Category: Diseases, Syndromes and Conditions

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Predicting the Next Viral Pandemic

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A group of experts has argued that trying to survey all of the viruses in the animal kingdom is a futile effort, and that we should rather focus on those most likely to cross over at the interface of humans and animals.

The observation that most of the viruses that cause human disease come from other animals has led some researchers to attempt “zoonotic risk prediction” to second-guess the next virus to cause a global pandemic. 
Zoonotic viruses, those that cross over from animal species into humans, have caused epidemics and pandemics in humans for centuries. This is exactly what is occurring today with the COVID pandemic: SARS-CoV-2—the coronavirus that causes the disease—emerged from an animal species, albeit which one is not yet known.

An essay published April 20th in the open access journal PLOS Biology, led by Dr Michelle Wille at the University of Sydney, Australia with co-authors Jemma Geoghegan and Edward Holmes outlines the great challenges in zoonotic risk prediction.

The authors argue that these zoonotic risk predictions are of limited value, and will not be able to predict which virus will cause the next great pandemic. Instead, they reason, the human-animal interface should be the target for intensive viral surveillance.

A key question is whether it is possible to predict which animal or which virus group will most likely cause the next pandemic. This has led to “zoonotic risk prediction,” in which researchers attempt to determine which virus families and host groups are most likely to carry potential zoonotic and/or pandemic viruses.

Dr Wille and her colleagues identified several key problems with zoonotic risk prediction attempts.

Firstly, they’re based on very small data sets. Despite decades of work, less than 0.001% of all viruses have likely been identified, even from the mammalian species from which the next pandemic virus is expected to emerge.

Second, these data are also already highly biased in favour of those the most infectious viruses  of humans or agricultural animals, or are already known to be zoonotic. Most animals have in fact not been surveyed for viruses, and that viruses evolve so quickly that any such surveys will soon be out of date and therefore be of limited value.

The authors instead argue that a new approach is needed, not trying to futilely survey all the viruses in the wild but instead undertaking extensive sampling at the animal-human interface. This would enable the detection of novel viruses as soon as they appear in humans. This kind of enhanced surveillance could help us forestall the next pandemic.

Source: Phys.Org

Journal information: Wille M, Geoghegan JL, Holmes EC (2021) How accurately can we assess zoonotic risk? PLoS Biol 19(4): e3001135. doi.org/10.1371/journal.pbio.3001135

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Encapsulated Clusters of Noroviruses are Resistant to Disinfection

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Encapsulated clusters of noroviruses which can cause stomach flu have been found to be resistant to detergent and ultraviolet disinfection.

Noroviruses are the leading cause of gastroenteritis around the world, with more than 21 million cases annually in the United States. The findings of this study show that there is a need to revise current disinfection, sanitation and hygiene practices which serve to protect against infection with noroviruses.

In 2018, the research team had found that noroviruses can be transmitted to humans in the form of membrane-enclosed packets that contain clusters of viruses. Previously, it was thought that viruses spread via exposure to individual virus particles, but the 2018 study, , showed how membrane-enclosed clusters arrive at a human cell and release a large number of viruses.

For the new study, Drs Danmeng Shuai, Nihal Altan-Bonnet and the study’s first author Mengyang Zhang, a doctoral student co-advised through a GW/NIH Graduate Partnerships Program, examined how such protected virus clusters behave in the environment. They found that the virus clusters could survive disinfection attempts with detergent solutions or even UV light. Water treatment plants use UV light to kill noroviruses and other pathogens, and is being widely used in the COVID pandemic.

“These membrane-cloaked viruses are tricky,” explained study co-author Danmeng Shuai, PhD, associate professor of civil and environmental engineering, George Washington University. “Past research shows they can evade the body’s immune system and that they are highly infectious. Our study shows these membrane enclosed viruses are also able to dodge efforts to kill them with standard disinfectants.”

“We have to consider these viral clusters cloaked in vesicle membranes as unique infectious agents in the public health arena,” added Nihal Altan-Bonnet, PhD, a senior investigator and the head of the Laboratory of Host-Pathogen Dynamics at the National Heart, Lung, and Blood Institute. “When it comes to virulence -; and now with this study, disinfection and sanitation -; the sum is much more than its parts. And these clusters are endowed with properties that are absent from other types of viral particles.”

