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Swiss studies show how important time is in responding to COVID-19 | Instant News


A new study published on preprinted servers medRxiv* in July 2020 revealed the important nature of time as a factor in controlling mortality rates in the current COVID-19 pandemic. The background of this paper is the outbreak in Switzerland, where around 30,000 people were infected with acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and more than 1,800 died from late February to early May 2020. This study shows that the introduction of NPI in March 2020 prevents thousands of virus-related deaths in Switzerland.

Study: Time is crucial: containment of the SARS-CoV-2 epidemic in Switzerland from February to May 2020. Image credit: Roger Gantner / Shutterstock

Plague Course in Switzerland

The first case in this country came from a region adjacent to the area affected by Italy, but the disease quickly spread to the small country. In response to the outbreak, a series of non-pharmaceutical interventions (NPI) were quickly introduced, including the closure of elementary schools, shops selling non-essential items, and restaurants, and limiting the gathering of more than five people on March 20, 2020.

The epidemic showed a decline after the introduction of these measures in March. On May 10, 2020, restrictions were lifted. The paper by researchers at the University of Bern aims to show how the timing of NPI implementation affects the course of the epidemic and its results.

New model number of infections, hospitalized patients, intensive care unit (ICU) occupancy, and deaths during the SARS-CoV-2 epidemic in Switzerland.  Solid lines show the maximum likelihood estimates of the model and shaded area according to the 95% prediction interval.  The model fits the data shown as white circles.  The number of reported infections (gray box) is shown for comparison.  The vertical dashed line shows the strengthening of social distance on March 17, 2020.

New model number of infections, hospitalized patients, intensive care unit (ICU) occupancy, and deaths during the SARS-CoV-2 epidemic in Switzerland. Solid lines show the maximum likelihood estimates of the model and shaded area according to the 95% prediction interval. The model fits the data shown as white circles. The number of reported infections (gray box) is shown for comparison. The vertical dashed line shows the strengthening of social distance on March 17, 2020.

Potential Effects of Previous or Next NPI

The researchers used modeling to estimate the effects of various scenarios on the Swiss epidemic. That is, if the NPI has been applied a week before or a week later, how has the incidence of infection, the number of cases treated at the hospital, and mortality, changed?

This study is based on a population-based transmission model and includes a gradual introduction of the NPI. Previous studies have shown that this causes a sharp reduction in the amount of effective reproduction (Re) in Switzerland.

Reduction of effective reproduction number of Re during the SARS-CoV-2 epidemic in Switzerland.  Solid lines show the maximum likelihood estimates of the model and shaded area according to the 95% compatibility interval.  We assume that the introduction of NPI sequentially results in a reduction in sigmoid transmission rates for about 2 weeks.  The vertical dashed line shows the strengthening of social distance on March 17, 2020.

Reduction of effective reproduction number of Re during the SARS-CoV-2 epidemic in Switzerland. Solid lines show the maximum likelihood estimates of the model and shaded area according to the 95% compatibility interval. We assume that the introduction of NPI sequentially results in a reduction in sigmoid transmission rates for about 2 weeks. The vertical dashed line shows the strengthening of social distance on March 17, 2020.

Using public data about the daily number of confirmed cases, hospitalization, admission to the intensive care unit (ICU), and virus-related deaths, the researchers found that initially, infections rose exponentially.

The researchers also estimate that the total number of infections is about ten times the number of cases diagnosed and confirmed initially. Then, the diagnosed cases account for around 20% of the total, but finally, after all the BOP is present, it drops again to around 10% of the total. The total estimate, therefore, amounts to around 264,000 cases.

Using a simulation of the previous NPI introduction, the model shows that around 2,000 deaths will occur if the NPI continues to negatively affect the number of deaths after May 10. If they had been implemented a week before, the model concluded that the peak number of hospitalizations would be much lower, at ~ 440, as would be the peak of ICU occupancy and death, respectively at ~ 88 and 400.

If the NPI is introduced a week later, these numbers will increase substantially, with a peak inpatient number of around 10,200, peak ICU occupancy of 1,900, and deaths of more than 8,000 each.

Doubling Time Triples with NPI

Current studies show that the effective reproduction rate (Re) fell from about 2.6 at the beginning to 0.64, which corresponds to a doubling time of about 3 days and 9 days at the start of the epidemic and post-lockdown phase, respectively. This underlines the urgency of the initial NPI in containing the spread of the virus.

The researchers commented, “One week of exponential increase in new infections during the spread of the initial epidemic requires 3.1 weeks of ‘locking’ to reduce the number of infections to the same level.”

Implications of this Study

This is the first study to analyze the possible effects of counterfactual scenarios regarding changes in the timing of NPI implementation. This finding is partly supported by lower mortality in Austria, which reported its first few cases at the same time as Switzerland, and who also fell victim to the spread from neighboring Lombardy, in Italy. However, the initial and strict introduction of the NPI within one week of the first case led to a reduction in the number of deaths.

In addition, the researchers showed that the high peak ICU occupancy rate of nearly 2,000 that could potentially result from a one-week delay in the NPI might flood the national health system, because the effective capacity of the ICU in Switzerland was only around 1,275 in April 2020.

In summary, this study concludes, “Our study illustrates that time is the most important when it comes to outbreak responses. We point out that while previous implementation of the NPI in Switzerland would result in a much lower number of cases and deaths being treated in hospitals, the steps taken succeeded in preventing the much higher morbidity and mortality burden associated with SARS-CoV-2. “

Because one week of exponential virus spread requires three weeks of locking to bring the number of daily cases back to their original level, the delay not only increases the number of deaths but extends the locking period. Therefore, the adoption of a stringent NPI will reduce the social and economic burden of these measures. Second, there are significant differences in the number of infections in various cantons, and this might indicate that new local outbreaks might be limited to separate areas.

* Important Notification

medRxiv publishing initial scientific reports that are not reviewed by colleagues and, therefore, should not be considered conclusive, guiding clinical practice / health-related behaviors, or treated as pre-existing information.

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“Winter is coming,” warns UK experts COVID-19 | Instant News


Famous lines of “Game of Thrones“About approaching the dangers of this winter might prove accurate, say, scientists at a new report. The researchers stated that the second wave of infections could hit Britain this winter, and this would be worse than the first wave that claimed as many as 120,000 lives.

