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Showing posts with label Medical Science. Show all posts
Showing posts with label Medical Science. Show all posts

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

Thursday, 23 January 2020

Alzheimer's disease: a crucial mechanism in the fight against the disease has been identified

Alzheimer's disease is a neurodegenerative disease that affects tens of millions of people worldwide today. It is characterized by two lesions: amyloid deposits and tangles of tau protein. Several treatments have been developed in recent years, targeting one or other of these lesions in order to delay the progression of the disease. But recently, researchers have identified a crucial mechanism of the disease: the process by which beta-amyloid causes tau tangles. A discovery that could lead to treatments far more effective than current therapies.

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Alzheimer's disease has long been characterized by the accumulation of two separate proteins in the brain: first beta-amyloid, which builds up in plaques, then tau, which forms toxic tangles that lead to cell death. . However, the way in which beta-amyloid leads to the toxicity of the tau protein has never been precisely known. Now a new study at the University of Alabama in Birmingham seems to describe this missing mechanism.

Published in the journal Science Translational Medicine , the study details a cascade of events. The accumulation of beta-amyloid activates a receptor which responds to a chemical signal from the brain called noradrenaline, commonly known to mobilize the brain and the body for action. Activation of this receptor by both beta-amyloid and norepinephrine stimulates the activity of an enzyme that activates the tau protein and increases the vulnerability of brain cells.

The role of norepinephrine in the virulence of Alzheimer's disease

Essentially, beta-amyloid bypasses the norepinephrine pathway to trigger a toxic build-up of tau, says Qin Wang, a neuropharmacology researcher in the Department of Cell, Developmental and Integrative Biology at the University of Alabama in Birmingham. " We really show that this norepinephrine is a missing piece of the whole Alzheimer's puzzle ."

This cascade explains why so many previous treatments for Alzheimer's disease have failed. Most of the drugs developed in recent decades have targeted the elimination of beta-amyloids. But new research suggests that norepinephrine amplifies the damage caused by this protein. Beta-amyloid itself can kill neurons, but only in very high doses.

Alzheimer's disease is characterized by two types of lesions: the amyloid plaques between the neurons and the tau neurofibrilar lesions (tangles) inside the neurons. Biologists have long missed the link between beta-amyloid and tau. But Wang's team has shown that norepinephrine plays the main role in this process. Credits: Dr Holland

Add norepinephrine and only 1-2% beta-amyloid is needed to kill brain cells in a laboratory can. So with treatments that targeted beta-amyloid but left the norepinephrine pathway intact, there was enough beta-amyloid left to do significant damage. But if the norepinephrine pathway is really crucial for the development of Alzheimer's disease, it suggests new ways of treating the disease.

Towards the development of a drug targeting the norepinephrine pathway

A drug that was developed to treat depression, but too ineffective to be approved, seems to work in this same direction. The drug, idazoxan, which has also been studied in schizophrenia, has already undergone the first clinical tests and has been shown to be safe. Wang is now looking to promote larger clinical trials of idazoxan to see if it can be used to effectively treat Alzheimer's disease at an early stage.

She hopes that in the long term, a drug which will act on this path linked to Alzheimer's disease in a more targeted manner can be developed, in order to minimize the side effects and maximize the effectiveness. Stephen Salloway, professor of psychiatry and neurology at Warren Alpert Medical School at Brown University, says he doesn't think Alzheimer will give in so easily to a new drug targeting the norepinephrine pathway.

“I doubt there is anything simple that will come out of it. I would be shocked if it works . ” Such a drug, however, could be part of a "therapeutic package" of treatments that could potentially advance Alzheimer's disease, he said. “ The goal is to gain a foothold on the biological level, then to develop it. The more goals we have, the greater the impact.”

The binding of beta-amyloid to norepinephrine would be responsible for the toxicity of the tau protein

Wang has a long history of norepinephrine because of its role in complex thinking and behavior. She came across the link with Alzheimer as part of this research. In two strains of mice and in human tissue in their new study, she and her colleagues showed that small pieces of beta-amyloid bind to a norepinephrine receptor, activating the enzyme GSK3-beta and causing the toxicity of tau.