Future studies are needed to determine whether certain kinds of cleaning solutions or more UV light exposure would degrade the protective membrane and/or kill the viruses inside. Such research would hopefully come up with improved disinfection methods that could be used for cleaning surfaces in the home, in restaurants and in places where norovirus can spread and cause outbreaks, like cruise ships.

“Our study’s findings represent a step towards recommendations for pathogen control in the environment, and public health protection,” Dr Altan-Bonnet said.

Source: News-Medical.Net

Journal information: Zhang, M., et al. (2021) Emerging Pathogenic Unit of Vesicle-Cloaked Murine Norovirus Clusters is Resistant to Environmental Stresses and UV254 Disinfection. Environmental Science and Technology. doi.org/10.1021/acs.est.1c01763.

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Discovery Offers New Treatment for Sickle Cell Anaemia

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In a promising step towards a new treatment for sickle cell anaemia, researchers have discovered a small molecule that boosts levels of foetal hemoglobin, a healthy form that adults normally do not make.

Current treatment options are few, including bone marrow transplants and gene therapy, and only address a subset of symptoms. Opioids are used for pain management, with their hazard for addiction and abuse.
The researchers presented their results at the spring meeting of the American Chemical Society (ACS).

“Using our proprietary small molecule probe and CRISPR guide RNA libraries, we screened a disease-relevant cell model that allowed us to pinpoint a treatment target,” said Ivan V Efremov, PhD, senior director, head of medicinal chemistry of Fulcrum Therapeutics.

Sickle cell disease occurs when genes for two of haemoglobin’s four proteins contains an error, resulting in a rigid, sickle-like shape. This has consequences in reduced oxygen transport, and painful blockages of the irregularly shaped cells called vaso-occlusive crises. The red blood cells die fast, leading to anaemia. These patients are also at high risk of developing stroke, heart disease, kidney failure and other potentially deadly conditions.

While in the womb, humans make “foetal” haemoglobin that carries oxygen normally but three or four months after birth, cells switch to an adult haemoglobin version. Although the adult haemoglobin expressed by sickle cell patients is defective, stem cells in their bone marrow still have the capacity to produce foetal haemoglobin.

Some individuals have a hereditary persistence of foetal hemoglobin, and so tap this resource automatically. “They have the sickle cell mutation, but additional mutations result in continued expression of fetal hemoglobin into adulthood,” said Christopher Moxham, PhD, chief scientific officer of Fulcrum Therapeutics. With foetal hemoglobin levels of around 25-30%, he said, enough red blood cells function well enough that patients may become asymptomatic.

The team developed a drug, called FTX-6058, that mimics the effect seen in patients with the hereditary persistence of foetal hemoglobin. It attaches to a protein inside bone marrow stem cells that will mature into red blood cells and reinstates their foetal haemoglobin expression. “What is really key is FTX-6058 upregulates fetal hemoglobin across all red blood cells, a pancellular distribution,” Dr Efremov said. “If some red blood cells did not express this, they could still sickle and cause disease symptoms.” Fulcrum began a phase 1 safety trial in healthy adult volunteers last year after preclinical experiments showed an increase in fetal hemoglobin levels to around 25-30%.

“What distinguishes FTX-6058 is that we are targeting the root cause of sickle cell disease,” Dr Moxham said. “Other drugs approved in this space, particularly since 2019, are treating the disease’s symptoms, either the anemia or the vaso-occlusive crises.”

Preclinical experiments showed that FTX-6058 outperformed another foetal heamoglobin booster, hydroxyurea, approved in the 1990s.

A phase 2 clinical trial is planned for people living with sickle cell disease which should begin by the end of 2021. The researchers are also further characterising the therapeutic molecule. Fulcrum is also considering exploring the use of FTX-6058 in people living with β-thalassemia, a blood disorder in which haemoglobin production is reduced.

Source: Medical Xpress

Categories : Diseases, Syndromes and Conditions NeurologyTags :

Mystery Brain Disease Baffles Canadian Doctors

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Doctors in Canada are struggling to explain a spate of cases involving memory loss, hallucinations and muscle atrophy.

For more than a year public health officials in New Brunswick province have been tracking a “cluster” of 43 cases of suspected neurological disease with no known cause.