The COVID-19 pandemic caused by acute coronavirus 2 (SARS-CoV-2) respiratory syndrome has gripped the world, and now experts warn that it is far from over. To date, the virus has infected 13.28 million people and claimed more than 577,000 lives worldwide.

Novel Coronavirus SARS-CoV-2 This transmission electron microscope image shows SARS-CoV-2 – also known as 2019-nCoV, the virus that causes COVID-19. isolated from a patient in the US, emerging from the surface of cells cultured in the lab. Images were captured and colored at NIAID’s Rocky Mountain Laboratories (RML) in Hamilton, Montana. Credit: NIAID

Current status in the UK

To date, there have been 292,931 cases of SARS-CoV-2 detected in the UK, and the infection has caused 45,053 deaths in the country. Over time the death rate and new cases have declined in the UK, and in July to date, there were 1,100 deaths, the researchers said. However, there may be no room for complacency that they warn.

According to the nation’s scientific advisors from Academy of Medical Sciences, which was asked to predict using modeling analysis, the worst is yet to come.

worst-case scenario that makes sense for the winter COVID-19 epidemic in the UK.  This model assumes that Rt rises to 1.7 from September 2020 to July 2021. (A) daily infections, (B) COVID-19 deaths caused in hospitals (ie excluding care homes and over-deaths in the community), (C ) general beds are occupied and (D) critical care beds are occupied.  Solid lines show medians, dark bands interquartile range, and pale bands at credible intervals of 95% (CrI).

The worst worst case scenario for the winter COVID-19 epidemic in the UK. This model assumes that Rt rises to 1.7 from September 2020 to July 2021. (A) daily infections, (B) COVID-19 deaths caused in hospitals (ie excluding care homes and over-deaths in the community), (C ) general beds are occupied and (D) critical care beds are occupied. Solid lines show medians, dark bands interquartile range, and pale bands at credible intervals of 95% (CrI).

Predictions and warnings

37 researchers in the team say that winter deaths can range between 24,500 and 251,000 in hospitals in the UK. This will be related to coronavirus infection. Deaths can peak between January and February 2021, they speculate.

These figures are predicted in a scenario where there are no locks or drugs available to treat any infection or vaccine to prevent COVID-19. At present, there is no specific drug that can be used to treat COVID-19, and the treatment is mainly supportive and symptomatic.

Around 120 vaccine candidates are currently undergoing clinical trials in various parts of the world, including one promising agent tested by Oxford researchers. However, nothing is available for use in humans.

Lockdown is the total closure of offices, businesses, schools and public transportation to break the transmission chain. The predicted number of deaths does not take into account locking, availability of effective drugs or vaccines during this winter.

Report

This report was requested by the chief British scientific advisor, Sir Patrick Vallance. The researchers write, “Risk … can be reduced if we take action immediately.” The actual status of a pandemic during winter is uncertain. However, what is clear is that the virus can survive better during winter and thus can spread easily among people who are trapped indoors during winter. The report states, “In cold, rainy or windy weather people are reluctant to open windows because they make cold winds and therefore they often have lower ventilation rates in winter. This can be a special challenge in modern airtight buildings that have a high level of infiltration very low for energy efficiency and for low income people who are trying to keep down heating costs. “

Burden on the health system

Thus, COVID-19 has a high level of infectivity but a low risk of complications and death. Only a small proportion of people – especially the elderly and those who suffer from other diseases, are at risk of complications.

These people may need intensive care and ventilation and are more at risk of dying. However, the spread of massive infections can also lead to extraordinary health care systems. This has been seen throughout Europe and in the United States for the past few months.

The NHS, too, is under pressure to meet the needs of thousands of patients. With the reduced number of COVID-19 cases, there has been a revival of flu cases and non-COVID-19 cases, the researchers explained.

The second wave of coronavirus infections can stretch the system to its capacity, they speculate. They say that there is a waiting list of non-coronavirus cases and this could reach 10 million by the end of this year if the situation with COVID-19 continues to worsen.

Expert talk

Prof. Stephen Holgate, a breathing specialist from the University Hospital of Southampton NHS Trust, is the chair of this report. He said in his statement, “This is not a prediction – but it is a possibility. Modeling shows that deaths could be higher with the new wave of COVID-19 this winter. But the risk of this event can be reduced if we take immediate action.”

He said that at this time, the numbers were low, and this could be “a window of critical opportunity to help us prepare for the worst that winter can throw at us.”

Co-author Prof. Dame Anne Johnson, from the Academy of Medical Sciences, said in a statement, “Facing these potential challenges, and after a difficult year, it will be easy to feel hopeless and helpless. But this report shows that we can act now to change things for the better. “He said,” COVID-19 has not disappeared. We need to do everything we can to stay healthy this winter. “

Health Secretary Matt Hancock has assured that the government already plans to handle the second wave this winter. A government statement said, “We remain vigilant, and the government will ensure the resources needed to avoid the second peak that will flood our NHS.”

Recommendations for prevention of the second wave

The report’s authors have made certain recommendations for overcoming problems with the second wave of the pandemic.

  • They urged further testing for infections and intensive tracking of all contacts of infected people to prevent the spread of infection.
  • A broad campaign to get more people vaccinated against seasonal flu to reduce the burden of flu cases this winter
  • Prevent transmission of coronavirus infection to other patients by making the area “corona-free” in the hospital.
  • Availability of adequate personal protective equipment (PPE) for health care workers to prevent infection and spread.

Window to act now

The researchers added that at present, many of these predicted figures are based on a modeling system, and if the parameters are changed slightly, the number of deaths and hospitalization can change significantly.

However, researchers urge the general public and policy makers to prepare for the worst case scenario while hoping for the best. “There’s a lot to do, and we don’t have much time to do it,” Johnson said. “A window to action now.”

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Patients with ARDS, COVID-19 experience severe financial toxicity | Instant News


Starting with shortness of breath. And for about a third of patients, acute respiratory distress syndrome, or ARDS, ends in death. For those who survived, their lives were often turned upside down. Michigan Medicine researchers have been investigating the downstream effects of ARDS for years. When the COVID-19 pandemic raged, their work had relevance for hundreds of thousands of new patients.