Graphs and microscopic images showing the efficacy of idazoxan (inhibitor of the enzyme GSK3-beta) on the activity of beta-amyloid; it is blocked and cannot bind to norepinephrine, greatly reducing the toxicity of the tau protein. Credits: Fang Zhang et al. 2020

They confirmed this relationship by blocking the receptor with idazoxan in two strains of middle-aged mice for eight weeks. This deactivated the enzyme and prevented tau from becoming toxic. For years, researchers have wondered how beta-amyloids and tau are linked, says Rudolph Tanzi, an expert in molecular genetics of Alzheimer's disease at Massachusetts General Hospital.

Scientists basically assumed that beta-amyloid had caused tau tangles through a complicated chain of events. Then in a 2014 article in Nature , Tanzi and colleagues used cultured human brain cells to reveal a problem with the theory: mice - the main source of research information on Alzheimer's disease - do not have the right form of tau which becomes entangled in humans.

Block the GSk3-beta enzyme to neutralize inflammation

Instead, researchers have shown that in human cells, beta-amyloid directly causes tangles of tau. Tanzi and his colleagues blocked a variety of different enzymes called kinases to try to stop the process. They found two, both of which blocked the GSK3-beta enzyme - the same one that Wang and his colleagues identified in their research.

In 2014, Wang and his team had already shown that 1-Azakenpaullone, an inhibitor of the GSK3-beta enzyme, neutralizes the formation of beta-amyloid responsible for the induction of tau toxicity (in yellow). Credits: R. Tanzi et al. 2014

Tanzi believes that inflammation is a key player in Alzheimer's disease, triggering the cascade that leads to the disease. He previously described beta-amyloid as the match and tangles of tau as brushwood that catches fire. Tanzi says he has unpublished data on dozens of drugs that prevent beta-amyloid from triggering tangles, many of which support what Wang and his colleagues found in their new document.


β-amyloid redirects norepinephrine signaling to activate the pathogenic GSK3β/tau cascade

Fang Zhang, Mary Gannon, Yunjia Chen, Shun Yan, Sixue Zhang3, Wendy Feng1, Jiahui Tao1, Bingdong Sha, Zhenghui Liu, Takashi Saito, Takaomi Saido, C. Dirk Keene, Kai Jiao, Erik D. Roberson, Huaxi Xu and Qin Wang

Science Translational Medicine  15 Jan 2020:
Vol. 12, Issue 526, eaay6931
DOI: 10.1126/scitranslmed.aay6931

Wednesday, 22 January 2020

Everything you need to know about coronavirus spreading from China

Wuhan hospital staff in protective gear, where patients were treated.

Recently, a new coronavirus causing a mysterious illness similar to SARS has spread to China and three other Asian countries since its first appearance in the central city of Wuhan. Initially, the authorities excluded human-to-human transmission, but according to the latest news and following the report of several deaths, it turns out that the virus can indeed be transmitted between humans.

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On December 31, 2019, the World Health Organization (WHO) was alerted by the Chinese authorities to a series of cases of pneumonia in Wuhan, a city of 11 million inhabitants. The patients had been quarantined and research into identifying the origin of the pneumonia had started.

The Centers for Disease Control and Prevention (CDC) in the United States had identified the potential origin of the virus: a seafood market in Huanan (Wuhan), China.

New coronavirus

On January 9, WHO said the Wuhan epidemic was caused by an unknown type of coronavirus , responsible for a wide range of illnesses, from colds to more serious conditions like SARS. The new coronavirus is currently called “Wuhan coronavirus”, or 2019-nCoV.

According to an official report, to date, 59 people have been infected, including seven who are in serious condition.

First Death

Chinese health officials said a first patient died of the virus on January 11. Shortly thereafter, the total number of patients was revised downwards to 41 cases.