A leaked memo from the province’s public health agency asking physicians to be on the lookout for symptoms similar to Creutzfeldt-Jakob disease (CJD), a rare, fatal and largely sporadic disease caused by prion proteins. Symptoms such as memory loss, vision problems and abnormal jerking movements were similar enough to trigger an alert with Canada’s CJD surveillance network. However, it was confirmed that this disease was not CJD.

“We don’t have evidence to suggest it’s a prion disease,” said Dr Alier Marrero, the neurologist leading New Brunswick’s investigation.
Patients initially reported unexplained pains, spasms and behavioural changes, easily misdiagnosed as anxiety or depression.

However, over 18 to 36 months they began to develop cognitive decline, muscle wasting, drooling and teeth chattering. Some also began experiencing frightening hallucinations, including the sensation of crawling insects on their skin.  

Each time a possible case arises, a battery of tests is administered to determine if they match the cluster. Cases have risen from only one in 2015 to 24 in 2020, and so far five people are believed to have died from the illness.

“We have not seen over the last 20-plus years a cluster of diagnosis-resistant neurological disease like this one,” said Michael Coulthart, head of Canada’s CJD surveillance network.

The majority of cases are linked a sparsely populated region of the province, with the overall number of cases in the cluster remaining low. However, New Brunswick has a population of fewer than 800 000 people.

Dr Marrero and his team have consulted experts in neurology, environmental health, field epidemiology, zoonotics and toxicology to better understand the possible cause of the mysterious illness.

A growing team of researchers are trying to pin down a common cause or perhaps environmental effect.

“We don’t know what is causing it,” said Dr Marrero. “At this time we only have more patients appearing to have this syndrome.”

Valerie Sim, a researcher of neurodegenerative diseases at the University of Alberta cautioned against jumping to conclusions. “I don’t really know if we even have a defined syndrome. There just isn’t enough information yet,” she said.

She observed that key markers for degenerative neurological illnesses had not been identified, with the cluster’s wide range of symptoms being “atypical” for most brain diseases. Conversely, the scope of symptoms could be explained by certain cancers, dementia or even misdiagnoses.

Frustratingly, when the ailment is unclear a number of tools can be deployed, “and then the patient somehow recovers. You come away never knowing what they actually had,” said Sim.

“We see odd neurological syndromes from time to time. Sometimes we figure them out. Sometimes we don’t.”

Source: The Guardian

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Premature Death Risk Doubled for Patients With Superbug on Their Skin

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Adults middle-aged or older who carry methicillin-resistant Staphylococcus aureus (MRSA) ‘superbug’ on their skin are twice as likely to die within the next decade as people who do not, according to a study by the University of Florida (UF).

“Very few people who carry MRSA know they have it, yet we have found a distinct link between people with undetected MRSA and premature death,” said lead author Arch Mainous, PhD, a professor in the department of health services research, management and policy at UF.

The findings suggest that routine screening for undetected MRSA may be warranted in older people to prevent deaths from infection.

A third of Americans carry Staphylococcus aureus, or staph, on their skin or in nasal passages, and of these about 1% carry MRSA, the notorious antibiotic resistant staph strain.

MRSA carriers may not even be aware that they carry the bacteria unless they develop an infection or are tested for it. A quarter of people who carry MRSA without an active infection, known as colonised MRSA for at least a year, eventually develop a MRSA infection.

“MRSA can be part of normal body flora, but it can lead to infection when immune systems are compromised, especially in people who are hospitalized, have underlying disease, or after antibiotic use,” said Prof Mainous, also vice chair for research in the UF College of Medicine’s department of community health and family medicine.

According to a 2017 Centers for Disease Control and Prevention report, 119 000 Americans experienced a staph bloodstream infection and nearly 20 000 died. Hospitalised patients with colonised MRSA may be particularly vulnerable to  infection in hospital or after discharge. Among carriers, wounds, surgical incisions and use of medical devices, such as catheters, may also lead to MRSA infection.

In this study, researchers analysed data from the 2001-2004 National Health and Nutrition Examination Survey, a nationally representative study combining survey questions with laboratory testing, which includes nasal swabs for detecting MRSA.

Adjusting for risk factors including gender and ethnicity, the researchers linked data on participants ages 40-85 with data from the National Death Index to track deaths over an 11-year period.

