentary brains . But until now, scientists have never tried the technique with reptile cells.

"No one knew anything about snake stem cells ," said Hans Clevers, molecular biologist at the Hubrecht Institute and one of the most renowned organoid researchers in the world." In fact, we had no idea if it was possible."

Mini-organs created from pluripotent stem cells

To find out, Clevers and his colleagues took venom gland stem cells from nine snake species, including the Cape Coral Snake ( Aspidelaps lubricus ) and the Western Diamondback Rattlesnake ( Crotalus atrox ). placed in a mixture containing in particular hormones and proteins, called growth factors.

To the surprise of the team, snake stem cells responded to the same growth factors as human and mouse cells. This suggests that certain properties of these stem cells appeared hundreds of millions of years ago, from a common ancestor of mammals and reptiles.

Miniature snake (organoid) venom glands, cultivated in the laboratory. Credits: Ravian van Ineveld / Princess Maxima Center

After a week immersed in the cocktail, the snake cells had become small clumps of tissue half a millimeter in diameter, visible to the naked eye. When scientists removed the growth factors, the growth factors began to develop into venom-producing epithelial cells in the glands of snakes. The mini-organs expressed genes similar to those of the actual venom glands, the team reports in the document.

Diagram summarizing the process of creation of organoids producing venom. Credits: Hans Clevers et al./Institut Hubrecht

Artificial venom-producing mini glands

Organoids have even produced venom. Chemical and genetic analysis of the secretions revealed that they correspond to the venom produced by real snakes. Tests have shown that laboratory-made venom is also dangerous: it disrupts the function of mouse muscle cells and rat neurons in the same way as real venom.

Until now, scientists have not known whether the many toxins found in snake venom are produced by a general type of cell or by specialized toxin-specific cells. By sequencing RNA from individual cells and examining gene expression, the Clevers team has determined that actual venom glands and organoids contain different types of cells that specialize in the production of certain toxins.

Organoids grown using stem cells from separate regions of the venom gland also produce toxins in different proportions, indicating that the location in the organ counts.

The proportions and types of toxins in the venom differ from one species to another, even within the same species. "This can be problematic for the production of antivenom," says study author Yorick Post, molecular biologist at the Hubrecht Institute. Most antivenoms are developed using a single type of venom, so they only work against the bite of a single type of snake.

Now that Clevers and his colleagues have developed a way to study the complexity of venom and venom glands without manipulating live and dangerous snakes, they plan to compile a "biobank" of frozen organoids from venomous reptiles around the world. , which could help researchers find broader treatments.

"It would make it easier to create antibodies," says Clevers. The biobank could also be a "rich resource for identifying new drugs," he adds. Scientists believe that snake venom may hold the key to the development of new treatments for pain, high blood pressure and cancer, for example.

Organoids created by the Clevers team will provide an unprecedented new opportunity to supplement genomic information on poisonous snakes.


ARTICLE| VOLUME 180, ISSUE 2, P233-247.E21, JANUARY 23, 2020

Snake Venom Gland Organoids

Yorick Post, Jens Puschhof, Joep Beumer, Michael K. Richardson, Nicholas R. Casewell, Hans Clevers


Monday, 27 January 2020

A new type of evolutionary process has been highlighted

Evolution and natural selection takes place at the DNA level, because genes mutate and genetic traits persist or get lost over time. But now biologists believe that evolution can take place on a whole new scale - transmitted not by genes, but by molecules linked to their surface and responsible for their methylation. This mechanism would allow the conservation of an epigenome by enzymatic processes through several tens of millions of years, according to a process analogous to that of the Darwinian evolution of the genome.

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These molecules, known as "methyl groups", modify the structure of DNA and can turn genes on and off. The alterations are known as "epigenetic changes". Many organisms, including humans, have DNA dotted with methyl groups, but creatures like Drosophila and roundworms have lost the genes necessary to do so during the evolutionary period.

Another organism, the yeast Cryptococcus neoformans , also lost key genes for methylation during the Cretaceous, about 50 to 150 million years ago. But remarkably, in its current form, the fungus still has methyl groups in its genome. Now, scientists theorize that C. neoformans was able to conserve epigenetic changes for tens of millions of years, thanks to a new mode of evolution. The study was published in the journal Cell.

Methyl groups present in C. neoformans

The authors generally study C. neoformans to better understand how yeast causes fungal meningitis in humans. The fungus tends to infect people with weak immune systems and causes about 20% of all AIDS-related deaths.

Hiten Madhani, professor of biochemistry and biophysics at the University of California, and his colleagues, spend part of their days researching the genetic code of C. neoformans , looking for critical genes that help yeast invade human cells.

But the team was surprised when reports emerged, suggesting that the genetic material was adorned with methyl groups. In vertebrates and plants, cells add methyl groups to DNA using two enzymes. The first, de novo methyltransferase, links methyl groups to unadorned genes.