The way COVID-19 kills patients is by depriving them of oxygen. But only one third or fewer of COVID-19 patients who experience respiratory failure die. Most survive, and we need research that helps them not only survive but also be completely cured. “

Theodore (Jack) Iwashyna, M.D., professor of critical care medicine

A team led by Iwashyna wanted to take a closer look at how to be hospitalized for people affected by ARDS months after they were discharged. They interviewed dozens of patients from all countries. “As we know from previous studies, people have new defects starting from general fatigue and weakness where they cannot remember things,” said Katrina Hauschildt from the U-M sociology department and the first author in this study. “Many people experience emotional difficulties to make peace with how sick they are – sort of PTSD because they are in the ICU.”

“What I did not expect,” Iwashyna said, “is the eternal chaos that caused respiratory failure that threw several of our patients and their families alive. Patients describe problems that come not only from medical bills – although there are many of them – but also because lost their jobs and lost their insurance. “Given the magnitude of the recession that struck at the same time as patients tried to recover from COVID-19, Iwashyna and Hauschildt worried that this could destroy many families.

A 55-year-old man described having to give up his small business because he could not work after leaving the intensive care unit (ICU). “I have to sell my business. I’m in disability now … I have a fire suppression company … We used to clean the kitchen exhaust system in restaurants across the state. Lower the number of restaurants, such as mufflers in the kitchen and on the roof. .. Yes, I sell everything. “

The team found that many respiratory failure patients experience what is known as financial toxicity, which is defined as financial burden and related medical care difficulties. In turn, this financial toxicity causes additional negative effects on their physical and emotional recovery.

Hospitalization for ARDS often results in weeks of intensive care, patients end up with medical bills ranging from tens of thousands to, in some cases, millions of dollars, and the proportion covered by insurance varies substantially.

A 49-year-old survivor of ARDS told the study team, “I almost didn’t make it, or my bills were delayed such as electricity, things and other items.” Another 55-year-old woman said, “I had to pay rent, food, and medicine and all that so I was a little lacking … They were rather difficult to pay after the hospital … Because I had to get more medicine and all of it. “

The team reported several consequences of hospitalization including emotional distress related to insurance problems and unpaid bills, reduced physical well-being due to the inability to receive further care due to costs, increased dependence on family and friends to help cover expenses and more. material difficulties. A patient said: “In the next few months, I might become homeless because of its financial aspects.”

Although these cases may seem extreme, they are not uncommon. And many patients illustrate having to make difficult choices about whether they are capable of rehabilitation – and stop early when their coverage runs out, even though they haven’t recovered. A 51-year-old man told the study team “[Physical therapy] very short, maybe a few weeks; then it’s all over, and basically I’m just lying there. My insurance doesn’t cover anymore, so they have to cut me. “

Another patient, a 61-year-old woman, described having no equipment when she tried to go home: “I can choose one item that I want,” from the hospital bed, wheelchair and walker she needs, “because insurance will only pay for one item. “

Hauschildt said the study outlined the need for doctors to be more aware of the financial poisoning faced by ARDS survivors, including those who had just recovered from COVID-19. “One of the biggest things that doctors who can engage in advanced care can do is anticipate that patients may have a real financial burden and know what resources are available so they can help,” he added.

However, he noted, what is available really depends on policy makers. For example, this study found that patients who had used public insurance before their illness reported a modest financial impact. “Communities that install safety nets for survivors of ARDS and COVID-19 will eventually have better healing and recovery. People who recover can go back to work and care for others and their communities; people who don’t.”

This work was supported by the National Institutes of Health, the National Heart, Lung and Blood Institute as part of the Early Prevention and Treatment Network for Acute Lung Injury (PETAL). The patients who participated in this interview gave consent for the words they were quoted, and all about nine months after moderate to severe ARDS.

Source:

Journal reference:

Hauschildt, K., et al. (2020) Financial Poisoning After Acute Respiratory Syndrome: A National Qualitative Cohort Study. Critical Care Medication. doi.org/10.1097/CCM.0000000000004378.

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How COVID-19 affects the nervous system | Instant News


A new paper published in the journal JAMA Neurology in May 2020 discussed the presentation and complications of COVID-19 with respect to the nervous system.

The COVID-19 pandemic has caused hundreds of thousands of cases of severe pneumonia and respiratory disorders, in 188 countries and regions in the world. The causative agent, SARS-CoV-2, is a new coronavirus, with well-recognized lung complications. However, evidence is increasing that the virus also affects other organs, such as the nervous system and heart.

The Coronaviruses: A Glimpse

That corona virus is a group of large spread RNA viruses that infect animals and humans. Human infections are known to be caused by 7 coronaviruses, namely human coronavirus (HCoV) –229E, HCoV-NL63, HCoV-HKU1, HCoV-OC43, MERS-CoV, SARS-CoV-1, and SARS-CoV-2.

Among these, the last three are known to cause severe human disease. While HCoV is more associated with respiratory manifestations, three of them are known to infect neurons: HCoV-229E, HCoV-OC43, and SARS-CoV-1.

Current research aims to contribute to the knowledge of the SARS-CoV-2 neurotropism, as well as post-infectious neurological complications. This virus infects humans through ACE2 receptors in various tissues, including airway epithelium, kidney cells, small intestine, proper lung tissue, and endothelial cells.

Because endothelium is found in blood vessels throughout the body, this offers a potential route for CoV to be localized in the brain. In addition, a recent report shows that ACE2 is also found in brain neurons, astrocytes, and oligodendrocytes, especially in areas such as substantia nigra, ventricles, middle temporal gyrus, and olfactory bulb.

Interestingly, ACE2 in neuron tissue is expressed not only on the surface but also in the cytoplasm. This finding could imply that SARS-CoV-2 can infect neuronal and glial cells in all parts of the central nervous system.

How does neuroinvasion occur with SARS-CoV-2?

Current knowledge indicates the possibility of nerve cell virus invasion by several mechanisms. These include the transfer of viruses across synapses of infected cells, entering the brain through the olfactory nerve, infection of endothelial blood vessels, and migration of infected white blood cells across the blood-brain barrier (BBB).

The corona virus has been shown to spread back along the nerves from the edge of the peripheral nerves, across synapses, and thus into the brain, in several small animal studies. This is facilitated by a pathway for endocytosis or exocytosis between motor cortex neurons, and other secretory vesicular pathways between neurons and satellite cells.

Axonal transport occurs rapidly using axonal microtubules, which allow the virus to reach the body of neuron cells with a retrograde version of this mechanism.

