#and now we have 2 new highly contagious and deadly viruses going around
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Something I've been wondering more and more about in the last few years is if this what people in the stories we tell about the apocalypse felt like. I don't think so. So often when we talk about the apocalypse it happens fast, a quick and violent transition from Before to After. They don't often get a chance to see it coming, for it to happen so slowly that everyone convinces themselves that it isn't happening. The chance to see the car crash coming, but be powerless to stop it because the people driving the car are too busy telling you nothing is wrong to steer you out of the way. I wonder if it's wrong to be so convinced that this is the End, but I don't know what other conclusion I'm supposed to come to. We won't go out with a bang, but with a wimper. I'm just sad we didn't get one of the fun apocalypses.
#end speaks#neg#covid isn't over#and now we have 2 new highly contagious and deadly viruses going around#and the way people are talking about it sounds a lot like december 2019
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How Do We Stop The Next Pandemic? Here's A New Strategy
April 20, 2021
MICHAELEEN DOUCLEFF
Shane Tolentino
In movies such as Contagion, a pandemic begins in a flash. A deadly virus spills over from an animal, like a pig, into humans and then quickly triggers an outbreak.
But that's not actually what happens, says Dr. Gregory Gray at the Duke Global Health Institute. "It's not like in the movies," he says, "where this virus goes from a pig in Indonesia and causes a pandemic."
Over the past few decades, the U.S. government has spent hundreds of millions of dollars hunting down new viruses in animals, largely wild animals, in hopes of stopping a pandemic. And yet those efforts failed to find – and stop — SARS-CoV-2, the virus that causes COVID-19, before it spread around the world.
Now, writing in the journal Viruses, Gray and his colleagues propose an alternative approach to hunting down new viruses, which, they believe, will have a better chance of stopping the next pandemic.
The approach takes into account the latest information about how human pathogens emerge from wildlife and how pandemics begin.
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Almost all viral infections come from animals, says virus expert Eddie Holmes at the University of Sydney. The virus hangs out in an animal — say a bat, pig or bird — for centuries, even millennia. And when given the opportunity, it jumps into a person. Scientists call this process "spillover."
Some viruses are particularly good at spilling over, and so they do it much more frequently. "Unfortunately, coronavirus is in that category," Holmes says. "If you look at the evolution of coronavirus, you see a lot of jumping around from host to host."
That's why scientists are so concerned about another coronavirus erupting — and causing a future pandemic. But which one?
There are likely thousands of coronaviruses across the planet living in virtually all animals, Holmes says. Finding the next "big one" is like looking for a submicroscopic needle in a haystack scattered across the globe — in forests, farms and caves.
For decades, scientists have hunted for undiscovered viruses before the spillover occurs. Specifically, they've looked for viruses inside wild animals, such as bats, where SARS-CoV-2 originates. They've trapped tens of thousands of bats, individually, and then taken samples from their saliva, feces and blood. (Here at Goats and Soda, we have reported on several studies such as this in Southeast Asia and in West Africa.)
This process is time-consuming, expensive, and, as Gray points out, it failed to stop the COVID-19 pandemic.
Why? Gray says one reason is you can't tell which viruses in the bats are going to be dangerous to people — and which ones will never leave the bats.
"These projects have discovered a lot of viruses, but those viruses have not always — and frankly, infrequently — been associated with illness in humans," he says.
But what if there is an approach to focus only on the viruses that are already spilling over into humans and making some people sick. "We'll get more bang for our buck. It'll be more efficient, and we'll pick up more viruses that are threatening people," he says.
What Gray and others are starting to realize is that virus spillover works a bit differently than how scientists originally thought. For starters, spillovers aren't rare. There are many hidden spillovers happening every day, Gray says.
"[New] viruses are assaulting humans' immune systems all the time," he says, especially for people who work closely and frequently with animals, such as farmers and ranchers.
But the vast majority of these spillovers are dead ends. A virus may jump into a person or two. And it might make them sick. But at this point, the virus doesn't have the ability to spread from one person to the next. And so the outbreak stops.
If the virus has the opportunity to spill over and over again, it may begin to evolve in ways to evade the human immune system and possibly even escape from the human body. At that point, the virus may begin to spread from one person to the next.
"The virus has to take hold. It has to adapt and then it can become highly transmissible," Gray says. "Evolutionary science would suggest that it's a process."
This step-by-step process takes years, decades, even centuries. And, Gray says, it gives scientists a more efficient way to zero in on the viruses in animals that are most dangerous to people. "We can catch viruses while they're crossing over before they fully adapted to humans," he says.
To do that, Gray says, scientists need to look inside people who are constantly in contact with animals, who are mostly likely to get sick from the initial spillovers before a virus becomes contagious.
For example, Gray and his colleagues recently searched for undiscovered coronaviruses in people sick with pneumonia — and quickly found one. The team screened about 400 samples from pneumonia patients in Sarawak in Malaysia. They found at least four people infected with a new coronavirus that likely came from an animal.
"I can't get into too many details because it's not published yet," he says. "But there's an inkling that other researchers are using a similar strategy, and they may have found another [new] virus, too."
In other words, this alternative approach may have already caught not one, but two new coronavirus pathogens, before a big outbreak has occurred.
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The 30 Day Pain Relief Challenge Kick Off
It’s 2021 and time to kick off the 30 Day Pain Relief Challenge!
But first I want to acknowledge what’s on everyone’s mind.
2020 began with an unexpected crisis, the COVID-19 pandemic. A new corona virus strain emerged; highly contagious and deadly for certain individuals, and for which there was no vaccine. As of this writing, over 85 million people worldwide have contracted the virus, with 1.85 million dying from it. The United States is being hit the hardest, with 20.8 million cases and 352,000 dead. The numbers are expected to spike following the holiday season, thanks to many people choosing to get together in large groups and ignoring the risk. So please, remain extra vigilant the next two weeks because chances are, there are more viruses around you than there were a month ago, ready to find a new host.
As we navigate through COVID-19 in 2021, life must still go on. I know many have been hurt economically, and their number-one priority is to find a way to get back on their feet. It is not an easy thing to do, especially if you lost your job and the life skills you possess are in an industry that has been permanently impacted by the pandemic. If this describes your situation, I sincerely hope you find a way to re-position or re-invent yourself, to get back to earning a living.
While COVID-19 dominates the news and peoples’ attention, we must not lose focus on the many other challenges life presents that also need our attention. How would you rate your health at the start of the new year? How about your energy levels and endurance?
Quarantining and social distancing have a way of discouraging exercising and promoting over-eating, a terrible combination to health. When one is restricted from going outside and going to a gym (although a gym is not necessary for staying fit, but I digress…) and constantly bombarded by news of doom and gloom, the tendency is to stay home, surf the web, and eat, more than you typically do (what else is there to do in such a scenario?). And for many, the choice is high-calorie comfort food. This can lead to unwanted weight gain, muscle atrophy, joint pain, and so on.
If you are not feeling 100%, then I encourage you to open all the emails I’ll be sending over the next 30 days—the 30 Day Pain Relief Challenge is about to kick off, and email is how it will be executed.
And what exactly is the challenge? It’s about challenging yourself to get out of your comfort zone and do all the things I will suggest in the coming days so that you can get out of pain, or significantly knock it down to levels you haven’t experienced in a long time.
The other reward may be that you will lose 10 pounds or more; will have more energy, and will notice that your mind/ thinking is clearer. This is because the methods I’ll go over target your body and all its systems; not just the area of pain. It is wholistic.