Spread beyond China

On January 13, the virus spread beyond the borders of China for the first time, with a case emerging in Thailand, according to the WHO. The victim is a Chinese woman suffering from mild pneumonia, who was returning from a trip to Wuhan.

On January 15, the Chinese health commission said that no human-to-human transmission of the virus that caused the Wuhan epidemic had been confirmed, but that the possibility "could not be excluded."

The following day, a first case of virus was confirmed in Japan, in a person who had stayed in Wuhan in early January.

American controls

On January 17, a second victim, a 69-year-old man, died in Wuhan, authorities said.

On the same day, the CDC announced that it would start screening passengers from Wuhan at three airports: San Francisco, JFK (New York) and Los Angeles.

Confirmation of human-to-human transmission

On January 20, a third death and more than 100 new cases are announced in China, causing concern before the annual Lunar New Year (or Chinese New Year) vacation, which begins on January 25 and sees hundreds of millions of Chinese traveling Across the country.

The virus is present in Beijing to the north, east of Shanghai and south of Shenzhen. More than 200 cases have been recorded. The virus has also been detected in South Korea in a Chinese man arriving by plane from Wuhan.

Chinese President Xi Jinping said during his first public comments on the epidemic that the virus must be "resolutely contained". Human-to-human transmission is "affirmative," Zhong Nanshan told state-run CCTV, a Chinese infectious disease specialist, on public television.

First case in the United States

The first case in the United States was reported a few days ago. It concerns a person in Washington State, near Seattle. The patient was hospitalized last week after a recent trip to Wuhan.

This article will be updated regularly.

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Tuesday, 21 January 2020

Cancer: discovery of new cell receptor could revolutionize T-cell therapies

Some current cancer therapies involve the use of genetically engineered T cells to destroy cancer cells. These particular white blood cells are able to recognize and neutralize any intruder in the body. However, these therapies are extremely restrictive and must be fully personalized due to the variability of the HLA receptor, allowing T cells to detect cancer cells. However, the discovery of a new invariant cellular receptor, which can neutralize different types of cancer, could revolutionize this therapy.

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The researchers behind the discovery note that the tests are still in their infancy, as they have only been performed on mice and human cells in the laboratory, not yet in living patients. But the preliminary results, published in the journal Nature Immunology , are promising and suggest that we may be on the verge of significant progress in T-cell therapies.

T cells are a type of white blood cell involved in the functioning of our immune system. When activated when they come into contact with defective or foreign cells in the body, they attack them, which helps us fight infection and disease.

T-cell therapies and HLA receptor variability

In T-cell therapy - the most common form of which is called CAR-T (for chimeric T cells of antigen receptors), scientists divert and increase this natural function of T cells to direct them to tumor cells in particular.

In CAR-T treatments, doctors extract T cells from patients' blood and genetically modify them in the laboratory to allow them to identify and specifically target cancer cells. The edited T cells are then multiplied in the laboratory before being administered to patients.

Diagram explaining the functioning of a CAR-T anticancer therapy. Credits:

Some of the limitations of the CAR-T technique are that edited T cells are only able to recognize a few types of cancer, and the whole therapy has to be personalized for different patients because of a T cell receptor (TCR) called “ human leukocyte antigen ”(HLA). HLA is what allows T cells to detect cancer cells, but it varies from person to person. And this is where this new discovery comes in.

MR1 receiver: an invariant and more suitable receiver

In the new study, led by biologists from Cardiff University in the UK, the researchers used CRISPR-Cas9 to discover a new type of TCR in T cells: a receptor molecule called MR1.

MR1 works similarly to HLA in terms of detecting and recognizing cancer cells, but one big difference is that, unlike HLA, it does not vary - which means that it could potentially form the basis of therapy for T cells that would work for a much wider range of people.