The possibility of spreading the olfactory route is marked by the occurrence of isolated anosmia and age. In such cases, the virus can pass through the latticed plate to enter the central nervous system (CNS) of the nose. However, more recent unpublished research shows that olfactory neurons lack ACE2, whereas cells in the olfactory epithelium do so. This could mean that a viral injury to the olfactory epithelium, and not the olfactory neuron, is responsible for anosmia, but further studies will be needed to confirm this.

Cross the BBB

This virus can also pass through the BBB through two separate mechanisms. In the first case, infected vascular endothelial cells can move the virus across blood vessels to neurons. Once there, the virus can start to bud and infect more cells.

The second mechanism is through infected white blood cells that pass through the BBB – a mechanism called Trojan horse, which is famous for its role in HIV. Inflamed BBB allows the entry of immune cells and cytokines, and even, possibly, viral particles into the brain. T-lymphocytes, however, do not allow viruses to replicate even though they can be infected.

Neurological features of COVID-19

From limited data on neurological manifestations related to COVID-19, it is clear that headaches, anosmia, and age are among the most common symptoms. However, other findings include stroke and an abnormal state of consciousness.

While headaches occur in up to one third of confirmed cases, anosmia or age shows a much more varied prevalence. In Italy, about one fifth of cases show this symptom, while almost 90% of patients in Germany have such symptoms.

The researchers said, “Given the reports of anosmia that appear as early symptoms of COVID-19, specific testing for anosmia can offer the potential for early detection of COVID-19 infection.”

Impaired consciousness can occur in up to 37% of patients, due to various mechanisms such as infection and direct brain injury, metabolic-toxic encephalopathy, and demyelinating disease. Encephalitis has not been documented as a result of COVID-19.

Toxic-metabolic encephalopathy can occur due to a number of disorders of metabolic and endocrine function. These include electrolyte and mineral imbalances, kidney disorders, and cytokine storms, hypo or hyperglycemia, and liver dysfunction. Patients who are elderly, ill, or already have symptoms of dementia, or are malnourished, are at higher risk for this condition.

Less common neurological complications include Guillain-Barre syndrome, which is a post-viral acute inflammatory demyelinating disease, and cerebrovascular events, including stroke.

Is COVID-19 Therapy Related to Neurological Manifestations?

Nowadays, many different drugs are used to treat this condition.

Chloroquine and hydroxychloroquine, for example, can cause psychosis, peripheral neuropathy, and the latter can worsen the symptoms of myasthenia gravis. Tocilizumab, an IL-6 blocker, is intended to reduce excessive cytokine release that occurs in severe inflammation. Although admission to CNS is limited, it can sometimes cause headaches and dizziness.

Precautions for COVID-19 Patients with Neurological Conditions

If a patient already has a neurological condition that requires special treatment, they tend to be at higher risk for COVID-19, due to existing lung, heart, or liver conditions, having kidney disease (dialysis), if they are overweight, or at immunosuppressive drugs. Also, it is likely that they may be in nursing homes, where many countries have reported severe outbreaks.

This study concludes: “Doctors must continue to monitor patients closely for neurological diseases. Early detection of neurological deficits can lead to improved clinical outcomes and better treatment algorithms. “

Journal reference:

  • Zubair, A. S. et al. (2020). Neuropathogenesis and Neurological Manifestations of Coronavirus in the Coronavirus Era 2019: Overview. JAMA Neurology. doi: 10.1001 / jamaneurol.2020.2065.

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SARS-CoV-2 is uniquely adapted to infect humans | Instant News


The new corona virus pandemic has sparked much debate about its origin, with some suggesting it might have been developed in a laboratory. Previous studies, however, mentioned that it was zoonotic, which means that the virus jumped from wild animals and found its way to humans.

Now, researchers claim that viruses have uniquely adapted to infect humans, demonstrating that virus theories planted in laboratories should not be completely excluded.

What is zoonotic disease?

Zoonotic disease or zoonosis is an infection caused by dangerous pathogens such as bacteria, viruses, fungi, and parasites that spread from animals to humans. Although many zoonotic diseases are common, some can cause serious illnesses, including hantavirus and corona virus.

Chengdu / China-Feb.2020: A security guard with a mask outside the local wet market. Image Credit: Amar Shrestha / Shutterstock

Animal pathogens can spread to human populations through direct contact with bodily fluids from infected animals, go to areas where animals live, be bitten by insects such as mosquitoes or fleas, and through the intake of contaminated food.

At present, the world is grappling with a new type of coronavirus, severe acute respiratory syndrome coronavirus (SARS-CoV-2), which causes coronavirus disease (COVID-19). The exact origin of this virus cannot be confirmed, but bats as a reservoir of known corona viruses are at the top of the list of ‘most likely’.

Hong Kong - March 10, 2017: Bird market in Kowloon, Hong Kong. Image Credit: Christian Mueller / Shutterstock

Bird market in Kowloon, Hong Kong. Image Credit: Christian Mueller / Shutterstock

The new corona virus has made sick more than 5.4 million people worldwide and caused the death of more than 345,000 people.

Uniquely adapted to infect humans

In the new study available at arXiv preprint server*, which has not been reviewed by colleagues, the researchers point to many reasons why viruses become so well adapted to humans, such as convergent evolution after exposure to human cells, exposure to human cells very early in a pandemic, and rare mutations that combine two species genes. All this raises new questions about whether the origin of SARS-CoV-2 is natural or can occur in the laboratory.

“The devastating impact of the COVID-19 pandemic caused by SARS coronavirus 2 (SARS-CoV-2) has raised important questions about the origin of this virus, the mechanism of zoonotic transfer from exotic animals to humans, whether companion animals or those used for commercial purposes can act as a reservoir for infection, and a reason for large variations in susceptibility across animal species, “the researchers wrote in the paper.

Professor Nikolai Petrovsky, from the Faculty of Medicine and Public Health at Flinders University, who has spent decades developing vaccines against influenza, SARS animals, and Ebola, said that the findings of this study were very unusual, opening the possibility that the virus might have originated from laboratory experiments .

However, he said that at this point it was impossible to rule out the theory that the virus was created in cell culture experiments.

Research findings show that the virus was specifically designed for humans, whether it occurs naturally, by chance, or by intention, remains to be investigated.

He also added that the virus is not unusual from animal to human infections because it can enter the human body immediately. Other pathogens in the past that have jumped from animals to humans usually strengthen when they adapt to new hosts, but for SARS-CoV-2, it seems to be perfectly adapted to infect humans.