But first let me explain how you will be measuring your results. After all, pain is subjective. You need some kind of tool to quantify your improvement, so read on.
Pain, aches, discomfort or whatever you want to call it affects your health. There is mental health and physical health; both important to happiness in different ways. Your physical and mental health are impacted, even just a little and perhaps unnoticeable to you, if you have chronic pain/aches/discomfort. Less-than-optimal physical and mental health impacts quality of life. Quality of life in this sense refers to your ability to physically do what you need or want to do; whether it be your job; recreational activity such as playing golf or swimming; or activities of daily living; i.e. taking care of yourself and your personal needs.
Why You Might Have a Disability if You Have Pain
If you live with chronic pain, you likely have some degree of disability.
“Me disabled?” you might be thinking. “No way!”
The word “disability” is often misconstrued. Disability doesn’t necessarily mean “disabled” and in a wheel chair. It simply means not being able to perform a certain task without some degree of difficulty or impediment; or not being able to do it at all.
Doctors (medical examiners) who issue disability certificates or write medical-legal reports are tasked to determine the degree to which someone is disabled. Their findings determine the patient’s disability compensation from the insurance company or government agency. They use observation, physical exam procedures, diagnostic tests like X-rays and nerve conduction; and instruments to measure strength, pain perception, reflexes, coordination, and range of motion. Any deficiency is expressed as a percent disabled, and there are laws that define levels of disability.
For example, in the insurance industry, the loss of both eyes, or the loss of two limbs equates to “100% disability.” Not being able to maintain a tight grip could be rated as 20% disability if the person’s occupation requires power gripping machinery.
Disability can also be subjectively quantified using Disability questionnaires where the patient rates his/ her ability to perform certain tasks on a scale of zero to some number; and the level of pain. In some questionnaires, the zero rating means you have zero difficulty doing the task (best score), while in others the zero rating means you cannot do the task at all (worst score).
For example, the following is one section of the Oswestry Low Back Pain Disability Questionnaire. Imagine having low back pain and rating yourself (0 to 5) on your ability to lift things:
LIFTING:
0 – I can lift heavy weights without extra pain
1 – I can lift heavy weights but it gives extra pain
2 – Pain prevents me from lifting heavy weights off the floor, but I can manage if they are conveniently positioned, i.e. on a table
3 – Pain prevents me from lifting heavy weights, but I can manage light to medium weights if they are conveniently positioned
4 – I can lift very light weights
5 – I cannot lift or carry anything at all
When rating yourself, you must try to be as objective as possible—don’t over rate your ability; nor under rate it. Give each question some thought.
Then, you add up the numbers, divide it by the total number of points and multiply by 100 to get a percentage score.
If the zero rating is assigned to “full ability to do the task” (like the Oswestry above), then the score is interpreted as “percent disabled.” So, an individual with no low back disability whatsoever will score zero out of 50 and his rating will therefore be zero percent disabled; i.e. 100% functional. If his score is 30, then 30/50 x (100) = 60% disabled.
Below is an example of an Oswestry Low Back Pain Disability Questionnaire completely filled out:
In the above example, the total points out of all ten questions is 19, which is considered a Moderate disability, out of No, Mild, Moderate, Severe and Total Disability. In this case, 19/50 x 100 = 38% disabled due to low back pain. Now this person has a baseline for his condition, and can set goals to lower it each time; perhaps to 20% after a month, then 10% after three months of therapy.
If the zero rating is instead assigned to “no ability to do the task,” the score is interpreted as “percent functional.” This is how the Upper and Lower Extremity Disability questionnaires are designed. So a score of zero in this case means zero percent functional (totally disabled), and 30% means you are 30% functional (you lost 70% function in that limb).
Please note that Disability questionnaires are used as tools to quantify and set baselines for pain and functional capacity; your scores do not officially establish any disability you may have, they simply provide a more tangible interpretation of pain.
Quantifying pain/disability, even if subjective, gives you a sense of how significant it is; i.e. how much it affects your life. Secondly, it can be used as a tool to measure your improvement over time, after doing some therapy and/or rehabilitation (strength and coordination exercises). This lets you know if what you did works for your condition, and therefore, whether to continue or discontinue it.
For example, if your baseline Oswestry score was 60%, and you were prescribed some McKenzie exercises for one week and a follow- up score was 40%, it suggests that those exercises improved your condition and you should continue or progress to the next level. If it was 60% or higher, you should discontinue the exercises and try another approach.
You don’t have to see a doctor to use Disability questionnaires to subjectively assess your disability. They are fairly straightforward to use and you can download the forms from the internet (see below; I’ve done it for you).
Determine Your Pain/Disability Baseline
If you have low back pain, neck pain, shoulder pain, or lower or upper limb pain then I suggest monitoring your condition using the appropriate disability questionnaire. If you are getting therapy, your doctor should be having you fill these forms (or something similar) out each visit and going over the results with you. It’s substandard care if you don’t know if the therapy you are getting or exercises you are doing is helping; these questionnaires will prompt you to think about the change or lack of change in your functional capacity, and will help you assess your care so that you can take appropriate action.
Below you will find forms to assess any musculoskeletal pain you are having. If you wish to participate in the 30 Day Pain Relief Challenge, print out the appropriate disability questionnaire; rate your abilities as objectively as you can and calculate your score; set it aside, and be ready to fill out a new questionnaire after 30 days of diligently doing the things I will cover over the next 30 days.
My goal is for participants to experience at least a 50% improvement in their pain/ disability scores. If you have any friends who might be interested in participating, please refer them to my site, https://PainandInjuryDoctor.com and have them enter their email in the opt in form.
