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Treatment gets five out of Intensive Care – Dominican Today

Posted: March 29, 2020 at 6:57 pm

At least five patients, including some doctors, have overcome the critical state of health in which they had fallen due to the coronavirus and been moved from the Intensive Care units to normal hospital wards, after undergoing an expensive treatment that is producing good results.

Of the patients who have responded adequately to treatment, there are four from Santiago: Dr. Daniel Rivera, president of the Board of Directors of the Unin Mdica Clinic, urologist Fausto Hernndez, ex-governor Jos Izquierdo and patient Juan Ramn. In Santo Domingo, the political leader of San Pedro de Macors, Senator Jos Hazim, while Dr. Felix Antonio Cruz Jiminin has presented significant improvement, although he is still in intensive care with mechanical respiration, admitted to the General Hospital of the Plaza de health.

The details were offered by the Minister of Public Health, Rafael Snchez Crdenas, on the eighth day of the virtual press conference to report the updates to the Covid-19.He said it is a non-over-the-counter medicine that is applied intravenously and is applied to critically ill patients with complicated pneumonia.

A drug used in the treatment of arthritis patients has been applied to these patients.It is tocilizumab, a biological medicine, which is supplied through the High-Cost Medicines Program of the Ministry of Public Health.

Tocilizumab (Actemra) is a biologic medication approved to treat rheumatoid arthritis (RA) in adults, polyarticular juvenile rheumatoid arthritis (JRA), and the systemic form of juvenile idiopathic arthritis (JIA) in children. It isused to suppress the immune system in autoimmune diseases.

Biological drugs are artificial and manufactured using genetic engineering techniques and are closely related to a protein that the body produces naturally.

Dr. Snchez Crdenas reported that there are nine doctors registered with the virus, of whom four were in the process of their work, and others were infected on a cruise or airplane trip, and about three nurses.

He recalled that the highest risk of death is in people over 60 years old and people with co-morbidities, so he called people to take more extreme care of older adults.

Cross-testsThe Minister of Public Health, Rafael Snchez Crdenas, announced that from yesterday the trial would begin with cross-tests at the Dr. Defill National Laboratory, in order to speed up the confirmation of Covid-19 cases.

THE PROCESSSnchez Crdenas revealed that starting today, Saturday, rapid tests of up to 15 minutes will be made, through blood collection obtained from the pulpejo, with patients who have tested positive for other types of tests, to confirm their effectiveness, and then put them into service.

The testsThe effectiveness of rapid tests can be as high as 95%, and the PCR tests, which are being applied in the laboratory, are a specific test with 95% effectiveness, said Crdenas.Those 15-minute rapid tests, of which there are already samples in the country, will be tested today with patients.

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The curious case of the cat with corona – The Brussels Times

Posted: March 29, 2020 at 6:57 pm

Among the headlines from yesterdays meetings of the newly-empowered government and the national security council, one that caught the eye was the announcement of a cat diagnosed with coronavirus caught from its owner.

The cat was reported to have caught the virus from close contact with its owner, who had recently returned from Italy. When the cat became ill, its stool was examined and traces of the virus discovered.

The experts were quick to reassure pet owners that the case was exceptional, that animals were not considered a vector for the disease, and that there was no reason to be afraid either for their pets or for themselves.

But one animal virologist has raised questions about the whole story.

Hans Nauwynck is a professor at the faculty of veterinary medicine at the University of Ghent, and a specialist in virology. The news of the corona cat took him by surprise.

Before sending this news out into the world, I would have had some other tests carried out, he told Het Laatste Nieuws. When you hear about this right now, I wouldnt wish to be a cat tomorrow.

The discovery was made by the vet faculty at Liege university, who concluded the infection passed from human to cat and not the other way around.

Look, I have no criticism of my colleagues at Liege university, he stressed. The diagnosis has been made, Ive no doubt about the result, but were dealing here with a PCR test, a way of identifying genetic material of the virus.

The polymerase chain reaction (PCR) test allows scientists to multiply a very small sample of genetic material to produce a quantity large enough to study.

Im simply questioning the interpretation of the results. The test is positive for corona, fine, but how was the test carried out? How was the sample taken, and can that result be trusted? I would advise people to slow down. There may somehow have been genetic material from the owner in the sample, and so the sample is contaminated.

To be absolutely certain, he said, more tests should have been done to confirm the initial result, and certainly before making an announcement to the world.

I think its too bad they didnt look further, he said. There should also have been research carried out to see if the cat had produced antibodies. Im worried that people will be scared by this news and animals will be the ones to suffer, and thats not right. As scientists we ought to put out clear and full information, and I dont think that has happened.

In the latest update, the cat is doing well. Its owner is also recovering, albeit more slowly.

Alan HopeThe Brussels Times

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Novartis new analysis further showed durable and potent LDL-C reduction with inclisiran, an investigational first-in-class siRNA cholesterol-lowering…

Posted: March 29, 2020 at 6:57 pm

EAST HANOVER, N.J., March 28, 2020 /PRNewswire/ --Novartis today announced results from a prespecified analysis of pooled data from three Phase III studies evaluating the safety and efficacy of inclisiran, its first-in-class investigational treatment for hyperlipidemia in adults. The data was presented during a Late Breaker session at the American College of Cardiology's Annual Scientific Session Together with World Congress of Cardiology (ACC.20/WCC Virtual). The pooled analysis of the ORION-9, -10 and -11 Phase III trials showed a durable and potent reduction in LDL-C of 51% when used in addition to other lipid-lowering therapies (LLT) over 17 months of treatment1. The prespecified analysis of pooled data is consistent with the efficacy and safety findings of the individual Phase III trial results recently published in The New England Journal of Medicine.

Additionally, a prespecified exploratory analysis using the safety reporting from all three trials indicated fewer MACE with inclisiran compared to placebo (7.1%, 9.4% respectively)1. The overall safety and tolerability profile was generally similar between the inclisiran and placebo groups. While these preliminary observations are based on a low number of events, they are consistent with the general concept that however LDL-C is lowered, it is thought to result in reduced risk of future cardiovascular events2. This further supports the research currently underway in the Phase III ORION-4 trial. The ORION-4 trial aims to recruit 15,000 participants from 150 sites in the United States and the United Kingdom with pre-existing atherosclerotic cardiovascular disease (ASCVD) and who are unable to achieve LDL-C goal. Expected to finish in 2024, this trial will bring additional information on inclisiran's effects on cardiovascular outcomes.