SARS-CoV-2 surge protein

The team used a structural silico homology modeling approach to characterize new coronavirus surge proteins, which predicted high affinity bonds to the human angiotensin 2 (ACE2) converting enzyme receptor.

SARS-CoV-2 virus binds to ACE-2 receptors in human cells, early stages of COVID-19 infection, 3D conceptual illustration Credit: Kateryna Kon / Shutterstock

SARS-CoV-2 virus binds to ACE-2 receptors in human cells, early stages of COVID-19 infection, 3D conceptual illustration Credit: Kateryna Kon / Shutterstock

Usually, traditional lab-based methods are used, but they may take longer to produce results. On the other hand, the silico modeling method can help produce information about newly emerging pathogens more quickly, providing insight into their behavior and effects on the body.

The SARS-CoV-2 virus binds to ACE-2 receptors in human cells, the early stages of COVID-19 infection, a conceptual 3D illustration credit: Kateryna Kon / Shutterstock

The SARS-CoV-2 virus binds to ACE-2 receptors in human cells, the early stages of COVID-19 infection, a conceptual 3D illustration credit: Kateryna Kon / Shutterstock

The team has found that the SARS-CoV-2 spike protein has the highest overall binding energy for human ACE2, more significant than all other tested species, including bats, the recommended viral source. Furthermore, the team revealed that SARS-CoV-2 is a highly adapted human pathogen. Pangolin, another animal source that claims an outbreak in Wuhan City in China, has the next highest binding affinity.

“Overall, the data show that SARS-CoV-2 is uniquely adapted to infect humans, raising the question whether it arose in nature by rare events or whether its origins lie elsewhere,” the team concluded.

The researchers added that given the seriousness of the ongoing COVID-19 pandemic, all efforts must be made to determine the source of the corona virus. It is important to determine whether coronavirus disease is caused by a natural coincidence, where it originates from a bat and jumps to humans through an intermediate host animal, or that COVID-19 has another origin.

The laboratory is growing

In the emergence of the novel coronavirus pandemic, many theories have emerged at the origin. One question raised a few months ago was whether the virus originated from the Wuhan laboratory, which is a Level 4 bio-safety laboratory that studies animal corona viruses.

The Wuhan Virology Institute has long isolated and obtained several coronaviruses from bats, according to laboratory director Wang Yanyi.

However, the director denied that the virus originated from the laboratory.

“After we examined the sample pathogen, we found it contained a new coronavirus. We have no prior knowledge, we also have never met, researched, or stored a virus, “he explained.

“The fact is, like others, we don’t even know about the presence of the virus, so how can it leak from our lab when we don’t have it?” she says.

Meanwhile, Chinese Foreign Minister Wang Yi said that false rumors that the virus was man-made were put there to stigmatize China. However, the country will be open to international participation to identify the source of SARS-CoV-2, as long as the investigation will be free from political interference.

Did SARS-CoV-2 adapt to humans long before the index case?

Other the latest study from Canada and the US suggests that severe acute coronavirus 2 (SARS-CoV-2) respiratory syndrome may have been adjusted before human transmission when it appeared at the end of 2019, which means that there may be progenitor populations still surviving from ancestral SARS-CoV-2 ancestors proficient. for human transmission and coronavirus disease (COVID-19) reappears.

* Important Notification

arXiv.org publishes preliminary scientific reports that are not reviewed by peers and, therefore, should not be considered conclusive, guide clinical practice / health-related behaviors, or be treated as established information.

Source:

Journal reference:

  • Piplani, S., Singh, P., Winkler, D., and Petrovsky, N. (2020). In silico comparisons of cross-species spike-ACE2 protein binding affinities; significance for the possible origin of the SARS-CoV-2 virus, https://arxiv.org/abs/2005.06199

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Heparin can stop host cells that infect SARS-CoV-2 | Instant News


Researcher at Sheffield University has developed a new test that can be used to assess the attachment of viruses to host cells and to test the potential inhibitors of viral infections.

Using the test, the team was able to demonstrate the binding of a spike protein in acute coronavirus 2 (SARS-CoV-2) respiratory syndrome to human cells expressing the angiotensin 2 converting enzyme (ACE2).

Spike proteins are the main structure used by SARS-CoV-2 to bind ACE2 receptors expressed on target cells, before infecting them and potentially causing coronavirus 2019 (COVID-19).

The SARS-CoV-2 virus binds to ACE-2 receptors in human cells, the initial stage of COVID-19 infection. Illustrated credit: Kateryna Kon / Shutterstock

The researchers also found that incubating cells with unfracted heparin stopped the surge of proteins that bind them.

The pre-printed version of paper can be accessed on the server bioRxiv*, while this paper underwent peer review.

SARS-CoV-2 infection mechanism

On binding to ACE2, the spike protein undergoes proteolytic division of the host cell into two subunits: S1, which contains receptor binding domains (RBD) and S2, which allow fusion with the host cell membrane and virus infusion.

“Serine host cell surface protein, TMPRSS2 [transmembrane serine proteinase 2]”It was also thought to be involved in virus entry and it was proposed to split S1 and S2, which led to the activation of the fusion machine,” wrote Peter Monk and colleagues.

The new test uses cells that express ACE2 and TMPRSS2

To investigate SARS-CoV-2 that binds to host cells, the team developed a new test using a transitional urinary bladder RT4 carcinoma cell line, which expresses ACE2 and TMPRSS2.

They found that the intact recombinant form of the viral surge protein containing both S1 and S2 (S1S2), but not only in the S1 domain, binds strongly to RT4 cells in a temperature-dependent manner.

The binding activity increased sharply at 37 ° C, indicating that proteolytic cleavage might be involved, the team said.

Are there other mechanisms for virus entry?

Monk and colleagues say that most cell types only express ACE2 levels that are low enough, suggesting that the surge protein might also interact with other receptor sites to get virus entry.

Certain viruses such as herpes simplex are known to bind to the host glycosaminoglycan called sulfuric deposits, the team said.

In addition, a study by one group suggested that soluble glycosaminoglycan heparin could inhibit the entry of SARS CoV-2 into “Vero” cells – cell lines derived from monkey kidney epithelium.

“These authors also demonstrated that heparin can interact with recombinant S1 RBD and cause conformational changes, leading to the suggestion that SARS-CoV-2 might use sulfate liver hosts as an additional site for attachment during infection,” the researchers wrote.