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India Blames a Virus Variant as its Covid-19 Crisis Deepens Doctors, the public and the media point to anecdotal evidence of infections even among the vaccinated. Scientists say the data is too thin and cite other reasons behind the country’s second wave. NEW DELHI — At Sir Ganga Ram Hospital, a huge facility in the middle of India’s capital, 37 fully vaccinated doctors came down with Covid-19 earlier this month. The infections left most with mild symptoms, but it added to their growing fears that the virus behind India’s catastrophic second wave is different. They wonder if a more contagious variant that dodges the immune system could be fueling the epidemic inside the world’s hardest-hit nation. So far the evidence is inconclusive, and researchers caution that other factors could explain the viciousness of the outbreak, which has overwhelmed India’s capital so quickly that hospitals are entirely overrun and crematories burn nonstop. Still, the presence of the variant could complicate the taming of India’s Covid-19 disaster. “The current wave of Covid has a different clinical behavior,” said Dr. Sujay Shad, a senior cardiac surgeon at Sir Ganga Ram Hospital, where two of the doctors needed supplemental oxygen to recover. “It’s affecting young adults. It’s affecting families. It’s a new thing altogether. Two-month-old babies are getting infected.” India’s outbreak worsened even further on Wednesday, as the authorities reported nearly 3,300 daily deaths. That brings the official total to nearly 201,200 people lost, though experts believe the true figure is much higher. Daily new infections also surged to nearly 357,700, another record. As supplies run dangerously low and hospitals are forced to turn away the sick, scientists are trying to determine what role variants of the virus might be playing. They are working with precious little data. India, like many other countries, has not built up a robust system to track viruses. India’s worries have focused on a homegrown variant called B.1.617. The public, the popular press and many doctors have concluded that it is responsible for the severity of the second wave. Researchers outside of India say the limited data so far suggests instead that a better-known variant called B.1.1.7 may be a more considerable factor. That variant walloped Britain late last year, hit much of Europe and is now the most common source of new infection in the United States “While it’s almost certainly true B.1.617 is playing a role, it’s unclear how much it’s contributing directly to the surge and how that compares to other circulating variants, especially B.1.1.7,” said Kristian Andersen, a virologist at the Scripps Research Institute in San Diego. Beyond the variants, scientists believe there are other, possibly more obvious factors that could be powering India’s deadly second wave. India has just scraped the surface in terms of vaccinating its population, with less than 2 percent fully vaccinated. Experts also blame lax public behavior after last year’s first wave and missteps by Prime Minister Narendra Modi, such as recently holding large political rallies that may have spread the disease and sent a message to the people that the worst was over. “There is a lot of jumping to conclusions that B.1.67 is the explanation for what’s happening,” said Jeffrey Barrett, director of the Covid-19 genomics initiative at the Wellcome Sanger Institute in Britain. “These other things are probably more likely to be the explanation.” Preliminary evidence suggests that the variant is still responsive to vaccines, although slightly less so. India relies heavily on the Oxford-AstraZeneca vaccine, which clinical trials show is less powerful than the vaccines made by Pfizer-BioNTech and Moderna and could perhaps be more easily thwarted by mutations. “For now the vaccines remain effective, but there is a trend toward less effectiveness,” said Dr. Céline Gounder, an infectious disease physician and epidemiologist at Bellevue Hospital in New York. Updated April 28, 2021, 8:29 a.m. ET In India, a number of doctors point to anecdotal evidence that people who have been fully vaccinated are getting sick. Those doctors also say they are seeing children with serious symptoms, such as severe diarrhea, acidosis and falling blood pressure, even among otherwise healthy patients. “This is very different from what we saw last year,” said Dr. Soonu Udani, head of critical care services at the SRCC Children’s Hospital in Mumbai. Researchers say other factors could lead to more infections among young people, such as India’s schools, which had started reopening in recent months after the country’s first wave. The variant in India is sometimes called “the double mutant,” though the name is a misnomer because it has many more mutations than two. It garnered the name because one of its three versions contains two genetic mutations found in other difficult-to-control variants of the coronavirus. One is present in the highly contagious variant that ripped through California earlier this year. The other is similar to one found in the variant first identified in South Africa and is believed to make the vaccines slightly less effective. “There are variants that are more transmissible than what we all coped with a year ago,” Dr. Barrett said of the many variants circulating in India. “Things can change really quickly, so if a country doesn’t react quickly enough, things can go from bad to very bad very quickly.” Scientists say that different variants seem to dominate specific parts of India. For instance, the B.1.617 variant has been detected in a large number of samples from the central state of Maharashtra. By contrast, the B.1.1.7 variant is rising quickly in New Delhi, said Dr. Sujeet Singh, director of India’s National Centre for Disease Control. It was prevalent in half of samples evaluated at the end of March, up from 28 percent just two weeks before. The B.1.617 variant is also circulating in New Delhi, he added. But ultimately, the data from India is too thin to parse the distribution of variants around the country. Despite the huge number of new infections, India is performing very little genomic sequencing. In December, the government tapped a group of 10 laboratories and set an ambitious target to sequence 5 percent of samples across the country every month. But so far, less than 1 percent of samples collected has been sequenced. A report in The Wire, an Indian online publication, pointed to logistical challenges, bureaucratic red tape and the lack of funding as some of the reasons. “They simply aren’t well-resourced enough, as sophisticated as their scientists and doctors might be,” Dr. Gounder said. Apart from Britain, few other countries have been monitoring variants closely. The United States was also sequencing less than 1 percent of samples and ramped up its efforts only in recent weeks. Officials in India are trying to track how many fully vaccinated people have fallen ill, a measure called the breakthrough infection rate. That could suggest how virulent any variant in India might be. They have focused on frontline medical workers, who are more likely to have received both doses of the AstraZeneca vaccine. So far, data from the Indian Council of Medical Research up to April 21 shows an extremely low breakthrough infection rate, though perhaps not as low as that of the United States. The data shows 0.02 percent to 0.04 percent of vaccinated people falling ill. The rate in the United States, which relies on different vaccines, is 0.008 percent. At Sir Ganga Ram hospital, the 37 doctors who became infected after immunization had received their first dose between late January to early February and then their second dose four to six weeks after that. The hospital employs about 500 doctors. Dr. Shad, the cardiac surgeon, was reluctant to jump to conclusions about variants breaking through the immunizations. “I don’t think anyone has the serological data” to answer that, he said. A broad lack of data plagues the scientific chase for variants and whether they are contributing to the severity of India’s crisis. Fast-moving mutations complicate the picture because it isn’t immediately clear how quickly they spread or how they respond to vaccines. In India, the health care system wasn’t on alert for the impact of variants at home, even as they began to spread globally, said Dr. Thekkekara Jacob John, a senior virologist in the southern state of Tamil Nadu. “We were not looking for variants at all,” he said. “In other words, we missed the boat.” Hari Kumar contributed reporting. Source link Orbem News #blames #Covid19 #crisis #Deepens #India #Variant #Virus
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How to find the next pandemic virus before it finds us
More than 100 years ago, a deadly flu virus circled the globe. It caused the influenza pandemic of 1918-1919. Before it was over, this disease had sickened an estimated 500 million people. That was one-third of everyone alive at that time. Some 20 million to 50 million people died.
Flash forward to the 1970s. People in a small Central Africa village fell ill with a mystery disease. It caused bleeding that would not stop. Soon, this Ebola virus would spread to other villages.
Explainer: What is a coronavirus?
What do these famous viral outbreaks have in common with the new coronavirus disease known as COVID-19? Scientists believe animals initially carried the viruses that cause all three. Such diseases are known as zoonoses (ZOH-wuh-NO-sees). That means they started in animals and later spread to people.
Flu likely came from birds. Researchers think that bats may have been the source of the Ebola virus and of COVID-19. “Roughly 75 percent of global pandemics and disease outbreaks caused by new viruses come from wild animals,” says Tracey Goldstein. She’s a virus detective at the University of California, Davis. She hunts for new viruses among the wild animals of Africa.
When viruses pass from wildlife to people, it’s called a spillover. Fortunately, spillovers that affect more than a handful of people are rare. But big spillovers do seem to be happening more often, Goldstein and others observe.
To prevent the next big outbreak, researchers around the world are scouting the role of wild animals in the emergence of new human diseases. Scientists want to understand which groups of animals or viruses pose the biggest risks. What they learn could help us all.
Virus hunters turn to bats
Viruses are tiny, infectious particles. They “live” but aren’t technically alive. They can reproduce only within the cells of a living host. That host can be an animal, plant, bacterium or fungus.
“Humans carry lots of viruses,” notes biologist Kevin Olival. He works for a group called the EcoHealth Alliance. Based in New York City, it tries to protect people and wildlife from new diseases. Measles and common skin warts are examples of viral diseases. But not all viruses are harmful, Olival notes. Some seem to have no effect on the body. It all depends on the virus and the host.
Scientists Say: Outbreak, Epidemic and Pandemic
“All mammals carry viruses,” Olival says. “But there’s something about bats that might be a little different or unique.” That’s why he has made bats — and the viruses they carry — a focus of his research.
Bats are thought to be the host for a number of relatively new viruses that can sicken people. Among them are the Ebola virus, Marburg virus, Nipah virus and SARS-CoV-2. That last one is the coronavirus responsible for COVID-19. In 2002, another coronavirus from bats caused a massive outbreak of SARS (severe acute respiratory syndrome) in China. Highly contagious, SARS showed some similarities to COVID-19.