"There remains a compelling need for new and novel LDL-C-lowering therapies given the residual risk faced by many patients with atherosclerotic cardiovascular disease and the inability of oral lipid-lowering therapy alone to achieve important LDL targets," said ORION-10 principal investigator R. Scott Wright, M.D., Professor of Medicine, Consultant in Cardiology, Mayo Clinic in Rochester, Minnesota. "Inclisiran harnesses the body's natural mechanisms for RNA silencing and lowers LDL-C. This analysis confirmed that twice-yearly dosing of inclisiran achieved durable and potent reductions in LDL-C in the phase III studies."

"After decades of declining cardiovascular disease mortality, it is on the rise again, renewing the urgency behind our longstanding commitment to and extensive experience in this space," said David Platt, M.D., Vice President, US Clinical Development and Medical Affairs, Cardiovascular, Renal & Metabolism Medical Unit, Novartis Pharmaceuticals. "We are excited by the results we have seen to date with inclisiran, and we look forward to the potential opportunity to make the first and only LDL-C-lowering treatment in the small interfering RNA (siRNA) class available to patients with ASCVD and familial hypercholesterolemia."

Inclisiran is currently under review by the U.S. Food and Drug Administration (FDA) and European Medicines Agency (EMA) for use in adults with ASCVD or heterozygous familial hypercholesterolemia (HeFH) who have elevated LDL-C while being on a maximum tolerated dose of a LLT. Inclisiran was administered subcutaneously with an initial dose, again at 3 months and then every 6 months, offering a unique dosing regimen. If approved, inclisiran will be the first and only LDL-C-lowering treatment in the siRNA class.

Hyperlipidemia refers to the high level of lipids (fats, cholesterol, triglycerides), such as LDL-C, found in the blood that are either acquired or from genetic disorders3. LDL-C is the most readily modifiable risk factor for ASCVD4-9. Despite the widespread use of therapies to reduce LDL-C, the majority of patients do not reach guideline-recommended treatment goals, leaving them at continued risk of a life-threatening condition10.

About the pooled analysisThe pooled analysis includes data from inclisiran's ORION-9, -10 and -11 trials, which are multicenter, double-blind, randomized, placebo-controlled,18-month studies evaluating inclisiran in patients with heterozygous familial hypercholesterolemia (ORION-9), ASCVD (ORION-10) and ASCVD or ASCVD risk equivalents (ORION-11). The primary endpoints for these studies were percentage change in LDL-C from baseline to 17 months and time-adjusted percentage change in LDL-C from baseline between 3 months and up to 18 months. The primary endpoints were achieved in all three studies. The prespecified analysis of pooled data assessed inclisiran's efficacy for lowering of LDL-C and other lipids/lipoproteins, as well as safety and tolerability, across these studies1.

In the prespecified analysis of pooled data, inclisiranresulted in placebo-adjusted LDL-C reduction at 17 months of 51% and a time-adjusted placebo-adjusted percentage reduction in LDL-C between 3 and 18 months of 51%. In a prespecified exploratory safety analysis, MACE were significantly lower with inclisiran versus placebo (7.1%, 9.4% respectively); measures included non-fatal myocardial infarction (5.2%, 7.8%), stroke (0.9%, 1.0%), cardiovascular death (0.9%, 0.8%) and resuscitated cardiac arrest (0.2%, 0.1%). The overall safety and tolerability profile was generally similar between inclisiran and placebo groups. No differences in adverse outcomes were observed between groups1.

About inclisiranInclisiran, an investigational cholesterol-lowering treatment, was added to the pipeline from the Novartis acquisition of The Medicines Company. Inclisiran will potentially be the first and only LDL-C lowering siRNA treatment. It is intended to be administered by a healthcare professional by subcutaneous injection with an initial dose, again at 3 months and then every 6 months thereafter. Its twice-yearly dosing by subcutaneous injection may integrate seamlessly into a patient's healthcare routine. As a siRNA, inclisiran is thought to harness the body's natural process of clearing LDL-C from the bloodstream. Inclisiran is a double-stranded siRNA, conjugated on the sense strand with triantennary N-acetylgalactosamine (GalNAc) to facilitate uptake by hepatocytes. In hepatocytes, inclisiran increases LDL-C receptor recycling and expression on the hepatocyte cell surface, thereby increasing LDL-C uptake by hepatocytes and lowering LDL-C levels in the circulation. Data from each of the Phase III studies was recently published online, ahead of print, in The New England Journal of Medicine11,12. A cardiovascular outcomes trial, ORION-4, is ongoing.

In the Phase III studies, inclisiran was reported to be well-tolerated with a safety profile similar to placebo. The most common adverse reactions reported (3% of patients treated with inclisiran and occurring more frequently than placebo) were, diabetes mellitus, hypertension, nasopharyngitis, arthralgia, back pain, dyspnea, bronchitis and upper respiratory tract infection. Adverse events at the injection site were more frequent with inclisiran than placebo and were generally mild and none were severe or persistent11,12.

Novartis has obtained global rights to develop, manufacture and commercialize inclisiran under a license and collaboration agreement with Alnylam Pharmaceuticals.

About Novartis in Cardiovascular-Renal-MetabolismBending the curve of life requires addressing some of society's biggest public health concerns. Novartis has an established and expanding presence in diseases covering the heart, kidney and metabolic system. In addition to essential treatment Entresto (sacubitril/valsartan), Novartis has a growing pipeline of potentially first-in-class molecules addressing cardiovascular, metabolic and renal diseases.