The mortality rate among participants without MRSA was about 18% compared with 36% among those with colonised MRSA. There was no increased mortality risk for those with non-MRSA staph bacteria on their skin.

Although some states and hospital systems require MRSA testing for patients before hospital admission, policies for testing and treatment of colonised MRSA, which may include antibiotics use, vary widely betweens hospitals, Prof Mainous said.

“Without a uniform strategy, we are missing an opportunity to help prevent deaths caused by MRSA,” he said. “Maybe we should know who is carrying MRSA.”

Source: Medical-News.Net

Journal information: Mainous, A. G., et al. (2021) Methicillin-Resistant Staphylococcus Aureus Colonization and Mortality Risk Among Community Adults Aged 40-85. Journal of the American Board of Family Medicine.

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Key Cellular Defence Functions Found for Heparanase

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A recent study has shown that there is a poorly understood protein, heparanase (HPSE), that is in fact a key regulator of cellular innate defence systems. High levels of HPSE are linked to cancer metastasis. 

Cellular innate defence systems are an array of built-in mechanisms that are common to species throughout evolution. These can be spurred into action by the presence of pathogens or environmental toxins and dysfunctional cells that may build up over time in the body. A clearer understanding of the interplay between these different processes has the potential to open up a whole new range of multi-target drugs to treat a wide range of conditions and diseases.

Researchers from the University of Illinois Chicago (UIC) used a systems approach to track changes in important components in cells and mice that have been genetically engineered to lack HPSE.

In this collaborative multidisciplinary study, Agelidis and coauthors for the first time demonstrated that HPSE is a mediator for antiviral immunity, proliferative signals and cell death.

“HPSE has been long known to drive late-stage inflammatory diseases yet it was once thought that this was primarily due to enzymatic activity of the protein breaking down heparan sulfate, a sugar molecule present in chains on the surface of virtually all cells,” Agelidis said.

While their study largely focussed on mechanisms of pathogenesis of herpes simplex virus (HSV-1), these findings hold a range of implications for treating diseases that involve the dysregulation of HPSE, including cancer, atherosclerosis and autoimmune disorders.

Source: Medical Xpress

Journal information: Alex Agelidis et al, Disruption of innate defense responses by endoglycosidase HPSE promotes cell survival, JCI Insight (2021). DOI: 10.1172/jci.insight.144255

Categories : Diseases, Syndromes and Conditions GeneticsTags :

Diphtheria Resurfacing as a Threat As it Evolves Antibiotic Resistance

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Diphtheria is resurfacing as a threat worldwide as it evolves antibiotic resistance and could escape vaccine containment, scientists warn.

Diphtheria cases in recent years have doubled what they were in previous decades, to 16 651 cases in 2018. Although babies are vaccinated against it in high-income countries, there is less coverage in middle- and low-income countries.

Diphtheria is mainly caused by Corynebacterium diphtheriae, spread by coughs and sneezes or close contact with the infected. Usually, the bacteria cause acute infections, driven by the diphtheria toxin—the main target of the vaccine. However, non-toxigenic C. diphtheria can also cause disease.

A team of researchers from the UK and India used genomics to map infections, including a subset from India, where more than half of the globally reported cases occurred in 2018.

Analysing the genomes of 61 bacteria isolated from patients and combining these with 441 publicly available genomes, the researchers were then able to understand how they spread. They also used this information to assess the presence of antimicrobial resistance (AMR) genes and assess toxin variation.

The researchers found clusters to genetically-similar bacteria isolated from different continents, most commonly Asia and Europe. This indicates that C. diphtheriae has been travelling with humans as they spread across the planet.

The diphtheria toxin ch is encoded by the tox gene, for which the researchers found 18 different variations, of which several had the potential to change the structure of the toxin.

Professor Gordon Dougan from the Cambridge Institute of Therapeutic Immunology and Infectious Disease (CITIID) said: “The diphtheria vaccine is designed to neutralise the toxin, so any genetic variants that change the toxin’s structure could have an impact on how effective the vaccine is. While our data doesn’t suggest the currently used vaccine will be ineffective, the fact that we are seeing an ever-increasing diversity of tox variants suggests that the vaccine, and treatments that target the toxin, need to be appraised on a regular basis.”