Olival and his colleagues at EcoHealth Alliance have been studying the coronaviruses hosted by bats. In China alone, they found 400 different strains of these viruses. Most of them probably wouldn’t sicken people, he says. To figure out which can, researchers will have to perform tests. That will involve taking human cells and infecting them with each virus in the lab, he explains.
See all our coverage of the new coronovirus outbreak
Or, researchers could survey people living near the bats and sample their blood. Olival’s colleagues at EcoHealth Alliance were part of a research team that did just that. They worked in rural Chinese villages. And there they found signs that mini coronavirus spillovers have been underway.
The researchers surveyed 1,585 people. They collected blood from 1,497 of them. Of these, 265 (almost one in every six people) reported some symptoms in the past year of a SARS- or flu-like disease. Nine people also tested positive for SARS-like coronaviruses that had previously been found in area bats. None of these nine remembered having any interactions with bats. However, the people who had reported SARS-like or other severe respiratory infections did say they had been exposed to wildlife and livestock.
This suggests that there may be zoonotic illness in these populations. And, the researchers add, the novel bat-linked viruses in the blood of some of these villagers offers “evidence for bat-borne coronavirus transmission to people.” Hongying Li of the EcoHealth Alliance and her colleagues reported their findings in the September 2019 Biosafety and Health.
Why bats?
Researchers don’t know precisely why bats are a good host for many deadly viruses. But they have some ideas. Bats are the only mammals that fly. (Other “flying” mammals don’t fly. They only glide.) Flying is hard work. A bat needs about twice as much energy for its flight muscles as a similar-sized rodent needs to run on the ground. Putting all their energy into flying could leave bats with less energy to fight off sickness or injury. But that doesn’t happen. Scientists think that flight may have led bats to evolve stronger immune systems than other mammals.
Judilee Marrow collects a saliva sample from a rodent in Gabon, Africa. She and her colleagues at Smithsonian’s National Zoo take these samples to the lab where they will be investigated for viruses.C. Whittier
A unique immune system might mean a unique response to viruses. For instance, one recent study showed that bats’ bodies can limit the ability of a virus to trigger dangerous inflammation. That response may push viruses to evolve in ways that let them rapidly spread from cell to cell. And if that altered virus now spreads to a species without such a strong immune system, the new victim might get super-sick — and quickly.
Olival’s work has mainly taken him to Malaysia. This Southeast Asian nation has more than 100 bat species. He wants to better understand how viruses there might spread between different groups of bats. So he collects genetic information from bats and bat viruses. He uses that to build computer models. These computer programs predict which bat viruses could cause real harm in people and other animals, he explains.
Explainer: What is a computer model?
Some, such as the Nipah virus, can infect a wide range of animals. Several species of fruit bats in Southeast Asia carry that virus without getting sick. But in 1999, Nipah virus triggered a deadly outbreak among Malaysia’s pigs and pig farmers.
Goldstein’s team performed similar work with bats in Sierra Leone. That’s a country in West Africa. Her group had suspected local bats carried the Ebola virus. It was not a wild guess. In 2014 and 2015, an Ebola outbreak killed nearly 4,000 West Africans. And in January 2015, researchers linked the start of that outbreak to a two-year old boy in Guinea. He liked to play in a hollow tree where insect-eating bats used to live.
Scientists perform lab work in Tanzania to look for new viruses from wild animals.USAID PREDICT
Villagers had burned the tree down. But insect-eating bats had been linked to earlier Ebola outbreaks. That made these animals the most likely suspects in the West African outbreak, explained Fabian Leendertz at the time. He works at the Robert Koch Institute in Berlin, Germany. His team described how its detective work led to this conclusion in the January 2015 EMBO Molecular Medicine.
“We wanted to see what other viruses were circulating in bats and other animals” in Sierra Leone, recalls Goldstein. That country shares a border with Guinea. Knowing what viruses the bats hosted might help researchers better understand their viral risks to people.
The bats in Sierra Leone carried Marburg virus, Goldstein’s team discovered. It’s a close relative to the Ebola virus. Marburg causes severe bleeding in people, just as Ebola does. But Marburg has not yet sickened anyone in Sierra Leone. The researchers found the disease in bats before any people got sick. But now Goldstein’s group knows that bats pose a Marburg risk there.
Protecting people and wildlife
Figuring out where potentially dangerous viruses come from is only part of the challenge. Research also needs to identify what activities put people at risk of exposure to animal viruses, note Goldstein and Olival.
These new viral diseases aren’t passing from wild animals to people because animals are going out of their way to mess with us. “It’s because we interfere with them,” says David Quammen. He’s a science journalist. And he researched the topic for a book he wrote eight years ago, Spillover: Animal Infections and the Next Human Pandemic.
Ecology is a branch of biology that explains how different living things interact with each other and their surroundings. And “humans are changing ecology,” observes Hellen Amuguni. She’s a veterinarian and infectious-disease researcher at Tufts University in North Grafton, Mass. People can alter ecology by cutting down trees in forests. Or they might build roads or cities through the landscape. Some might hunt down wild animals for pets or food, explains Amuguni. All of these activities can impact the local ecology in ways that scientists are just beginning to understand.
One new study backs that up. Christine K. Johnson of UC Davis and her colleagues published it April 8 in the Proceedings of the Royal Society B. They found that hunting, wildlife trade, habitat destruction and the spread of cities into areas that were previously wildlands all increase the risk of virus spillovers. Selling wild animals at markets or shrinking their natural habitat can jumble together species that wouldn’t normally meet.
Hongying Li visits a live-animal food market in China. All animals, including these, may harbor harmful viruses. Li’s team is surveying the types of wildlife and livestock that local consumers might encounter.EcoHealth Alliance
Scientists think that the new coronavirus might have come from a live animal market in China. The virus could have passed directly from a bat to a human. Or it could have passed from a bat to another animal that was touched by a human. Wild animals kept in cages come into close contact with people and other animals. That provides more chances for viruses to spill over from one species to another.
And these events can be just as bad for wildlife as for people, points out Christopher Whittier. He’s a veterinarian at Tufts who studies human diseases that spill over into wildlife. “Understanding what viruses are in wildlife can help us to protect wild animals, too,” he notes.
The human measles virus can sicken and even kill mountain gorillas. Researchers in Africa discovered this back in 1988. People would gather to watch the apes in Rwanda’s national parks. At the time, no one knew that someone’s sneeze can infect local primates with colds and other viral diseases. And there’s plenty of opportunity for that. Each year, park gorillas and chimps were exposed to more people — and their germs — than would visit the average person’s house over a lifetime.
After scientists realized that these wild animals could get sick, practices changed. Today, people visiting wildlife parks in Africa are asked to keep at least 7 meters (23 feet) away from apes to avoid spreading germs.
When you really think about it, human health, animal health and the environment are all connected, says Olival. Preventing the next pandemic will take the work of doctors, veterinarians and scientists. Each field contributes something different to the understanding of new zoonotic diseases. “If we all come together,” he says, “we can improve the health of humans and the planet.”
Chris Whittier and his colleagues in the Central African Republic collect blood and saliva samples from this western lowland gorilla. These great apes can become infected with human viruses, including measles. The researchers’ goal is to protect gorillas, such as this adult female, from human viruses. This sedated animal will be released once she wakes up. C. Whittier/WWF
How to find the next pandemic virus before it finds us published first on https://triviaqaweb.tumblr.com/
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Covid19
FRI FEB 28 2020
I was really surprised to see that the stock market took a huge shit this week. Just after hitting another all time high, last Wednesday, the 19th, it began to drop last Thursday, and then all five days this week, Nasdaq, S&P, all of them across the board just kept dropping lower and lower every day, with the only thing stopping it being the closing bell of trading today.