DisclaimerThis press release contains forward-looking statements within the meaning of the United States Private Securities Litigation Reform Act of 1995. Forward-looking statements can generally be identified by words such as "potential," "can," "will," "plan," "may," "could," "would," "expect," "anticipate," "seek," "look forward," "believe," "committed," "investigational," "pipeline," "launch," or similar terms, or by express or implied discussions regarding potential marketing approvals, new indications or labeling for the investigational or approved products described in this press release, or regarding potential future revenues from such products. You should not place undue reliance on these statements. Such forward-looking statements are based on our current beliefs and expectations regarding future events, and are subject to significant known and unknown risks and uncertainties. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those set forth in the forward-looking statements. There can be no guarantee that the investigational or approved products described in this press release will be submitted or approved for sale or for any additional indications or labeling in any market, or at any particular time. Nor can there be any guarantee that such products will be commercially successful in the future. In particular, our expectations regarding such products could be affected by, among other things, the uncertainties inherent in research and development, including clinical trial results and additional analysis of existing clinical data; regulatory actions or delays or government regulation generally; global trends toward health care cost containment, including government, payor and general public pricing and reimbursement pressures and requirements for increased pricing transparency; our ability to obtain or maintain proprietary intellectual property protection; the particular prescribing preferences of physicians and patients; general political, economic and business conditions, including the effects of and efforts to mitigate pandemic diseases such as COVID-19; safety, quality, data integrity or manufacturing issues; potential or actual data security and data privacy breaches, or disruptions of our information technology systems, and other risks and factors referred to in Novartis AG's current Form 20-F on file with the US Securities and Exchange Commission. Novartis is providing the information in this press release as of this date and does not undertake any obligation to update any forward-looking statements contained in this press release as a result of new information, future events or otherwise.

About NovartisLocated in East Hanover, NJ Novartis Pharmaceuticals Corporation an affiliate of Novartis is reimagining medicine to improve and extend people's lives. As a leading global medicines company, we use innovative science and digital technologies to create transformative treatments in areas of great medical need. In our quest to find new medicines, we consistently rank among the world's top companies investing in research and development. Novartis employs about 15,000 people in the United States. For more information, please visit http://www.novartis.us.

Novartis is on Twitter. Sign up to follow @Novartis at http://twitter.com/novartisnews For Novartis multimedia content, please visit http://www.novartis.com/news/media-libraryFor questions about the site or required registration, please contact media.relations@novartis.com

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You can’t kill the coronavirus. That’s OK. – Mashable SE Asia

Posted: March 29, 2020 at 6:57 pm

Some viruses look like moon landers.

Called phages, they hijack bacteria by landing on the hapless cells and injecting them with a ream of genetic material. Then, the phages use the commandeered cells to multiply.

Similar to the new coronavirus, these phages are excellent parasites. They can be aggressive, dogged, and seem to act with purpose. Yet, many microbiologists who know viruses best say it's a stretch to call any virus truly alive. And so, they can't be killed only disarmed, like pulling the plug on an appliance.

But today, with a rapidly spreading viral pandemic that's stirring serious unease in American emergency rooms, it doesn't really matter if a virus meets biologists' definitions of dead or alive. Whatever these entities are, they're powerful.

"It's more of a philosophical question," said Ryan Relich, a medical microbiologist at Indiana University's School of Medicine, of whether viruses are alive or not.

"What's more important is that they're winning," he said.

Today, the coronavirus isn't just winning. It's dominating us. It's closed our arenas. Shut down our bars. Emptied California beaches. The increasingly austere governor of New York is now demanding ventilators from the federal government. Our best, and most critical, defense until a vaccine is developed in a year at the earliest is social distancing: We're avoiding infected persons and hiding from the microbes themselves, which are basically genes surrounded by a shell.

Viruses, like coronavirus, have become globally dominant because they evolved to become master replicators. But they can't multiply alone, so they take over other cells and exploit this cellular machinery to multiply. It's exquisite parasitism. A single coronavirus-infected cell can manufacture millions of coronaviruses.

"Parasitism is an old, venerated way of making a living," said Siobain Duffy, who researches the evolution of viruses at Rutgers University.

6/

Now, lets get it out of the way: viruses are not alive. They do not possess all the characteristics of a living organisms so, no, you cannot kill them. You can, however, inactivate them, denature them, neutralize them, etc. pic.twitter.com/ODGVoa5q1J

Efra Rivera-Serrano, PhD (@NakedCapsid) March 17, 2020

A colorized image of a cell (brown) from a patient infected with coronavirus (pink).

Yet, unlike parasites such as intestinal worms, viruses are almost completely dependent upon the cells they hijack. "Viruses don't actually do anything on their own," explained Relich.

They don't breathe. They don't eat. They don't make energy. They appear mindless, floating around with the possibility of landing on a cell. "They don't get up and go to work every day," said Relich. "I dont consider them to be living. But hey, maybe you want to consider them to be alive so that its easier to personify them or rationalize things in a more palatable way."

So, microbiologists can make a good argument that viruses don't have the same hallmarks of living as do amoebas, elephants, and emus.

But maybe viruses are alive just in another sense of alive. After all, life has been evolving on Earth for some 3.8 billion years, noted Duffy. There are all kinds of curious things out there that might blur the boundary between alive and not alive. For example, there are viruses with longer genomes than bacteria (which we all agree are alive), and viruses that make some bacteria better at things, like photosynthesis. Our human DNA is embedded with some viral genetic material, too, noted Relich.

"Life continues to astound us."

"People want a clear dividing line between life and non-life," said Duffy. But that line might be blurrier than we think, she added.

The quandary of whether a virus can ever be killed, then, is a bottomless philosophical hole that may never have a certain answer. But it's safe to say, at least, that there are effective ways "to inactivate viruses or otherwise render them kaput," said Relich.

Chemicals like bleach and rubbing alcohols can massively damage the exterior wrappings of viruses, which for some include a fatty membrane envelope, making viruses useless. Thorough hand washing destroys these viral shells, too. Though there are no proven antiviral medications for coronavirus (and there may not be for many months), these types of drugs are designed to disrupt a virus' activity. For instance, the HIV drug Enfuvirtide blocks the virus from even attaching to human cells. Other drugs stop viruses from replicating, once they've already slipped inside a cell.

There's another very certain thing about viruses. Humanity has a ton to learn about them. There are countless species, and they're everywhere. "There are more viruses in this world than there are cells," said Duffy. But only 6,828 virus species have been formally named by scientists. Meanwhile, there could be millions more species out there. Finding and understanding theses microscopic entities could reveal much more about their nature, and "lives."