Unfracted heparin completely stops the bond

Given that the new test seems to mimic some features of SARS-CoV-2 infection, the researchers used it to test the effect of incubating RT4 cells with heparin at 37 ° C.

The team reports that unfrracted heparin (UFH) actually inhibits the binding of S1S2 cells to RT4.

Treating cells with two low molecular weight heparin (LMWHs) that has been used clinically also inhibits binding, but only partially and not as strongly.

“This shows that heparin, especially the non-diffracted form, can be considered to reduce the clinical manifestations of COVID-19 by inhibiting ongoing viral infections,” wrote Monk and the team.

Can spike proteins also bind to the host cell’s sulfate supply?

The authors say the interaction they observed between heparin and protein spike suggests that it might also bind to sulfate liver cells.

To test this hypothesis, they treated RT4 cells with a mixture of heparinase I and III, enzymes that degrade sulfate molecules, before testing the binding of S1S2.

Treatment did not result in a significant reduction in RT4 cell binding, indicating that sulfate exposure did not play a significant role in the attachment of the SARS-CoV-2 surge protein to host cells:

“Although our data support UFH inhibitory activity, it does not support the notion that sulfate deposits are very important for viral infections,” the team wrote.

What are the implications of this research?

The researchers say that LMWHs, which have been used to treat COVID-19 patients and have been shown to improve results, are much smaller than UFH and have a more predictable pharmacokinetics.

Monks and colleagues argue that their research shows that previous use of heparin should be considered when a viral infection is still an important factor in influencing the severity of the disease.

“The use of UFH rather than LMWH must also be considered, although we note that the administration and safety profile of UFH might prevent this in some cases,” they added.

Finally, the researchers said their newly developed flow cytometric test to assess the binding of SARS-CoV-2 spike protein to the host cell supports the previous findings that heparin can inhibit viral attachment to monkey kidney epithelial cells.

“Our new test could be the first screen to be useful for new inhibitors of coronavirus infection,” concluded the team.

* Important Notification

bioRxiv publishing initial scientific reports that are not reviewed by colleagues and, therefore, should not be considered conclusive, guide clinical practice / health-related behaviors, or be treated as pre-existing information.

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Studies show the wide geographical spread and evolution of betacoronaviruses from African bats | Instant News


A research group from Nigeria found evidence of long-distance transmission and spread between bats corona virus isolated in Africa and Europe and Asia, as described in a new paper available on preprinted servers bioRxiv*.

The pandemic coronavirus 2019 (COVID-19), caused by acute acute coronavirus 2 (SARS-CoV-2) acute respiratory syndrome, is the current decisive global public health crisis. This virus belongs to a large group of coronaviruses, which are known to have zoonotic potential to spread from animals to humans.

Novel Coronavirus SARS-CoV-2 This scanning electron microscope image shows SARS-CoV-2 (yellow) – also known as 2019-nCoV, the virus that causes COVID-19 – isolated from a patient in the US, emerging from the cell surface (pink ) cultured in the lab. Images were taken and colored at NIAID’s Rocky Mountain Laboratories (RML) in Hamilton, Montana. Credit: NIAID

The rich fauna and biodiversity in Africa create hotspots for emerging viral diseases. Additional opportunities for viruses are various bats that can function as reservoirs, and which can efficiently spread pathogens (for example, African fruit bats are known to reach thousands of miles during their migration cycle).

Evidence shows African bats as a potential reservoir for some betacoronaviruses that can cause serious outbreaks. Some studies also suggest that SARS-CoV-2 might be extended to the human population by zoonotic events involving SARS-related betacoronavirus.

As a result, a research group from PT Federal Medical Center in Abeokuta, Agreement University at Otta, and Ibadan University in Nigeria decided to assess the phylogenetic diversity and dynamics of the evolution of African betacoronavirus among bats, and their possible spread across continents.

Analyzing evolution trees

Three data sets were generated from the Pathogen Virus resource database for the purpose of this study. More specifically, the authors obtained a partial RNA-dependent RNA polymerase (RdRP) gene sequence from bat coronaviruses from seven African countries, four European and three Asian countries.

Information such as host species, country of origin, and date of collection are combined with sequence data to make accurate phylogenetic determination. Cluster analysis is carried out with special software to identify sequence similarities and reduce data duplication.

Phylogenetic trees were concluded using MEGA software for manual and automatic sequence alignment, distribution analysis (both geographically and evolutionally) carried out using the Monte Carlo Markov Chain implemented in BEAST (platform for Bayesian phylogenetic molecular sequence analysis) and visualized with the SpreaD3 platform interactive.

Viruses that leap over continents

The most common bat species sampled in this study is the Peters dwarf dwarf batMicropteropus pusillus). At the same time, Cameroon is the country with the highest distribution of sample bat species in this study. However, recognized data gaps must be taken into account when assessing study findings.

Peter

Peter’s Dwarf Epauletted Fruit Bat (Micropteropus pusillus). Image Credit: Dave Montreuil / Shutterstock

“These results do not always represent a true picture of the diversity of bat species in Africa, because some countries do not have sequence information for bats due to lack of supervision,” the study authors caution.

In fact, so far, only a handful of studies have been carried out in Africa on the corona virus among bats, which has left a considerable gap in epidemiological information about beta bat coronavirus in Africa.

This study adds additional knowledge about the phylogeny of the beta coronavirus sequence, which revealed that most African strains included in the D derivative – consisted of strains from Cameroon, Democratic Republic of Congo, Kenya, Madagascar, and Nigeria. This corroborates previous reports that identified a clade circulating throughout the African continent.

In addition, the researchers hinted at inter-species transmission among the lineage betacorona D virus, which allows for the potential recombination and rapid evolution of this lineage. Also, the circulation of two different B and C lineages between African bat species is indicated.

Finally, the phylogenic spread of bat coronaviruses reveals a large number of inter-continental and intra-continental spread events. The first shows the spread of the virus from China and Hong Kong to Central and South Africa, while the second shows the spread between Cameroun, the Democratic Republic of Congo and South Africa, and directly from Cameroon to Madagascar.

Study the shortcomings and conclusions

Although this insight is very important for further tracking of the corona virus, one major limitation of research is the inability to analyze the protein sequence data for these spike viruses. Such an approach will provide more relevant data about their evolution regarding transmission and infectivity.

In addition, the population demographics reported in this study may not realistically describe virus populations because the size of the dataset used is limited and may not represent the true demographic population of the bat corona virus in Africa.