It’s been the worst week of decline since October of 2008, with the banking collapse, after the housing bust was already in full swing... but this time, it was due to a sudden panic about Covid19, the coronavirus that emerged in China back in December.
There had been some global concern about Covid19 through January, when it was still contained mostly to China, but through February, cases have been showing up in other concentrated spots all around the globe, leading to a low level panic that finally affected the stock market.
Trump, of course, didn’t bother to address it at all until he saw his precious stock market was falling, and... it was actually his announcement about putting his VP Pence in charge of the virus that really caused the markets to break loose and go into free fall... because in the press conference, it was so painfully obvious to everybody, that Trump has no clue how to deal with a pandemic, and neither does Pence.
And it’s not just stocks, but other market warning signs are flashing, and... as mentioned above, people are talking about 2008, and everybody’s getting into their crash positions for another big recession suddenly.
Well... many are getting into crash positions. Other pundits are assuring us that everything will rally back to normal next week, like the market’s been doing over and over again for the entire Trump administration.
Of course, my model here, holds that the economy since the early twenty-teens has been a self-driving one, kept on the road by AI bots who have gone to great lengths to fend off the panics that should otherwise have tanked it by now, being caused by a rogue US President and his incendiary tweets... not to mention insane policies like jacking up tariffs on China last year.
And they’re so good at what they do, that I’ve maintained for this entire blog so far, even through Trump’s Impeachment hearings... that a market crash, and/or recession was off the table... no matter how fortuitous one might be in getting Trump removed from office.
So I’ve been truly surprised this week to see this happening.
And now I have to speculate as to why it’s happening.
Are the bots behind this?
The short answer is no. Their prime directive is, to the best of their ability, to keep the economy on track no matter what. Same as a self driving car, which only wants to keep driving, avoid accidents, obey the rules of the road, and get from point A to point B as quickly, but safely as possible.
But just like with a self driving car, there are some factors outside their control. One of these factors is Presidential tariffs... an arbitrary tax thrown in by one man on the outside, at his whim.
I’ve spent many an entry speculating about how the bots must have not only identified Trump as, essentially a virus attacking the system... but went so far as to form a coalition with smarter, more robust AI bots out there on the deep web, to hold Trump to account... by finding and leaking damning evidence to the House, who has the power to impeach him.
And that kind of worked... because Trump forgot about his tariffs. He wasn’t removed, but the economically destructive behavior he’d been engaging in, was put on indefinite pause... which was good enough to keep things rolling and buy time to find a more effective solution.
As for elections... two entries ago, I talked about how this bot coalition is not interested in tampering with elections. They’ll step in to prevent tampering if they can, like by crippling the Shadow app in Iowa, which was designed to subvert democracy... but this is a coalition of humanitarian bots, and economy bots, so... they all want to play by the rules, while also avoiding big upsets to society... like an assassination or something.
But when something like Covid19 appears on the landscape... well, it’s even further outside their control than rogue tariffs.
Real viruses... the biological kind, are an extremely ancient form of life, operating under the complex rules of natural selection, on a very root level. They’re unpredictable, and can be quite ruthless to higher life forms when they hit on a novel strategy for which existing biological immune systems are not prepared.
That said, biological immune systems are also insanely advanced, and do a very good job of neutralizing viruses... especially when they are helped along by human doctors who can study the DNA of the viruses and produce vaccines to teach immune systems how to fight them before they attack.
This is how we’ve managed to nearly wipe out polio, small pox, and dozens of other deadly viruses... and how we defend the world’s population every year against the latest strains of influenza*.
That said, I’m not convinced that Covid19 is the deadly pandemic threat that everybody’s terrified it could be at the moment.
Because it began in China... an authoritarian nation, we don’t have any reliable information about this virus at all. We can’t trust their numbers, either of infected or of deaths... we can’t trust their information about it’s transmission methods, contagiousness, incubation period, symptoms, or it’s origin... not just because we can’t trust them to tell the world the truth... but because we can’t even trust them to properly assess this kind of data.
Autocracies are notorious for brain drain, and clueless bureaucrats running big agencies they don’t understand, so... their data is useless.
Meanwhile, as far as news on the ground in China, all we have is a random sampling of smart phone footage, mixed with state reports, and first hand accounts from people supposedly spying from within China on behalf of the free world... but we have no idea what the true context is for any of this material... or what the agenda is of people who’ve fed this back to us over social media.
Long story short here, I do believe at the moment, that the panic is overblown, and that it’s being overblown by several layers of trolls around the world, who just want to create global panic for the lols.
People in the free world have been studying Covid19 in their own countries, as it’s spread to them, and are sharing that information but... we’re talking about three weeks worth of study on small sample sizes. There just hasn’t been enough time to fully understand how dangerous this virus really is.
Earlier this week, the big panic was essentially triggered by comparing global death toll numbers, to global estimates for how many have been infected... and that’s resulted in the estimated fatality for Covid19 at 2%... compared to 0.1% for Influenza.
If accurate, that would be a Spanish Flu magnitude pandemic... highly contagious, and extremely deadly.
But... if the infection numbers turn out to be far higher than we realize... it brings both the contagiousness factor, and the fatality percentage waaay down.
And just here at the end of the week, this is what it’s starting to look like.
We’re starting to understand that Covid19 is probably a lot more like the common cold, than the common flu... and that the vast number of victims simply mistake it for a mild cold, and get over it quickly.
This, based on the way it’s beginning to pop up with people who are very far removed from any possible contact with known vectors.
Does it still get serious and cause pneumonia in some victims, taking some of their lives, yes... but this may turn out to be a very small percentage of all infected... more like the 0.1% who die from the common flu.
If so, standard precautions are enough to keep the threat at bay, globally until a vaccine can be produced next year.
Maybe I’m wrong here, but, this is my best guess based on the knowledge we have at the moment... minus the disinformation and trolling.
Based on that... I’d predict that the markets go back to normal in the coming two weeks, as the deadly pandemic fails to materialize. We shall see.
In other news, the South Carolina Primary is tomorrow.
Most polling suggests that Joe Biden will take first place, by a comfortable margin over Bernie Sanders, who will follow a distant second. Some outlier polls had Sanders within only one or two points of Biden, earlier in the week, but the conventional wisdom tonight, is that Biden will enjoy a big win in SC.
I still think Bernie can pull off an upset and win SC.
This is based on the fact that Bernie has so far, consistently over performed his polling... while Biden has consistently under performed his own polling.
You can poll well, but will those supporters actually go out and vote on election day? That’s the name of the game.
Biden’s supporters tend to be over represented in the polls, because they are the kind of people the pollsters know how to query... but they aren’t necessarily motivated enough to actually follow through.
With Bernie, it’s the opposite... his followers are under represented by contemporary polling techniques, but are also highly motivated to get out and vote for their candidate... thanks to his extraordinary ground game.
We’ll see tomorrow.
One thing is for certain... after doing so poorly in the first three states, and losing so much ground to Bloomberg in the polling for Super Tuesday states... Biden needs an unmitigated blow out in SC to stay relevant.
And even an unmitigated blow out might not be enough to save his campaign, as there are only two full days between the SC and Super Tuesday, for him to try and leverage the big win enough to influence voters.