"We need more research, we need more researchers, we need more funding for research," said Relich.

Only in 1977 did humanity discover the third domain of life, a massive, ancient group of organisms called archaea (the other two domains are bacteria and eukaryotes which include humans.) What might the great diversity of viruses in this domain, still being discovered, tell us?

"Life continues to astound us," said Duffy. Indeed.

For now, we're focused on the minority of viruses that can threaten our ability to breathe, like the new coronavirus which can result in the serious respiratory disease COVID-19. And for good reason.

"It's to our own advantage to know our enemies as well as possible," said Relich.

Even if they can't be killed.

"Whether or not theyre alive, viruses influence life," said Duffy.

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Eight strains of the coronavirus are circling the globe. They’re giving scientists clues – Stuff.co.nz

Posted: March 29, 2020 at 6:57 pm

At least eight strains of the coronavirus are making their way around the globe, creating a trail of death and disease that scientists are tracking by their genetic footprints.

While much is unknown, hidden in the virus'unique microscopic fragments are clues to the origins of its original strain, how it behaves as it mutates and which strains are turning into conflagrations while others are dying out thanks to quarantine measures.

KATHRYN GEORGE/STUFF

Scientists are tracking eight strains of the coronavirus by their genetic footprints.

Huddled in once bustling and now almost empty labs, researchers who oversaw dozens of projects are instead focused on one goal: tracking the current strains of the SARS-CoV-2 virus that cause the illness Covid-19.

Labs around the world are turning their sequencing machines, most about the size of a desktop printer, to the task of rapidly sequencing the genomes of virus samples taken from people sick with Covid-19. The information is uploaded to a website called NextStrain.org that shows how the virus is migrating and splitting into similar but new subtypes.

READ MORE:* Three months into the pandemic, here is what we know about the coronavirus* Coronavirus isn't alive and that's why it's so hard to kill* Coronavirus vaccine hunters: meet the scientists racing to find a cure* Key terms of the coronavirus outbreak, explained: From asymptomatic to zoonotic

While researchers caution they're only seeing the tip of the iceberg, the tiny differences between the virus strains suggest shelter-in-place orders are working in some areas and that no one strain of the virus is more deadly than another. They also say it does not appear the strains will grow more lethal as they evolve.

"The virus mutates so slowly that the virus strains are fundamentally very similar to each other," said Charles Chiu, a professor of medicine and infectious disease at the University of California, San Francisco School of Medicine.

The SARS-CoV-2 virus first began causing illness in China sometime between mid-November and mid-December. Its genome is made up of about 30,000 base pairs. Humans, by comparison, have more than 3 billion. So far even in the virus's most divergent strains scientists have found only 11 base pair changes.

That makes it easy to spot new lineages as they evolve, said Chiu.

"The outbreaks are trackable. We have the ability to do genomic sequencing almost in real-time to see what strains or lineages are circulating," he said.

So far, most cases on the USWest Coast are linked to a strain first identified in Washington state. It may have come from a man who had been in Wuhan, China, the virus' epicentre, and returned home on January 15. It is only three mutations away from the original Wuhan strain, according to work done early in the outbreak by Trevor Bedford, a computational biologist at Fred Hutch, a medical research centrein Seattle.

On the East Coast there are several strains, including the one from Washington and others that appear to have made their way from China to Europe and then to New York and beyond, Chiu said.

BEWARE PRETTY PHYLOGENETIC TREES

This isn't the first time scientists have scrambled to do genetic analysis of a virus in the midst of an epidemic. They did it with Ebola, Zika and West Nile, but nobody outside the scientific community paid much attention.

"This is the first time phylogenetic trees have been all over Twitter," said Kristian Andersen, a professor at Scripps Research, a nonprofit biomedical science research facility in La Jolla, California, speaking of the diagrams that show the evolutionary relationships between different strains of an organism.

The maps are available on NextStrain, an online resource for scientists that uses data from academic, independent and government laboratories all over the world to visually track the genomics of the SARS-CoV-2 virus. It currently represents genetic sequences of strains from 36 countries on six continents.

While the maps are fun, they can also be "little dangerous" said Andersen. The trees showing the evolution of the virus are complex and it's difficult even for experts to draw conclusions from them.

"Remember, we're seeing a very small glimpse into the much larger pandemic. We have half a million described cases right now but maybe 1000 genomes sequenced. So there are a lot of lineages we're missing," he said.

MANU FERNANDEZ/AP

Health workers applaud in support of the medical staff that are working on the Covid-19 virus outbreak in Spain.

DIFFERENT SYMPTOMS, SAME STRAINS

Covid-19 hits people differently, with some feeling only slightly under the weather for a day, others flat on their backs sick for two weeks and about 15 per centhospitalised. Currently, an estimated 1 per centof those infected die. The rate varies greatly by country and experts say it is likely tied to testing rates rather than actual mortality.

Chiu says it appears unlikely the differences are related to people being infected with different strains of the virus.

"The current virus strains are still fundamentally very similar to each other," he said.

The Covid-19 virus does not mutate very fast. It does so eight to 10 times more slowly than the influenza virus, said Anderson, making its evolution rate similar to other coronaviruses such as Ebola, Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS).

It's also not expected to spontaneously evolve into a form more deadly than it already is to humans. The SARS-CoV-2 is so good at transmitting itself between human hosts, said Andersen, it is under no evolutionary pressure to evolve.

GETTY IMAGES

The Covid-19 virus does not mutate very fast. It does so eight to 10 times more slowly than the influenza virus.

SHELTER IN PLACE WORKING IN CALIFORNIA

Chiu's analysis shows California's strict shelter in place efforts appear to be working.

Over half of the 50 SARS-CoV-2 virus genomes his San Francisco-based lab sequenced in the past two weeks are associated with travel from outside the state. Another 30 per centare associated with health care workers and families of people who have the virus.

"Only 20 per centare coming from within the community. It's not circulating widely," he said.

That's fantastic news, he said, indicating the virus has not been able to gain a serious foothold because of social distancing.