Diagram explaining the functioning of methylation via the intervention of de novo methyltransferase and maintenance methyltransferase. Credits: Nature

The enzyme adds to each half of the helical DNA strand the same methyl group pattern, creating a symmetrical design. During cell division, the double helix unwinds and builds two new strands of DNA from the corresponding halves. At this stage, an enzyme called "maintenance methyltransferase" intervenes to copy all the methyl groups from the original strand to the newly constructed half.

De novo methyltransferase loss and maintenance of methyltransferase compensation

Madhani and his colleagues examined existing evolutionary trees to trace the history of C. neoformans over time and found that, during the Cretaceous period, the ancestor of the yeast had the two enzymes necessary for the methylation of l DNA. But somewhere along the line, C. neoformans lost the gene needed to make de novo methyltransferases

During its evolutionary process, C. neoformans lost de novo methyltransferase and retained the maintenance methyltransferase. Credits: Sandra Catania et al. 2020

Without the enzyme, the body could no longer add new methyl groups to its DNA - it could only copy existing methyl groups by using its maintenance enzyme. In theory, even when working alone, the maintenance enzyme could keep DNA covered with methyl groups indefinitely - if it could make a perfect copy every time.

Natural selection at the origin of the conservation of a methylation mechanism

In reality, the team discovered that the enzyme makes mistakes and loses track of methyl groups every time the cell divides. When grown in a petri dish, C. neoformans cells occasionally gain new methyl groups in the same way that random mutations occur in DNA. However, cells lost methyl groups about 20 times faster than they could gain new ones.

In about 7,500 generations, each last methyl group would disappear, leaving nothing to be copied by the maintenance enzyme, the team estimated. Given the speed at which C. neoformans multiplies, the yeast should have lost all of its methyl groups in about 130 years. Instead, it retained the epigenetic changes for tens of millions of years.

Despite the loss of DNMT, C. neoformans can still use methylation thanks to compensation by its maintenance methyltransferase. A process preserved by natural selection. Credits: Sandra Catania et al. 2020

“ Because the rate of loss is higher than the rate of gain, the system would slowly lose methylation over time if there were no mechanism to maintain it. This mechanism is natural selection, ”explains Madhani. In other words, even if C. neoformans gained new methyl groups much more slowly than it lost them, methylation considerably increased the endurance of the organism, which meant that it could surpass individuals with less methylation.

Use methylation to control transposons

Enduring individuals have prevailed over those with fewer methyl groups, and thus, methylation levels have remained higher over millions of years. But what evolutionary advantage could these methyl groups offer to C. neoformans ? Well, they could protect the yeast genome from life-threatening damage.

Transposons, also known as "jumping genes", jump into the genome at will and often fit into very impractical places. For example, a transposon could jump to the center of a gene necessary for cell survival; this cell could malfunction or die. Fortunately, the methyl groups can cling to the transposons and lock them in place. It may be that C. neoformans maintain a certain level of DNA methylation to control transposons.

Understanding methylation in C. neoformans

Many mysteries still surround DNA methylation in C. neoformans . Besides copying methyl groups between strands of DNA, maintenance methyltransferase appears to be important in terms of how yeast causes infection in humans, according to a 2008 study by Madhani. Without the intact enzyme, the body cannot attack cells as effectively.

The enzyme also requires large amounts of chemical energy to function and copies only the methyl groups on the pristine half of the replicated DNA strands. In comparison, the equivalent enzyme in other organisms does not require additional energy to function and sometimes interacts with naked DNA, devoid of any methyl group. Further research will reveal exactly how methylation works in C. neoformans and whether this new form of evolution occurs in other organisms.


Evolutionary Persistence of DNA Methylation for Millions of Years after Ancient Loss of a De Novo Methyltransferase

Sandra Catania, Phillip A. Dumesic, Harold Pimentel,  Ammar Nasif
Caitlin I. Stoddard
Jordan E. Burke
Jolene K. Diedrich
Sophie Cook
Terrance Shea
Elizabeth Geinger
Robert Lintner
John R. Yates III
Petra Hajkova
Geeta J. Narlikar
Christina A. Cuomo
Jonathan K. Pritchard
Hiten D. Madhani

Published:January 16, 2020


Friday, 24 January 2020

Snakes are believed to be the cause of reported coronavirus disease in China

Since late December, a new coronavirus respiratory disease has emerged in China. It has already caused several hundred victims. Now, the new strain of coronavirus baptized 2019-nCoV by the WHO, has spread to several other countries. To better understand the virus, virologists must trace its origin and the animal host through which it first passed before infecting humans. A recent study shows that 2019-nCoV was transmitted to humans in the Wuhan market from snakes.