On the other hand, all Bernie needs to do is come in a close second... close that gap to single digits... and he’s looking formidable.
Like I said, I think Bernie can overtake Biden tomorrow, at least by a few points... and if he does... he will crush Super Tuesday.
Exciting times.
But I’m going to bed.
*It should be noted here that unlike bacteria... which can be treated with antibiotics, viruses can only be neutralized by the immune system itself... once it knows how to identify the threat.
That’s why some viruses, like HPV, which causes common warts, can be so stubborn and near impossible to eradicate... because they’re good at avoiding immune system detection... but also don’t kill, or even seriously harm their hosts. To kill a wart virus... the only real treatment is salicylic acid applied directly to the spot, nearly constantly, for extremely long periods... months if not years.
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You’re Likely to Get the Coronavirus
Most cases are not life-threatening, which is also what makes the virus a historic challenge to contain.
BY JAMES HAMBLIN | Published February 24, 2020 | The Atlantic | Posted February 27, 2020 |
(Updated at 7:43 p.m. on Feb. 25, 2020.)
In May 1997, a 3-year-old boy developed what at first seemed like the common cold. When his symptoms—sore throat, fever, and cough—persisted for six days, he was taken to the Queen Elizabeth Hospital in Hong Kong. There his cough worsened, and he began gasping for air. Despite intensive care, the boy died.
Puzzled by his rapid deterioration, doctors sent a sample of the boy’s sputum to China’s Department of Health. But the standard testing protocol couldn’t fully identify the virus that had caused the disease. The chief virologist decided to ship some of the sample to colleagues in other countries.
At the U.S. Centers for Disease Control and Prevention in Atlanta, the boy’s sputum sat for a month, waiting for its turn in a slow process of antibody-matching analysis. The results eventually confirmed that this was a variant of influenza, the virus that has killed more people than any in history. But this type had never before been seen in humans. It was H5N1, or “avian flu,” discovered two decades prior, but known only to infect birds.
By then, it was August. Scientists sent distress signals around the world. The Chinese government swiftly killed 1.5 million chickens (over the protests of chicken farmers). Further cases were closely monitored and isolated. By the end of the year there were 18 known cases in humans. Six people died.
This was seen as a successful global response, and the virus was not seen again for years. In part, containment was possible because the disease was so severe: Those who got it became manifestly, extremely ill. H5N1 has a fatality rate of about 60 percent—if you get it, you’re likely to die. Yet since 2003, the virus has killed only 455 people. The much “milder” flu viruses, by contrast, kill fewer than 0.1 percent of people they infect, on average, but are responsible for hundreds of thousands of deaths every year.
Severe illness caused by viruses such as H5N1 also means that infected people can be identified and isolated, or that they died quickly. They do not walk around feeling just a little under the weather, seeding the virus. The new coronavirus (known technically as SARS-CoV-2) that has been spreading around the world can cause a respiratory illness that can be severe. The disease (known as COVID-19) seems to have a fatality rate of less than 2 percent—exponentially lower than most outbreaks that make global news. The virus has raised alarm not despite that low fatality rate, but because of it.
Coronaviruses are similar to influenza viruses in that they both contain single strands of RNA.* Four coronaviruses commonly infect humans, causing colds. These are believed to have evolved in humans to maximize their own spread—which means sickening, but not killing, people. By contrast, the two prior novel coronavirus outbreaks—SARS (severe acute respiratory syndrome) and MERS (Middle East respiratory syndrome, named for where the first outbreak occurred)—were picked up from animals, as was H5N1. These diseases were highly fatal to humans. If there were mild or asymptomatic cases, they were extremely few. Had there been more of them, the disease would have spread widely. Ultimately, SARS and MERS each killed fewer than 1,000 people.
COVID-19 is already reported to have killed more than twice that number. With its potent mix of characteristics, this virus is unlike most that capture popular attention: It is deadly, but not too deadly. It makes people sick, but not in predictable, uniquely identifiable ways. Last week, 14 Americans tested positive on a cruise ship in Japan despite feeling fine—the new virus may be most dangerous because, it seems, it may sometimes cause no symptoms at all.
[Read: The new coronavirus is a truly modern epidemic SEE BELOW]
The world has responded with unprecedented speed and mobilization of resources. The new virus was identified extremely quickly. Its genome was sequenced by Chinese scientists and shared around the world within weeks. The global scientific community has shared genomic and clinical data at unprecedented rates. Work on a vaccine is well under way. The Chinese government enacted dramatic containment measures, and the World Health Organization declared an emergency of international concern. All of this happened in a fraction of the time it took to even identify H5N1 in 1997. And yet the outbreak continues to spread.
The Harvard epidemiology professor Marc Lipsitch is exacting in his diction, even for an epidemiologist. Twice in our conversation he started to say something, then paused and said, “Actually, let me start again.” So it’s striking when one of the points he wanted to get exactly right was this: “I think the likely outcome is that it will ultimately not be containable.”
Containment is the first step in responding to any outbreak. In the case of COVID-19, the possibility (however implausible) of preventing a pandemic seemed to play out in a matter of days. Starting in January, China began cordoning off progressively larger areas, radiating outward from the city of Wuhan and eventually encapsulating some 100 million people. People were barred from leaving home, and lectured by drones if they were caught outside. Nonetheless, the virus has now been found in 24 countries.
Despite the apparent ineffectiveness of such measures—relative to their inordinate social and economic cost, at least—the crackdown continues to escalate. Under political pressure to “stop” the virus, last Thursday the Chinese government announced that officials in Hubei province would be going door-to-door, testing people for fevers and looking for signs of illness, then sending all potential cases to quarantine camps. But even with the ideal containment, the virus’s spread may have been inevitable. Testing people who are already extremely sick is an imperfect strategy if people can spread the virus without even feeling bad enough to stay home from work.
Lipsitch predicts that within the coming year, some 40 to 70 percent of people around the world will be infected with the virus that causes COVID-19. But, he clarifies emphatically, this does not mean that all will have severe illnesses. “It’s likely that many will have mild disease, or may be asymptomatic,” he said. As with influenza, which is often life-threatening to people with chronic health conditions and of older age, most cases pass without medical care. (Overall, about 14 percent of people with influenza have no symptoms.)
Lipsitch is far from alone in his belief that this virus will continue to spread widely. The emerging consensus among epidemiologists is that the most likely outcome of this outbreak is a new seasonal disease—a fifth “endemic” coronavirus. With the other four, people are not known to develop long-lasting immunity. If this one follows suit, and if the disease continues to be as severe as it is now, “cold and flu season” could become “cold and flu and COVID-19 season.”
At this point, it is not even known how many people are infected. As of Sunday, there have been 35 confirmed cases in the U.S., according to the World Health Organization. But Lipsitch’s “very, very rough” estimate when we spoke a week ago (banking on “multiple assumptions piled on top of each other,” he said) was that 100 or 200 people in the U.S. were infected. That’s all it would take to seed the disease widely. The rate of spread would depend on how contagious the disease is in milder cases. On Friday, Chinese scientists reported in the medical journal JAMA an apparent case of asymptomatic spread of the virus, from a patient with a normal chest CT scan. The researchers concluded with stolid understatement that if this finding is not a bizarre abnormality, “the prevention of COVID-19 infection would prove challenging.”
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Even if Lipsitch’s estimates were off by orders of magnitude, they wouldn’t likely change the overall prognosis. “Two hundred cases of a flu-like illness during flu season—when you’re not testing for it—is very hard to detect,” Lipsitch said. “But it would be really good to know sooner rather than later whether that’s correct, or whether we’ve miscalculated something. The only way to do that is by testing.”