First author Robert Will, a PhD student at CITIID, said: “The C. diphtheriae genome is complex and incredibly diverse. It’s acquiring resistance to antibiotics that are not even clinically used in the treatment of diphtheria. There must be other factors at play, such as asymptomatic infection and exposure to a plethora of antibiotics meant for treating other diseases.”

Erythromycin and penicillin are commonly recommended to treat early-stage diphtheria, although there are other classes capable of it. Variants resistant to six of these classes in isolates from the 2010s were identified by the team.

Study leader Dr Ankur Mutreja from CITIID, said: “It’s more important than ever that we understand how diphtheria is evolving and spreading. Genome sequencing gives us a powerful tool for observing this in real time, allowing public health agencies to take action before it’s too late.
“We mustn’t take our eye off the ball with diphtheria, otherwise we risk it becoming a major global threat again, potentially in a modified, better adapted, form.”

Source: Medical Xpress

Journal information: Will, RC et al. Spatiotemporal persistence of multiple, diverse clades and toxins of Corynebacterium diphtheria. Nat Comms; 8 Mar 2021; DOI: 10.1038/s41467-021-21870-5

Categories : Diseases, Syndromes and Conditions ImmunologyTags :

New Bacteria-based Atopic Dermatitis Treatment Proves Effective

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A skin bacteria-based treatment for atopic dermatitis (AD) was successful in clinical trials, with no serious adverse effects and indications that it reduces eczema symptoms as well.

Atopic dermatitis (AD) is a common, chronic skin disorder which can have great impacts on the lives of sufferers. The disorder seems to result from the complex interplay between the skin, environmental effects and the immune system. Treatment involves a multifaceted approach that involves education, optimal skin care practices, anti-inflammatory treatment with topical corticosteroids and/or topical calcineurin inhibitors, the management of pruritus, and the treatment of skin infections. Severe flare-ups or more difficult-to-control disease may be treated with systemic immunosuppressive agents. Topical corticosteroids are the first-line treatment of choice, and seem to be prophylactic against flareups.

AD is associated with S. aureus colonisation, which induces a proteolytic breakdown of the epidermal barrier and dermal immune dysregulation. Inflammation results in further dysregulation of the skin microbial system. Commensal, coagulase-negative staphylococci (CoNS) were observed to produce bacteriocins which inhibit bacteria such as S. aureus, and these were not seen in the skin of most patients with AD. They hypothesised that reintroduction of CoNS would improve AD in patients.

Patients treated with MSB-0221, which incorporated the naturally occurring skin bacteria S. hominis (ShA9), had fewer AD-related adverse events (AEs) as compared with patients treated with a topical placebo, reported Richard L Gallo, MD, PhD, of the University of California San Diego and co-founder of the company developing MSB-0221.

“Besides its effect on decreasing the redness and itch in a subset of patients, and dramatically and rapidly decreasing the colonisation by Staph aureus, one of the unique aspects of this is that it’s specific for this organism,” said Dr Gallo. “It was not detrimental to other members of the microbiome that could help restore balance.”

Applying MSB-0221 to 54 adults, they found a reduction in S. Areus, which was associated with a significant decrease in AD symptoms compared to placebo.

The next step would be a larger, 150 patient clinical trial over 12 weeks.

“We don’t fully understand all of the ramifications, but there seems to be at least a subset of patients with atopic dermatitis whose disease is influenced and exacerbated by certain bacteria, such as Staph aureus,” said Bruce Brod, MD, of the University of Pennsylvania. “There is still sort of a chicken-and-egg aspect to the relationship. Did the skin inflammation come first or the Staph aureus?“

“This is a proof-of-concept study that provides some evidence that shifting the balance of another bacteria that’s not pathogenic might have some therapeutic benefit in some patients with atopic dermatitis,” he added. “It provides support for larger studies looking at safe bacteria to shift the flora to a more favourable environment. At this point, it’s just another piece of a puzzle that could one day lead to different therapies. It’s probably not the whole picture, but in some patients, it may play a significant role.”

Source: MedPage Today

Journal information: Nakatsuji T, et al “Development of a human skin commensal microbe for bacteriotherapy of atopic dermatitis and use in a phase I randomized clinical trial” Nature Med 2021; DOI: 10.1038/s41591-021-01256-2.