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Snakes - Chinese krait and Chinese cobra - may be the initial source of the newly discovered coronavirus that triggered the onset of a deadly infectious respiratory disease in China this winter. The disease was first reported in late December 2019 in Wuhan, a large city in central China, and quickly spread. Since then, sick travelers from Wuhan have infected people in China and other countries, including the United States.

Using samples from the virus isolated from patients, Chinese scientists determined the genetic code of the virus and observed it. The pathogen responsible for this pandemic is a new coronavirus. It belongs to the same family of viruses as the well-known severe acute respiratory syndrome coronavirus SARS-CoV, and the Middle East respiratory syndrome coronavirus (MERS-CoV), which have killed hundreds of people in the past 17 years. The World Health Organization (WHO) has named the new coronavirus “2019-nCoV”.

What is coronavirus?

The name of the coronavirus comes from its shape, which resembles a crown or a solar crown when imaged using an electron microscope. The coronavirus is transmitted by air and mainly infects the upper respiratory and gastrointestinal tracts of mammals and birds.

Although most members of the coronavirus family cause only mild flu-like symptoms during infection, SARS-CoV and MERS-CoV can infect the upper and lower respiratory tract, causing severe respiratory illness and other complications in humans.

The 2019-nCoV coronavirus observed under the electron microscope. Credits: CDC Chine

2019-nCoV causes symptoms similar to those of SARS-CoV and MERS-CoV. People infected with these coronaviruses suffer from a severe inflammatory reaction. Unfortunately, no approved antiviral vaccine or treatment is available for coronavirus infection. A better understanding of the 2019-nCoV life cycle, including the source of the virus, how it is transmitted and how it replicates is necessary to prevent and treat the disease.

2019-nCoV: an initial transmission from animals to humans

SARS and MERS are classified as zoonotic viral diseases, which means that the first infected patients acquired these viruses directly from animals. This was possible because, in the host animal, the virus had acquired a series of genetic mutations which allowed it to infect and multiply inside humans.

These viruses can now be transmitted between humans. Field studies have revealed that the original source of SARS-CoV and MERS-CoV is the bat and that masked palm civets (a mammal native to Asia and Africa) and camels , respectively, are used intermediate hosts between bats and humans.

This graph shows the origins of the different coronaviruses. The initial strains all come from bats. Credits: Science

In the case of this coronavirus epidemic in 2019, reports indicate that most of the patients in the first hospital group were workers or customers of a local wholesale seafood market which also sold processed meats and consumable animals living.

Including poultry, donkeys, sheep, pigs, camels, foxes, badgers, bamboo rats, hedgehogs and reptiles. However, as no one has ever reported finding a coronavirus infecting aquatic animals, it is plausible that the coronavirus may have originated from other animals sold in this market.

A disease transmitted by bats?

The hypothesis that nCoV 2019 comes from an animal on the market is strongly supported by a new publication in the journal Journal of Medical Virology . Virologists have analyzed and compared the genetic sequences of 2019-nCoV and all other known coronaviruses.

Study of the 2019-nCoV genetic code reveals that the new virus is most closely linked to two samples of bat SARS-type coronavirus from China, initially suggesting that, like SARS and MERS, the bald -mouse could also be behind 2019-nCoV.

The authors further found that the DNA coding sequence for the 2019-nCoV peak protein, which forms the crown of the viral particle that recognizes the receptor on a host cell, indicates that the bat virus may have mutated before infecting people. But when the researchers performed a more detailed bioinformatic analysis of the 2019-nCoV sequence, it suggested that this coronavirus could have come from snakes.

2019-nCoV: it would have gone from the bat to the snake

The researchers used an analysis of the protein codes favored by the new coronavirus and compared it to the protein codes of the coronaviruses found in different animal hosts, such as birds, snakes, marmots, hedgehogs, manis, bats and humans. Surprisingly, they found that the 2019-nCoV protein codes are most similar to those used in snakes.

Snakes often hunt bats in the wild. Reports indicate that the snakes were sold in the local seafood market in Wuhan, raising the possibility that 2019-nCoV has passed from the host species - bats - to snakes, and then to humans at the start of this. coronavirus epidemic. However, how the virus could adapt to both cold-blooded and warm-blooded hosts remains a mystery.

The authors of the report and other researchers must verify the origin of the virus by laboratory experiments. The first thing to do is to find the 2019-nCoV sequence in snakes. However, since the epidemic, the seafood market has been disinfected and closed, making it difficult to trace the source animal of the new virus.

DNA sampling from market animals and wild snakes and bats is necessary to confirm the origin of the virus. However, the results reported will also provide information on the development of prevention and treatment protocols.


RESEARCH ARTICLE:  Homologous recombination within the spike glycoprotein of the newly identified coronavirus may boost cross‐species transmission from snake to human

Wei Ji  Wei Wang  Xiaofang Zhao  Junjie Zai  Xingguang Li

First published: 22 January 2020

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