It's like a wildfire, Chiu said. A few sparks might fly off the fire and land in the grass and start new fires. But if the main fire is doused and its embers stomped out, you can kill off an entire strain. In California, Chiu sees a lot of sparks hitting the ground, most coming from Washington, but they're quickly being put out.

An example was a small cluster of cases in Solano County, northeast of San Francisco. Chiu's team did a genetic analysis of the virus that infected patients there and found it was most closely related to a strain from China.

At the same time, his lab was sequencing a small cluster of cases in the city of Santa Clara in Silicon Valley. They discovered the patients there had the same strain as those in Solano County. Chiu believes someone in that cluster had contact with a traveller who recently returned from Asia.

"This is probably an example of a spark that began in Santa Clara, may have gone to Solano County but then was halted," he said.

The virus, he said, can be stopped.

CHINA IS AN UNKNOWN

So far researchers don't have a lot of information about the genomics of the virus inside China beyond the fact that it first appeared in the city of Wuhan sometime between mid-November and mid-December.

The virus's initial sequence was published on January 10 by professor Yong-Zhen Zhang at the Shanghai Public Health Clinical Center. But Chiu says scientists don't know if there was just one strain circulating in China or more.

"It may be that they haven't sequenced many cases or it may be for political reasons they haven't been made available," said Chiu. "It's difficult to interpret the data because we're missing all these early strains."

Researchers in the United Kingdom who sequenced the genomes of viruses found in travellers from Guangdong in south China found those patients' strains spanned the gamut of strains circulating worldwide.

"That could mean several of the strains we're seeing outside of China first evolved there from the original strain, or that there are multiple lines of infection. It's very hard to know," said Chiu.

THE VIRUS DID NOT COME FROM A LAB

While there remain many questions about the trajectory of the Covid-19 disease outbreak, one thing is broadly accepted in the scientific community: The virus was not created in a lab but naturally evolved in an animal host.

SARS-CoV-2's genomic molecular structure - think the backbone of the virus - is closest to a coronavirus found in bats. Parts of its structure also resemble a virus found in scaly anteaters, according to a paper published earlier this month in the journal Nature Medicine.

Someone manufacturing a virus targeting people would have started with one that attacked humans, wrote National Institutes of Health Director Francis Collins in an editorial that accompanied the paper.

Andersen was lead author on the paper. He said it could have been a one-time occurrence.

"It's possible it was a single event, from a single animal to a single human," and spread from there.

- USA Today

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Bone Therapeutics appoints Stefanos Theoharis as Chief Business Officer – OrthoSpineNews

Posted: March 29, 2020 at 6:54 pm

Gosselies, Belgium, 26March 2020, 7am CET BONE THERAPEUTICS(Euronext Brussels and Paris: BOTHE), the bone cell therapy company addressing high unmet medical needs in orthopaedics and bone diseases, today announces that it is further strengthening its management team with the appointment of Stefanos Theoharis, PhD, as Chief Business Officer (CBO).

Stefanos will be responsible for the companys corporate development activities and executing its business strategy. His immediate priorities will be concentrating on partnering Bone Therapeutics products and in-licensing innovations. He will also further develop the commercial strategies for the product portfolio and cell therapy platform.

At this stage of the development of Bone Therapeutics, it is very important to appoint a proven executive with a high level of business experience to achieve our next set of commercial goals,said Miguel Forte, MD, PhD, Chief Executive Officer of Bone Therapeutics. Stefanos has gathered considerable achievements in business development at both rapidly growing biotech and global biopharma companies, coupled with an extensive expertise in cell therapy drug development and manufacturing. His diverse skill set, which includes licensing, M&A transactions and R&D partnerships, will be invaluable to bolster our business initiatives as we continue to advance our mid- to late stage product pipeline through clinical development with a potential commercialization in sight.

Stefanos will contribute more than 15 years of business development experience in the pharma and biotech industry to Bone Therapeutics, specifically in the cell and gene therapy space. This includes his achievements as Senior Vice-President at Cell Medica, a clinical-stage biotech company, where he expanded the companys allogeneic T-cell immunotherapy platform through strategic partnerships with leading research institutions and targeted acquisitions. Prior to Cell Medica, Stefanos was Chief Business Officer at apceth GmbH, a company developing genetically-engineered mesenchymal stromal (MSC) cell products and also acting as a contract manufacturer in the ATMP space. He led all apceths business development activities, including in- and out-licensing and service contracts negotiations. He also held positions as Head of Business Development at the antisense RNA drug specialist Antisense Pharma (now Isarna), and Director Business Development at Roche, focused on partnering activities in emerging science and technologies. Stefanos also worked at Lazard, the global investment bank, advising to a variety of life sciences firms on M&As and financing transactions. Stefanos achieved an MSc. in Molecular Medicine and a PhD in Pathology and Immunology from Imperial College London.

I really wanted to join a cell therapy company where I was able to make a significant difference to the company, the wider field and patients outcomes.With an innovative allogeneic, off the shelf, cell therapy platform and a potentially best-in-class knee osteoarthritic pain treatment, Bone Therapeutics is uniquely positioned to make a meaningful difference in the lives of patients with severe orthopaedic conditions,said Stefanos Theoharis, PhD, Chief Business Officer of Bone Therapeutics. As both products are entering advanced stage clinical trials, Im delighted to join the company at such a critical time and I look forward to working with its talented leadership and scientific teams to take these promising treatments to market.

About Bone Therapeutics

Bone Therapeutics is a leading biotech company focused on the development of innovative products to address high unmet needs in orthopedics and bone diseases. The Company has a broad, diversified portfolio of bone cell therapies and an innovative biological product in later-stage clinical development, which target markets with large unmet medical needs and limited innovation.

Bone Therapeutics is developing an off-the-shelf protein solution, JTA-004, which is entering PhaseIII development for the treatment of pain in knee osteoarthritis. Positive PhaseIIb efficacy results in patients with knee osteoarthritis showed a statistically significant improvement in pain relief compared to a leading viscosupplement. The clinical trial application (CTA) for the pivotal PhaseIII program has been approved by the Danish relevant authorities allowing the start of the study.