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Bacteria in Cystic Fibrosis Use Slimy Shield to Ward off Drugs

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Research has revealed that a common bacteria found in the lungs of those with cystic fibrosis produces a slime that acts as a defence against a variety of therapeutic drugs.

Dr Laura Jennings, a research assistant professor in UM’s Division of Biological Sciences and an affiliate with the University’s Center for Translational Medicine, headed the research.

A life threatening-condition caused by a genetic mutation, cystic fibrosis causes persistent lung infections and gradually reduces a person’s breathing capacity. A common strain of bacteria, Pseudomonas aeruginosa, often thrives in the lungs of people with cystic fibrosis,  and when a P. aeruginosa infection is established, it can be extremely hard to remove.
The research showed that stubborn bacteria dwelling in the lungs of cystic fibrosis patients produce a carbohydrate slime, which both shields them against antibiotics and also mucus-reducing drugs.

“We found the first direct evidence that these carbohydrates are produced at the sites of infection,” Dr Jennings said. “We showed that one of the carbohydrates, called Pel, sticks to extracellular DNA, which is abundant in the thick mucus secretions prominent in cystic fibrosis lungs.

“This interaction makes a slimy protective layer around the bacteria, making them harder to kill,” she said. “As such, it reduces the pathogen’s susceptibility to antibiotics and drugs aimed at reducing the thickness of airway mucus by digesting DNA.”

She explained that the research supports a theory that these carbohydrates also support the aggregation of these bacteria in the lungs of cystic fibrosis patients.

“This is important because we know that physically breaking up bacterial aggregates can restore bacterial susceptibility to killing with antibiotics and cells of the immune system,” Jennings said. “Therefore, understanding the mechanisms that promote bacterial aggregation may facilitate new therapeutic approaches aimed at digesting the carbohydrates holding bacterial cells together.”

Source: Medical Xpress

Journal information: Laura K. Jennings et al. Pseudomonas aeruginosa aggregates in cystic fibrosis sputum produce exopolysaccharides that likely impede current therapies, Cell Reports (2021). DOI: 10.1016/j.celrep.2021.108782

Categories : Diseases, Syndromes and Conditions Medical Research & TechnologyTags :

Researchers Study Enzyme Processes for New Drugs

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Traditional discovery has produced drugs that effectively target proteins directly involved with disease, but options are starting to run out and researchers are looking to more complex and obscure interactions for drug targets.

So far, drug discovery has used the ‘small molecule’ approach, where a specific protein is targetted in a cancer cell to shut it down and bring down the cancer cell as a whole. Up until this point, traditional drugs have only been able to target proteins that are involved in the disease that also have activities that are amenable to the small molecule approach, leaving a vast number of proteins unaddressed. Many of these other proteins may be involved in disease processes behind the scenes.

“It’s starting to get to the point where we’ve kind of taken traditional drug discovery as far as we can, and we really need something new,” explained University of Nevada, Las Vegas biochemist Gary Kleiger.

“Cancer cells are clever,” Kleiger said. “They can evolve very, very quickly. So, a drug might be working at first—targeting an enzyme and telling that enzyme, ‘stop doing your activity,’ which can stop the cancer cells from growing. Those cancer cells appear to lie dormant, but all the while there are still little things that happen that eventually enable those cancer cells to bypass that drug.” Therefore, in order to stay ahead of cancer’s capacity to evolve drug resistance, it is necessary to target many additional disease-causing proteins, and thus, limiting the landscape of druggable proteins is a serious disadvantage.

The new approach by investigated by Kleiger and collaborators uses a family of human enzymes called ubiquitin ligases found in human cells. Of about 20 000 known proteins in the human body, some 5-10% are enzymes.

Kleiger’s team uses cutting edge cryo electron microscopes that can image the ubiquitin ligases when they’re at work. To test their hypotheses, Kleiger and collaborators measure the activity of ‘mutated’ enzymes that should now be defective in their activities.

Kleiger compared the process to how a 50 000 year old society might view a bicycle. They could identify its purpose and general properties, but could test the importance of a certain gear; if it was bent, the bicycle would no longer function. “We can do that at the molecular level with the enzymes,” he said.

Source: Medical Xpress

Journal information: Daniel Horn-Ghetko et al, Ubiquitin ligation to F-box protein targets by SCF–RBR E3–E3 super-assembly, Nature (2021). DOI: 10.1038/s41586-021-03197-9