“However, we have demonstrated the importance of molecular surveillance of zoonotic potentials such as coronaviruses,” the study authors said. “We advocate for broader cross-continent research involving the full genome sequences of betacoronavirus to better understand the causes of their emergence and the spread of zoonoses into human populations,” they concluded.

However, we must be aware that coronavirus-related SARS bats will continue to spread to human populations. Other possible deadly pandemics are rare; However, that opportunity increases with the frequency of the spillover. Thus the scientific community must remain vigilant.

* Important Notification

bioRxiv publishing initial scientific reports that are not reviewed by colleagues and, therefore, should not be considered conclusive, guide clinical practice / health-related behaviors, or be treated as pre-existing information.

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Symptomatic COVID-19 patients tend to be smokers | Instant News


When the COVID-19 pandemic rages in many parts of the world, a new study shows that smoking may not play an important role in increasing the severity of the disease in these patients. This study was published on a preprinted server medRxiv* in May 2020.

It is now known that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes COVID-19 disease, is more likely to cause severe pneumonia which often causes severe acute respiratory distress, multi-organ dysfunction, or both, causing Dead. Predisposing factors for serious or critical illness include older age, underlying medical conditions such as asthma, high blood pressure, diabetes, and cardiovascular disease.

However, does active smoking increase the risk? Little is known about the role of this factor, which is driving current research.

Smoking Can Increase Viral Entry – But What Is It?

Smoking increases the expression of angiotensin-converting enzyme 2 (ACE2) molecules in smokers’ tissues. ACE2 is known as the main receptor for viral attachment and entry into host cells in humans. Logically, it seems that smoking increases the risk of infection.

The SARS-CoV-2 virus binds to ACE-2 receptors in human cells, the initial stage of COVID-19 infection. Image Credit: Kateryna Kon / Shutterstock

However, some studies contradict this assumption, on the contrary showing the opposite. In Chinese studies, for example, only about 1.4% to 12.6% of COVID-19 patients are smokers. Likewise, only about 5% of New York patients, who are part of a very severe outbreak, are smokers.

Compared with national smoking statistics in the two countries, respectively around 25% and 17%, as taken from https://worldpopulationreview.com/countries/smokingrates-by-country, this is so low that the absence of direct links becomes clear. Current research is driven by the need to examine the existence of an inverse relationship between smoking and the possibility of infection with COVID-19.

How was the Smoking-COVID-19 Research conducted?

The researchers conducted a retrospective study of about 440 patients with COVID-19, all admitted sequentially to the tertiary level center in Parma, Italy. All of them have confirmed infection with nasopharyngeal swabs proved positive with the reverse transcriptase-polymerase chain reaction (rt-PCR).

The researchers took demographic, clinical, laboratory, and death data from hospital electronic health records. They also attempted to confirm smoking data with direct contact with patients or their relatives, in 423 of 441 cases.

What does the Cigarette Study show about COVID-19?

The results showed that about 62% of patients were male, and the median age was 71 years. 35% of patients died during their hospital stay, with 65% excluded after clinical recovery.

About 5% of them actively smoked at the time of the study, while 10% were smokers but had quit. The rest are not smokers.

With a closer analysis of clinical characteristics, it was observed that more men died from this disease. Although they constitute 62% of the total patients, they account for 72% of deaths and only 59% of survivors. Those who died were also older, at an average age of 76 years, compared to 67 years for those who survived. However, this is not statistically significant.

Again, the presence of certain medical diseases that coexist is significantly more common among deaths. For example, patients with a history of cardiovascular disease each contribute 21% and 10% of those who die and survive.

While hypertension was present in 61% and 56% of deaths and survivors, respectively, while diabetes was present in 26% and 18% respectively, this was not significant.

The median level of D-dimers, which is a marker of inflammation, is almost double the value in those who die compared to those who survive. There was a much smaller but significant increase in the median level of C-reactive protein, which also increased inflammation, among those who died.

However, with smoking, around 6% and 4% of those who die and live are current smokers, which means there is no significant difference. Similarly, the number of former smokers and never smokers was almost identical in the two groups.

What Does This Study Mean for People Affected by COVID-19?

Italy has experienced the second highest number of COVID-19 deaths in the European Union (EU). However, in this retrospective study, only 5% of smokers patients currently, even though the prevalence of the smoking population is 24% in Italy. This finding, therefore, agrees with previous research in China and the US.

This study did not include asymptomatic patients by design, and therefore the conclusions should be limited to cases of COVID-19 hospitalized or symptomatic.

The researchers said, “Current research shows that smokers can carry several types of protective mechanisms from symptomatic SARS-CoV-2 infections.” However, as scientists have warned, carefully designed controlled studies alone can validate this impression.

The mechanism underlying the low prevalence of smoking in the population of COVID-19 patients treated in this hospital is purely speculative at this time. For example, exposure to cigarette smoke can suppress the immune response, which contributes to low systemic inflammation compared to those who have never smoked.

By modulating the normal intensity and spectrum of the immune system against viruses, due to “continuous inflammatory insults,” cytokine storms may be less likely to occur in COVID-19 patients, making them less susceptible to severe or symptomatic disease.

The importance of ensuring the protective role for smoking in this pandemic is that, according to the researchers, “it can help uncover the molecular mechanisms underlying predisposition to SARS-CoV-2 infection, then also potentially being exploited by newly designed protective drugs. “

* Important Notification

medRxiv publish initial scientific reports that are not reviewed by colleagues and, therefore, should not be considered conclusive, guide clinical practice / health-related behaviors, or be treated as pre-existing information.

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Italy develops vaccine candidates that neutralize SARS-CoV-2 in mice | Instant News


As the world wrestles with coronavirus (COVID-19), scientists race to develop treatments and vaccines to fight viral infections. Although many ongoing trials show hope in fighting the new coronavirus, Italian researchers claim they have developed a vaccine that can neutralize the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in animal cells.

Team of Takis Biotech, a biotechnology company based in Rome, Italy, has conducted tests at Lazzaro Spallanzani Hospital in Rome, which specializes in infectious diseases. The results of this initial study in mice were very positive. After a single dose, five DNA-based vaccine candidates were able to induce a strong antibody response to the SARS-CoV-2 protein spike in just 14 days.