Diagram showing how new genetically engineered T cells use the MR1 receptor to identify and kill cancer cells. Credits: University of Cardiff

Preliminary laboratory experiments involving MR1 are indeed promising, even if the researchers point out that the results must be reproduced safely in clinical trials before they can confirm that it is a treatment suitable for humans.

In laboratory tests using human cells, T cells equipped with MR1 killed the multiple cancer cell lines tested (lung, melanoma, leukemia, colon, breast, prostate, bone and ovaries) that did not share common HLA. Tests on mice with leukemia - in which the animals were injected with MR1 cells - revealed signs of cancer regression and led the mice to live longer than the control mice.

Towards a new T cell therapy?

At the moment, we do not yet know how many types of cancer a technique based on this receptor could treat. That said, the first results certainly suggest that a varied range could be sensitive to it. If these types of effects can be replicated in humans - something scientists hope to start testing this year - T-cell therapies could take a big step.

To this end, the team's next step - in addition to organizing future clinical trials - will be to learn more about the mechanisms that allow MR1 to identify cancer cells at the molecular level.


Genome-wide CRISPR–Cas9 screening reveals ubiquitous T cell cancer targeting via the monomorphic MHC class I-related protein MR1

Michael D. Crowther, Garry Dolton, Mateusz Legut, Marine E. Caillaud, Angharad Lloyd, Meriem Attaf, Sarah A. E. Galloway, Cristina Rius, Colin P. Farrell, Barbara Szomolay, Ann Ager, Alan L. Parker, Anna Fuller, Marco Donia, James McCluskey, Jamie Rossjohn, Inge Marie Svane, John D. Phillips & Andrew K. Sewell

Nature Immunology (2020)


Sunday, 15 December 2019

Major research shows that certain common genes are linked to the majority of psychiatric disorders

A large-scale study has shown that the development of certain psychiatric illnesses can originate from the same gene. A discovery that could lead to the development of new treatments.

Psychiatric disorders affect more than 25% of the population each year. The numerous studies carried out in this field have made it possible to link variants (or mutations) of certain genes in the appearance of these disorders. But recently, scientists from Massachusetts General Hospital (MGH), in association with an international consortium of scientists specializing in genomic analyzes for psychiatric disorders, have shown that some of these variants can cause more than one disorder. psychiatric.

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In order to identify these genes, they gathered genomic data from around 500,000 healthy people, as well as from 230,000 others suffering from at least one of the eight most common psychiatric disorders. Result: 109 gene variants would increase the risk of developing more than one psychiatric illness.

They also found that the expression of the latter is greatly increased during the second trimester of pregnancy, a crucial phase for the development of the fetal brain.

The researchers then separated into three groups the different psychiatric pathologies, according to the gene variants that they have in common: mood and psychotic disorders (schizophrenia, bipolar disorder and depression), disorders responsible for compulsive behaviors (disorders obsessive compulsive, or anorexia nervosa), and developmental disorders of the nervous system (autism, attention deficit, or Tourette syndrome).

"  Understanding how specific genetic variations can contribute to a broad spectrum of diseases could tell us something about the degree to which these disorders can have a shared biology ," says lead study author Jordan Smoller.

Although this type of large-scale research has never been done in the past, the large number of variants identified was predictable for scientists. Indeed, most genes are pleiotropic, that is, they can have many roles in the body. It was therefore highly likely that a significant number of variants whose role is the proper development and functioning of the nervous system could be involved in more than one disease.

"Understanding how disorders are linked biologically can shed light on how we classify and diagnose mental health problems, " says bioinformatician Phil H. Lee of MGH. He also adds that this discovery could help characterize the biological pathways contributing to the development of these pathologies.

The researchers are confident that their study will allow the development of clinical trials in the future in order to develop new diagnoses and treatments that can be used for more than one disorder.

"  To the extent that these genes can have far-reaching effects, they could be potential targets for the development of new treatments that could benefit multiple conditions, " says Smoller.


Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

Cross-Disorder Group of the Psychiatric Genomics Consortium 1

Jordan W. Smoller