Bone Therapeutics other core technology is based on its cutting-edge allogeneic cell therapy platform (ALLOB) which can be stored at the point of use in the hospital, and uses a unique, proprietary approach to bone regeneration, which turns undifferentiated stem cells from healthy donors into bone-forming cells. These cells can be administered via a minimally invasive procedure, avoiding the need for invasive surgery, and are produced via a proprietary, scalable cutting-edge manufacturing process. Following the CTA approval by the Belgian regulatory authority, the Company is ready to start the PhaseIIb clinical trial with ALLOB in patients with difficult tibial fractures, using its optimized production process.

The ALLOB platform technology has multiple applications and will continue to be evaluated in other indications including spinal fusion, osteotomy and maxillofacial and dental applications.

Bone Therapeutics cell therapy products are manufactured to the highest GMP (Good Manufacturing Practices) standards and are protected by a broad IP (Intellectual Property) portfolio covering ten patent families as well as knowhow. The Company is based in the BioPark in Gosselies, Belgium. Further information is available at http://www.bonetherapeutics.com.

Contacts

Bone Therapeutics SAMiguel Forte, MD, PhD, Chief Executive OfficerJean-Luc Vandebroek, Chief Financial OfficerTel: +32 (0) 71 12 10 00investorrelations@bonetherapeutics.com

International Media Enquiries:Image Box CommunicationsNeil Hunter / Michelle BoxallTel: 44 (0)20 8943 4685neil@ibcomms.agency / michelle@ibcomms.agency

For French Media and Investor Enquiries:NewCap Investor Relations & Financial CommunicationsPierre Laurent, Louis-Victor Delouvrier and Arthur RouillTel: + 33 (0)1 44 71 94 94bone@newcap.eu

Certain statements, beliefs and opinions in this press release are forward-looking, which reflect the Company or, as appropriate, the Company directors` current expectations and projections about future events. By their nature, forward-looking statements involve a number of risks, uncertainties and assumptions that could cause actual results or events to differ materially from those expressed or implied by the forward-looking statements. These risks, uncertainties and assumptions could adversely affect the outcome and financial effects of the plans and events described herein. A multitude of factors including, but not limited to, changes in demand, competition and technology, can cause actual events, performance or results to differ significantly from any anticipated development. Forward looking statements contained in this press release regarding past trends or activities should not be taken as a representation that such trends or activities will continue in the future. As a result, the Company expressly disclaims any obligation or undertaking to release any update or revisions to any forward-looking statements in this press release as a result of any change in expectations or any change in events, conditions, assumptions or circumstances on which these forward-looking statements are based. Neither the Company nor its advisers or representatives nor any of its subsidiary undertakings or any such person`s officers or employees guarantees that the assumptions underlying such forward-looking statements are free from errors nor does either accept any responsibility for the future accuracy of the forward-looking statements contained in this press release or the actual occurrence of the forecasted developments. You should not place undue reliance on forward-looking statements, which speak only as of the date of this press release.

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What Does Our Body Temperature Say About Our Health? – The New York Times

Posted: March 29, 2020 at 6:54 pm

Such a substantial change in average temperature over a fairly short period of history could have other, unforeseeable impacts. Parsonnet points out that there are more microbial organisms in us than there are human cells, which creates a complex ecosystem. And like a human-size version of climate change, were seeing probably a change in our ecosystem thats associated with this drop in temperature. Yet were only beginning to understand all the ways temperature influences that ecosystem to help determine how we function.

Our body temperature is controlled by the hypothalamus, which acts as a thermostat, keeping the temperature of vital organs fairly constant. (Its this core temperature that a thermometer approximates.) Temperature sensors in nerve endings, which produce the sensation of being hot or cold, prompt the hypothalamus to initiate adjustments like shivering to warm up or sweating to cool down. At any given time, your skin might be 10 degrees cooler or warmer than your core. And that difference and thus how much energy the body has to expend to keep the core stable seems to affect how the immune system functions. For instance, in 2013 Elizabeth Repasky of the Roswell Park Comprehensive Cancer Center and co-authors reported in P.N.A.S. that raising the room temperature improved the ability of laboratory mice to fight off cancer after they got it. Repasky and others are also experimenting with heating tumor cells to kill them or make them more susceptible to chemotherapy. Already, certain abdominal cancers are treated with hot chemotherapy, in which the drug is heated to 103 degrees, which has been shown to increase how much of it is absorbed by cancer cells. Separately, the heat from a fever may help fight infection, because, as Mark Dewhirst, an emeritus professor of radiation oncology at the Duke University School of Medicine, puts it, a lot of bacteria and other pathogens dont fare well at elevated temperatures.

Scientists struggle, though, to explain how a cooler average body temperature has been associated with longevity. A lower metabolic rate, and thus a lower temperature, has been linked to a longer life span in experimental settings with reduced calorie intake, when the body slows to conserve energy. But Bruno Conti, a professor of molecular medicine at the Scripps Research Institute, and colleagues have also found that mice genetically engineered to have a body temperature a half-degree lower than average lived longer than ordinary mice, even if they ate as much as they wanted. What other effects this has on an organism is unknown. For instance, he says, a brain at a lower temperature might not function as well.

At the same time, other bodily systems might benefit from being cooler. H. Craig Heller, a biology professor at Stanford, and colleagues have shown that muscle fatigue is caused by heat, which they believe triggers a temperature-sensitive enzyme that acts as a safety valve, stopping the production of chemicals that power muscle contractions in order to prevent the tissue from burning up. When Heller cools muscle during physical activity using special gloves that chill blood as it moves through the hands, the muscle just keeps on going, he says. Ive had freshmen doing more than 800 push-ups.

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COVID-19 breakthrough: researchers from U of T and McMaster successfully isolate virus – Varsity

Posted: March 29, 2020 at 6:54 pm

Scientists at Sunnybrook Hospital, the University of Toronto, and McMaster University successfully isolated and cultured SARS-CoV-2, the virus that causes the COVID-19 disease, from two patients, accelerating progress toward a COVID-19 vaccine.

The discovery was announced on March 12, and comes almost three months after the outbreak of COVID-19, which started as an epidemic in Wuhan, China in December 2019. One day earlier, on March 11, the World Health Organization (WHO) had declared the virus spread across the globe to be a pandemic.