Binding the coronavirus (red) spike protein to the ACE2 receptor (blue) in human cells leads to virus penetration in cells, as illustrated in the background. Credit Illustration: Juan Gaertner / Shutterstock

One step closer

Pressure continues to burn for most pharmaceutical companies to develop coronavirus vaccines for SARS-CoV-2. Although there are many promising candidates, a strong and effective landing requires hard work.

However, in the world’s first breakthrough, scientists developed the SARS-CoV-2 vaccine candidate by growing antibodies in mice. This is the first time scientists have found a way to neutralize SARS-CoV-2. The biotech company said it would begin human trials in June.

“According to the Spallanzani Hospital, as far as we know, we are the first in the world so far to have demonstrated the neutralization of the corona virus with a vaccine. We hope this happens to humans too, “Luigi Aurisicchio, CEO of Takis Biotech, said in a statement.

Tests conducted by Italian scientists show that the vaccine has the potential to work against SARS-CoV-2 in humans. Furthermore, the company is exploring another sophisticated platform with the drug company, LineaRx, in an effort to develop further vaccines.

To succeed in this endeavor, biotech companies need support from not only the Italian government but also international institutions and partners who might want to help speed up the process.

Aurisicchio stressed that this is not competition or race, and if companies and scientists join hands, the world can win against the deadly virus.

Will there be a vaccine at the end of this year?

Director of the National Institute of Allergy and Infectious Diseases, Dr. Anthony Fauci, said it might take a year and a half before the world can have a vaccine for the new corona virus.

The statement came after Pfizer, a pharmaceutical company, claimed it could have a vaccine ready for emergency use in September. However, Fauci said the most realistic date was January. Normally, vaccines can take around five to 15 years before reaching the market, but by tracking the process quickly, it may be shorter.

At present, the record for developing a vaccine is four years, while the general vaccine is for chicken pox and influenza takes 28 years to develop. The vaccine for measles comes at an accelerated rate of four years. However, the coronavirus vaccine is still far away, given the process required for its approval for human use.

Some say that the usual barriers to vaccine development have been removed amid a coronavirus pandemic, therefore, making it faster to have a vaccine that works around early next year. Take, for example, the 2009 H1N1 outbreak where scientists could develop a vaccine against the virus in just five months.

Meanwhile, the World Health Organization said that deliberately infecting healthy volunteers with viruses could accelerate vaccine studies on SARS-CoV-2. Although such studies can pose a danger to participants, this is needed in dire situations such as the coronavirus pandemic.

Challenge studies, where vaccines, prevention and treatment are tested directly on volunteers who have information, can help speed up the development and approval of vaccines needed.

“They can be substantially faster to conduct than vaccine field trials, in part because far fewer participants need to be exposed to experimental vaccines to provide initial estimates and efficacy and safety. Such studies can be used to compare efficacy many vaccine candidates and therefore choose the most promising vaccine for larger studies, “the report wrote.

With more than 100 vaccine candidates currently, health agencies see the feasibility and safety of conducting a challenge study.

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Researchers show how bats carry the MERS coronavirus | Instant News


The University of Saskatchewan (USask) research team has revealed how bats can carry Middle Eastern respiratory syndrome (MERS) coronavirus without getting sick – research that can explain how corona virus make the jump to humans and other animals.

Corona viruses such as MERS, Severe Acute Respiratory Syndrome (SARS), and more recently the SARS-CoV-2 virus that causes COVID19, are thought to originate from bats. Although these viruses can cause serious and often fatal diseases in humans, for reasons not previously well understood, bats do not appear to be injured.

Bats do not get rid of viruses and do not get sick. We want to understand why the MERS virus doesn’t kill the bat’s immune response like humans do, “

Vikram Misra, USask Microbiologist, University of Saskatchewan

In a new study published in Scientific Report, the team has shown for the first time that cells from insect-eating bats can be continuously infected with the MERS corona virus for months, because of the important adaptation of bats and viruses that work together.

“Instead of killing bat cells as viruses do with human cells, the MERS coronavirus enters a long-term relationship with the host, which is maintained by the bat’s unique” super “immune system,” said Misra, the corresponding author in the newspaper. “SARS-CoV-2 is estimated to operate in the same way.”

Misra said teamwork showed that pressure on bats – such as wet markets, other diseases, and possible loss of habitat – might have a role in spreading the corona virus to other species.

“When bats experience stress on their immune system, it disrupts the balance of the immune-virus system and allows the virus to multiply,” he said.

The research was conducted at the USask Vaccine and Infectious Disease Organization – International Vaccine Center (VIDO-InterVac), one of the largest level 3 detention research facilities in the world, by a team of researchers from USask College of Veterinary Medicine and VIDO-InterVac.

“We see that MERS coronaviruses can quickly adapt to certain niches, and although we don’t fully understand what’s happening, this shows how coronaviruses can jump from species to species so easily,” said VIDO-InterVac scientist Darryl Falzarano, who led the bat study, developed the first potential treatment for MERS-CoV, and led the VIDO-InterVac effort to develop a vaccine against COVID-19.

So far, the SARS-CoV-2 virus has infected more than 3.5 million people worldwide and killed seven percent of those infected. In contrast, the MERS virus infected nearly 2,500 people in 2012 but killed one out of every three infected. There is no vaccine for SARS-CoV-2 or MERS. While camels are known as MERS-CoV brokers, bats are thought to be ancestral hosts.

Corona viruses quickly adapt to the species they are infected with, Misra said, but little is known about the molecular interactions of these viruses with their natural bat hosts. A study led by USask 2017 shows that bat coronaviruses can survive in their natural bat host for at least four months of hibernation.

When exposed to the MERS virus, bat cells adapt – not by producing inflammatory proteins that are a sign of illness, but by maintaining a natural antiviral response, a function that is turned off in other species, including humans. Simultaneously, the MERS virus also adapts to bat host cells very quickly to mutate one particular gene, he said.

Operating together, this adaptation produces the virus that is left in the long run in bats but is considered harmless until something – such as a disease or other stress trigger – disturbs this delicate balance.

Next, the team will shift its focus to understanding how the MERS virus borne by bats adapts to infection and replication in camels (a group of even-ended ungulates that include camels) and human cells.

“This information may be important for predicting the next bat virus that will cause a pandemic,” Misra said.

Source:

Journal reference:

Banerjee, A., et al. (2020) Selection of viral variants during persistent infection of insect-eating bat cells with Middle Eastern syndrome coronavirus. Scientific Report. doi.org/10.1038/s41598-020-64264-1.

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