Originally, doctors in the U.S. were advised not to test people unless they had been to China or had contact with someone who had been diagnosed with the disease. Within the past two weeks, the CDC said it would start screening people in five U.S. cities, in an effort to give some idea of how many cases are actually out there. But tests are still not widely available. As of Friday, the Association of Public Health Laboratories said that only California, Nebraska, and Illinois had the capacity to test people for the virus.
With so little data, prognosis is difficult. But the concern that this virus is beyond containment—that it will be with us indefinitely—is nowhere more apparent than in the global race to find a vaccine, one of the clearest strategies for saving lives in the years to come.
Over the past month, stock prices of a small pharmaceutical company named Inovio have more than doubled. In mid-January, it reportedly discovered a vaccine for the new coronavirus. This claim has been repeated in many news reports, even though it is technically inaccurate. Like other drugs, vaccines require a long testing process to see whether they indeed protect people from disease, and do so safely. What this company—and others—has done is copy a bit of the virus’s RNA that one day could prove to work as a vaccine. It’s a promising first step, but to call it a discovery is like announcing a new surgery after sharpening a scalpel.
Though genetic sequencing is now extremely fast, making vaccines is as much art as science. It involves finding a viral sequence that will reliably cause a protective immune-system memory but not trigger an acute inflammatory response that would itself cause symptoms. (While the influenza vaccine cannot cause the flu, the CDC warns that it can cause “flu-like symptoms.”) Hitting this sweet spot requires testing, first in lab models and animals, and eventually in people. One does not simply ship a billion viral gene fragments around the world to be injected into everyone at the moment of discovery.
Inovio is far from the only small biotech company venturing to create a sequence that strikes that balance. Others include Moderna, CureVac, and Novavax. Academic researchers are also on the case, at Imperial College London and other universities, as are federal scientists in several countries, including at the U.S. National Institutes of Health. Anthony Fauci, the head of the NIH’s National Institute of Allergy and Infectious Diseases, wrote in JAMA in January that the agency was working at historic speed to find a vaccine. During the SARS outbreak in 2003, researchers moved from obtaining the genomic sequence of the virus and into a phase 1 clinical trial of a vaccine in 20 months. Fauci wrote that his team has since compressed that timeline to just over three months for other viruses, and for the new coronavirus, “they hope to move even faster.”
New models have sprung up in recent years, too, that promise to speed up vaccine development. One is the Coalition for Epidemic Preparedness (CEPI), which was launched in Norway in 2017 to finance and coordinate the development of new vaccines. Its founders include the governments of Norway and India, the Wellcome Trust, and the Bill & Melinda Gates Foundation. The group’s money is now flowing to Inovio and other small biotech start-ups, encouraging them to get into the risky business of vaccine development. The group’s CEO, Richard Hatchett, shares Fauci’s basic timeline vision—a COVID-19 vaccine ready for early phases of safety testing in April. If all goes well, by late summer testing could begin to see if the vaccine actually prevents disease.
[Read: Coronavirus is devastating Chinese tourism SEE TIMELINE]
Overall, if all pieces fell into place, Hatchett guesses it would be 12 to 18 months before an initial product could be deemed safe and effective. That timeline represents “a vast acceleration compared with the history of vaccine development,” he told me. But it’s also unprecedentedly ambitious. “Even to propose such a timeline at this point must be regarded as hugely aspirational,” he added.
Even if that idyllic year-long projection were realized, the novel product would still require manufacturing and distribution. “An important consideration is whether the underlying approach can then be scaled to produce millions or even billions of doses in coming years,” Hatchett said. Especially in an ongoing emergency, if borders closed and supply chains broke, distribution and production could prove difficult purely as a matter of logistics.
Fauci’s initial optimism seemed to wane, too. Last week he said that the process of vaccine development was proving “very difficult and very frustrating.” For all the advances in basic science, the process cannot proceed to an actual vaccine without extensive clinical testing, which requires manufacturing many vaccines and meticulously monitoring outcomes in people. The process could ultimately cost hundreds of millions of dollars—money that the NIH, start-ups, and universities don’t have. Nor do they have the production facilities and technology to mass-manufacture and distribute a vaccine.
Production of vaccines has long been contingent on investment from one of the handful of giant global pharmaceutical companies. At the Aspen Institute last week, Fauci lamented that none had yet to “step up” and commit to making the vaccine. “Companies that have the skill to be able to do it are not going to just sit around and have a warm facility, ready to go for when you need it,” he said. Even if they did, taking on a new product like this could mean massive losses, especially if the demand faded or if people, for complex reasons, chose not to use the product.
Making vaccines is so difficult, cost intensive, and high risk that in the 1980s, when drug companies began to incur legal costs over alleged harms caused by vaccines, many opted to simply quit making them. To incentivize the pharmaceutical industry to keep producing these vital products, the U.S. government offered to indemnify anyone claiming to have been harmed by a vaccine. The arrangement continues to this day. Even still, drug companies have generally found it more profitable to invest in the daily-use drugs for chronic conditions. And coronaviruses could present a particular challenge in that at their core they, like influenza viruses, contain single strands of RNA. This viral class is likely to mutate, and vaccines may need to be in constant development, as with the flu.
“If we’re putting all our hopes in a vaccine as being the answer, we’re in trouble,” Jason Schwartz, an assistant professor at Yale School of Public Health who studies vaccine policy, told me. The best-case scenario, as Schwartz sees it, is the one in which this vaccine development happens far too late to make a difference for the current outbreak. The real problem is that preparedness for this outbreak should have been happening for the past decade, ever since SARS. “Had we not set the SARS-vaccine-research program aside, we would have had a lot more of this foundational work that we could apply to this new, closely related virus, ” he said. But, as with Ebola, government funding and pharmaceutical-industry development evaporated once the sense of emergency lifted. “Some very early research ended up sitting on a shelf because that outbreak ended before a vaccine needed to be aggressively developed.”
On Saturday, Politico reported that the White House is preparing to ask Congress for $1 billion in emergency funding for a coronavirus response. This request, if it materialized, would come in the same month in which President Donald Trump released a new budget proposal that would cut key elements of pandemic preparedness—funding for the CDC, the NIH, and foreign aid.
These long-term government investments matter because creating vaccines, antiviral medications, and other vital tools requires decades of serious investment, even when demand is low. Market-based economies often struggle to develop a product for which there is no immediate demand and to distribute products to the places they’re needed. CEPI has been touted as a promising model to incentivize vaccine development before an emergency begins, but the group also has skeptics. Last year, Doctors Without Borders wrote a scathing open letter, saying the model didn’t ensure equitable distribution or affordability. CEPI subsequently updated its policies to forefront equitable access, and Manuel Martin, a medical innovation and access adviser with Doctors Without Borders, told me last week that he’s now cautiously optimistic. “CEPI is absolutely promising, and we really hope that it will be successful in producing a novel vaccine,” he said. But he and his colleagues are “waiting to see how CEPI’s commitments play out in practice.”
These considerations matter not simply as humanitarian benevolence, but also as effective policy. Getting vaccines and other resources to the places where they will be most helpful is essential to stop disease from spreading widely. During the 2009 H1N1 flu outbreak, for example, Mexico was hit hard. In Australia, which was not, the government prevented exports by its pharmaceutical industry until it filled the Australian government’s order for vaccines. The more the world enters lockdown and self-preservation mode, the more difficult it could be to soberly assess risk and effectively distribute tools, from vaccines and respirator masks to food and hand soap.