Research teams from all across the world have started accepting grants to work on developing a potential vaccine. Even though COVID-19 shares genomic and structural similarities with severe acute respiratory syndrome better known as SARS another strain of coronavirus that was identified and previously researched in 2003, the WHO has said that it would take at least 18 months to develop a vaccine.

Dr. Rob Kozak, a clinical microbiologist at U of T and at Sunnybrook Hospital, told Sunnybrook News that researchers from these world-class institutions came together in a grassroots way to successfully isolate the virus in just a few short weeks.

Lab-grown copies of the virus will help researchers around the world enhance their understanding of the virus biology and evolution in order to develop better treatments and a potential vaccine.

One of the primary uses of the isolated virus will be as a control group to see whether the tests currently being used by health care providers are performing as expected, according to Dr. Samira Mubareka, an infectious diseases physician and microbiologist whos at U of T and Sunnybrook.

Researchers can also use the isolated virus to measure the effectiveness of the vaccines and drugs that are currently in development.

As Kozak explained to U of T News, From a bigger picture standpoint, having a virus isolate that can be shared with other labs to perform other experiments to better understand the virus and how to stop it is critical.

Karen Mossman, a professor of pathology and molecular medicine at McMaster University, told The Globe and Mail that she and her colleagues would be using the isolated virus to understand how COVID-19 counteracts the human immune response.

As of time of publication, the virus has infected more than 662,000 people in over 177 countries and regions, and caused more than 30,800 deaths. While there is more work to be done, there is cause for hope, as the isolation of SARS-CoV-2 could eventually help quell the outbreak and save many lives worldwide.

Now that we have isolated the SARS-CoV-2 virus, we can share this with other researchers and continue this teamwork, said Dr. Arinjay Banerjee, Natural Sciences and Engineering Research Council of Canada postdoctoral fellow at McMaster University, to Sunnybrook News, emphasizing that this collaboration will continue.

The more viruses that are made available in this way, the more we can learn, collaborate and share, he added.

Tags: coronavirus, COVID-19

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This is how my team isolated the new coronavirus to fight the global pandemic – ThePrint

Posted: March 29, 2020 at 6:54 pm

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As most people rush to distance themselves from COVID-19, Canadian researchers have been waiting eagerly to get our (gloved) hands on the hated virus.

We want to learn everything we can about how it works, how it changes and how it interacts with the human immune system, so we can test drugs that may treat it, develop vaccines and diagnostics and prevent future pandemics.

This is what researchers live to do. Much of our everyday work is incremental. Its important and it moves the field forward, but to have a chance to contribute to fighting a pandemic is especially inspiring and exciting.

Viruses are fascinating. They are inert microscopic entities that can either hide out, innocuous and undetected, or wreak pandemic havoc.

They are simultaneously complex and simplistic, which is what makes them so interesting especially new, emerging viruses with unique characteristics. Researching viruses teaches us not only about the viruses we study, but also about our own immune systems.

The emergence of a new coronavirus in a market in Wuhan, China, in December 2019 set in motion the pandemic we are now witnessing in 160 countries around the world. In just three months, the virus has infected more than 360,000 people and killed more than 16,000.

The outbreak sent researchers around the world racing to isolate laboratory specimens of the virus that causes COVID-19. The virus was later named severe acute respiratory syndrome coronavirus 2, or SARS-CoV-2.

In countries that experienced earlier outbreaks, including China, Australia, Germany and the United States, researchers were able to isolate the virus and develop their own inventories of SARS-CoV-2, but logistical and legal barriers prevented them from readily sharing their materials with researchers beyond their borders.

What Canadian researchers needed to join the fight in earnest was a domestic supply of clean copies of the virus preferably from multiple Canadian COVID-19 cases. Even in a pandemic, developing such a supply is not as easy as it might sound, and multiple teams in Canada set out to isolate and develop pure cultures of the virus, not knowing which would be successful, or when.

Ultimately two teams in Canada would isolate the virus for study: one at the University of Saskatchewan and one that featured researchers from McMaster University, Sunnybrook Health Sciences Centre and the University of Toronto.

Arinjay Banerjee, a postdoctoral research fellow at McMaster who typically works in my virology lab, volunteered his special expertise. We were proud to have him share his talent with the team in Toronto, where he set to work with physicians and researchers Samira Mubareka, Lily Yip, Patryk Aftanas and Rob Kozak.

For Banerjee, it was like a batter being called to the plate with the score tied in the bottom of the ninth. He had come to work at McMaster because of its Institute for Infectious Disease Research and its Immunology Research Centre, and because the university maintains a research colony of bats.

Banerjees PhD work at the University of Saskatchewan, and now at McMaster, has focused on bats and how their viruses, including coronaviruses, interact with bat and human antiviral responses. Over the past few years, studies have shown that bat coronaviruses have the capacity to infect human cells. Multiple researchers had predicted a coronavirus that would evolve and jump into humans.

Also read:Modis India isnt Maos China. Silly forecasts assume well let corona kill millions of us

Isolating a virus requires collecting specimens from patients and culturing, or growing, any viruses that occur in the samples. These viruses are obligate intracellular parasites, which means that they can only replicate and multiply in cells. To isolate a particular virus, researchers need to provide it with an opportunity to infect live mammalian cells, in tiny flasks or on tissue culture plates.

Viruses adapt to their hosts and evolve to survive and replicate efficiently within their particular environment. When a new virus such as SARS-CoV-2 emerges, it isnt obvious what particular environment that virus has adapted to, so it can be hard to grow it successfully in the lab.

We can use tricks to draw out a virus. Sometimes the tricks work and sometimes they dont. In this case, the researchers tried a method Banerjee and the team had previously used while working on the coronavirus that causes Middle Eastern Respiratory Syndrome: culturing the virus on immunodeficient cells that would allow the virus to multiply unchecked. It worked.

Since specimens from patients are also likely to contain other viruses, it is critical to determine if a virus growing in the culture is really the target coronavirus. Researchers confirm the source of infection by extracting genetic material from the virus in culture and sequencing its genome.

They compare the sequence to known coronavirus sequences to identify it precisely. Once a culture is confirmed, researchers can make copies to share with colleagues.

All this work must be done in secure, high-containment laboratories that mitigate the risk of accidental virus release into the environment and also protect scientists from accidental exposure. The more versions of a virus that can be isolated, the better. Having multiple virus isolates allows us to monitor how the virus is evolving in humans as the pandemic progresses. It also allows researchers to test the efficacy of vaccines and drugs against multiple mutations of the virus.

Transmission electron microscopic image of an isolate from the first U.S. case of COVID-19. The spherical viral particles, colourized blue, contain cross-sections through the viral genome, seen as black dots. (U.S. CDC)

Both the Saskatchewan and Ontario teams are now able to make and share research samples with other Canadian scientists, enabling important work to proceed, using a robust domestic supply that reflects the evolving virus in its most relevant mutations.

That in turn gives Canadian researchers a fighting chance to deliver a meaningful blow to COVID-19 while there is still time. Im glad our colleagues at other Canadian institutions will also have versions of the virus to use in their research.

There is still so much work for all of us to do.

Karen Mossman, Professor of Pathology and Molecular Medicine and Acting Vice President, Research, McMaster University

This article is republished from The Conversation.

Also read:Lesson from Black Death: Coronavirus will transform economic life for longer than we expect

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How sick will the coronavirus make you? The answer may be in your genes – Science Magazine

Posted: March 29, 2020 at 4:49 am

A patient in Italy receives intensive care for COVID-19. Human geneticists are coming together to look for genes that make some people more vulnerable to the disease.

By Jocelyn KaiserMar. 27, 2020 , 3:25 PM

Sciences COVID-19 reporting is supported by the Pulitzer Center.

COVID-19, caused by the new pandemic coronavirus, is strangelyand tragicallyselective. Only some infected people get sick, and although most of the critically ill are elderly or have complicating problems such as heart disease, some killed by the disease are previously healthy and even relatively young. Researchers are now gearing up to scour the patients genomes for DNA variations that explain this mystery. The findings could be used to identify those most at risk of serious illness and those who might be protected, and they might also guide the search for new treatments.

The projects range from ongoing studies with DNA for many thousands of participants, some now getting infected with the coronavirus, to new efforts that are collecting DNA from COVID-19 patients in hard-hit places such as Italy. The goal is to compare the DNA of people who have serious cases of COVID-19 (which stands for coronavirus disease 2019)but no underlying disease like diabetes, heart or lung diseasewith those with mild or no disease. We see huge differences in clinical outcomes and across countries. How much of that is explained by genetic susceptibility is a very open question, says geneticist Andrea Ganna of the University of Helsinkis Institute for Molecular Medicine Finland (FIMM).

Its hard to predict what will pop out from these gene hunts, some researchers say. But there are obvious suspects, such as the gene coding for the cell surface protein angiotensin-converting enzyme 2 (ACE2), which the coronavirus uses to enter airway cells. Variations in the ACE2 gene that alter the receptor could make it easier or harder for the virus to get into cells, says immunologist Philip Murphy of the National Institute of Allergy and Infectious Diseases, whose lab identified a relatively common mutation in another human cell surface protein, CCR5, that makes some people highly resistant to HIV.

Ganna heads up a major effort to pool COVID-19 patients genetic data from around the world. The idea came quite spontaneously about 2 weeks ago when everyone was sitting at their computers watching this crisis, says Ganna, who is also affiliated with the Broad Institute, a U.S. genomic powerhouse.

He and FIMM Director Mark Daly quickly created a website for their project, the COVID-19 Host Genetics Initiative, and reached out to colleagues who run large biobank studies that follow thousands of volunteers for years to look for links between their DNA and health. At least a dozen biobanks, mostly in Europe and the United States, have expressed interest in contributing COVID-19 data from participants who agreed to this. Among them are FinnGen, which has DNA samples and health data for 5% of the 5 millionperson Finnish population, and the 50,000-participant biobank at the Icahn School of Medicine at Mount Sinai.

The UK Biobank, one of worlds largest with DNA data for 500,000 participants, also plans to add COVID-19 health data from participants to its data set, the project tweeted this month. And the Icelandic company deCODE Genetics, which is helping test much of the nations population to see who is infected with the new coronavirus, has received government permission to add these data and any subsequent COVID-19 symptoms to its database, which contains genome and health data on half of Icelands 364,000 inhabitants, says its CEO Kri Stefnsson. We will do our best to contribute to figuring this out, Stefnsson says.

Another effort to identify protective or susceptibility DNA variants is the Personal Genome Project led by Harvard Universitys George Church, which recruits people willing to share their full genome, tissue samples, and health data for research. Earlier this month, it sent questionnaires to its thousands of participants, asking about their COVID-19 status. More than 600 in the United States responded within 48 hours. It seems that most people want to do their part, says Church, whose group isnt yet part of Gannas collaboration.

Other researchers working with Gannas initiative are recruiting COVID-19 patients directly within hospitals for such genomics studies. Italian geneticist Alessandra Renieri of the University of Siena expects at least 11 hospitals in the nation to give ethics approval for her team to collect DNA samples from willing patients. It is my opinion that [host] genetic differences are a key factor for susceptibility to severe acute pneumonia, Renieri says.

Pediatrics researcher Jean-Laurent Casanova at the Rockefeller University, who specializes in identifying rare genes that can make healthy young people susceptible to certain serious diseases, is drawing on a network of pediatricians around the world to look for the relatively few young people who develop COVID-19 serious enough to get admitted to intensive care. We study exclusively patients who were previously healthy and under 50, as their serious COVID-19 illness is more likely to have a genetic basis, he explains.

In addition to genetic variants of the ACE2 receptor, scientists want to see whether differences in the human leukocyte antigen genes, which influence the immune systems response to viruses and bacteria, affect disease severity. And some investigators want to follow up a finding, which a Chinese team reported in a preprint: that people with type O blood may be protected from the virus. Were trying to figure out if those findings are robust, says Stanford University human geneticist Manuel Rivas, who is contributing to Gannas initiative.

The catastrophic spread of the coronavirus should soon increase the number of COVID-19 patients available to these gene hunts. And that could speed findings. Ganna expects the first susceptibility genes could be identified within a couple of months.

With reporting by Elizabeth Pennisi.

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