Italy, Iran, and South Korea are now among the countries reporting quickly growing numbers of detected COVID-19 infections. Many countries have responded with containment attempts, despite the dubious efficacy and inherent harms of China’s historically unprecedented crackdown. Certain containment measures will be appropriate, but widely banning travel, closing down cities, and hoarding resources are not realistic solutions for an outbreak that lasts years. All of these measures come with risks of their own. Ultimately some pandemic responses will require opening borders, not closing them. At some point the expectation that any area will escape effects of COVID-19 must be abandoned: The disease must be seen as everyone’s problem.
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* This story originally stated that coronaviruses and influenza viruses are single strands of RNA; in fact, influenza viruses can contain multiple segments of single-strand RNA.
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JAMES HAMBLIN, MD, is a staff writer at The Atlantic. He is also a lecturer at Yale School of Public Health and author of the forthcoming book Clean.
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The New Coronavirus Is a Truly Modern Epidemic
New diseases are mirrors that reflect how a society works—and where it fails.
By ED YOUNG | Published February 3, 2020 | The Atlantic Magazine | Posted February 27, 2020 |
On Thursday, Nahid Bhadelia left rural Uganda, where she had been helping to set up a center for studying viruses such as Ebola. Before she left, she was peppered with concerned questions about when 2019-nCoV—the new coronavirus that has rapidly spread through China—would appear there. The virus had already reached 23 other countries, and when Bhadelia, an infectious disease physician at Boston University School of Medicine, arrived in Amsterdam on Friday morning for a layover, she noticed that a quarter of the people in Schiphol Airport seemed to be wearing face masks. When she landed in Paris for a second stop, she paused to deal with the barrage of tweets and emails that she had been getting about the new virus. “I’m not as worried by the disease as from people’s reactions to it,” she told me over Skype. “People are freaking out.”
The virus emerged in the city of Wuhan in December, and has infected more than 17,200 people. The large majority of cases have been in mainland China, but more than 140 have been detected elsewhere. At least 361 people have died in China, and one in the Philippines. In response, the World Health Organization recently declared a “public-health emergency of international concern” (PHEIC)—a designation that it has used on five previous occasions, for epidemics of H1N1 swine flu, polio, Ebola, Zika, and Ebola again. The invocation of a PHEIC is a sign that the new coronavirus should be taken seriously—and as the sixth such invocation in a little more than a decade, it is a reminder that we live in an age of epidemics.
Each new crisis follows a familiar playbook, as scientists, epidemiologists, health-care workers, and politicians race to characterize and contain the new threat. Each epidemic is also different, and each is a mirror that reflects the society it affects. In the new coronavirus, we see a world that is more connected than ever by international travel, but that has also succumbed to growing isolationism and xenophobia. We see a time when scientific research and the demand for news, the spread of misinformation and the spread of a virus, all happen at a relentless, blistering pace. The new crisis is very much the kind of epidemic we should expect, given the state of the world in 2020. “It’s almost as if the content is the same but the amplitude is different,” Bhadelia said. “There’s just a greater frenzy, and is that a function of the disease, or a function of the changed world? It’s unclear.”
Certainly, the new epidemic has grown at a pace unprecedented in recent history. The official case count has more than tripled within the past week, from about 4,500 on Monday to more than 17,200 now. In Wuhan, the number of ill people is straining the health care system, testing kits are in short supply, and hospitals are so full that some patients are being sent home to quarantine themselves, Amy Qin of The New York Times reports. The virus seems to have rapidly eclipsed SARS, which infected only about 8,100 people throughout eight months in 2002 and 2003.
[ Read: The deceptively simple number sparking coronavirus fears SEE TIMELINE]
But several experts note that this comparison is misleading. SARS hit a world that was unaware of how far and fast a new virus could spread, and that was unprepared for such a threat. Many cases were likely never recorded because tests were slow to arrive and affected people weren’t sick enough to seek treatment. By stark contrast, the panic about the new coronavirus might lead to an uptick in known cases “because people are more conscious of it and are reporting their illness and seeking out testing,” says Angela Rasmussen, a virologist at Columbia University.
Diagnostic tests are already available for 2019-nCoV, even though the virus still lacks a formal name. In the U.S., the Centers for Disease Control and Prevention has already sent testing kits to state labs. In China, thousands of people are being tested every day, and that pace will only rise as two new hospitals finish construction. More testing means that, in addition to cases of very recent infections, doctors will start identifying people who had caught the virus earlier but hadn’t yet been diagnosed—a trend that inevitably leads to ballooning numbers. “It’s not that we’re getting this many new cases every single day,” says Maia Majumder, an epidemiologist at Harvard Medical School and Boston Children’s Hospital. The number of cases is rising because the medical system is not only playing catch-up to a virus, but also, reassuringly, closing the gap between infection and diagnosis.
But the number of new infections is rising. “We’re getting numbers faster, but that’s partly because there are more numbers,” says Tom Inglesby, a health-security expert at Johns Hopkins Bloomberg School of Public Health. “It’s not just an observation bias. It’s a real disease on the move.” And that movement is easier than ever: The number of people traveling by plane every year has more than doubled since SARS first emerged, in 2003.
The rate at which scientists can analyze a new threat has also increased dramatically. Zika spread through the Americas for 16 months before anyone even knew it was there. Ebola spread through West Africa for several months before any researcher managed to sequence its genes. But this time, in a matter of weeks, researchers recognized a new respiratory virus in the middle of flu season, identified it as a coronavirus, isolated it, sequenced its genome dozens of times over, and worked out how it sticks to human cells. “I’ve never seen anything like this before,” Majumder says. Researchers (and the WHO) have particularly praised Chinese scientists for their speed and transparency in releasing viral genomes and clinical data. China was heavily criticized for withholding and downplaying information during the SARS outbreak. This time around, “it’s a completely different ball game,” says Rebecca Katz, a health-security expert at Georgetown University. “There’s a tremendous amount of information being shared.”
[Read: A virus with a deadly boring Name]
Despite that information, many unknowns remain. How transmissible is the virus? Once infected, how much time passes before people show symptoms, and how likely are they to die? Which people are most at risk? It seems that, on average, infected people spread the virus to two or three others. Thus far, only a minority of those who’ve been infected have become severely ill, and most of those people were either elderly or had prior medical complications. But there are still many uncertainties—and that is entirely normal. “These are the same questions you’d ask in every single outbreak ever—and given that this is a novel virus, we’re getting a lot of answers very quickly,” Katz says.
The unusual speed of discovery partly stems from better avenues for scientific communication. In the past decade, scientists have developed open portals for sharing and analyzing viral genomes, used preprint servers to quickly post new papers, and created rich networks on Twitter and other social media. Researchers can share data and refine ideas faster than ever—but they’re doing so in full view of a concerned citizenry. “You want the free flow of scientific information, but that information is being shared with the public at the same speed, while the scientific community is still digesting it,” Bhadelia told me.
Preliminary data that might once have run the gantlet of peer review before being published can now be downloaded by anyone, sparking misinterpretations and conspiracy theories. Epidemiological arcana, such as the R0 number, are suddenly the subject of widespread discussion. Uncertainties that academics are used to dealing with, about fatality rates or transmissibility, are stoking fear. “It’s not that we should know this by now and we don’t,” Majumder says. “What’s uncommon is not so much these epidemiological factors but the amount of public interest in them.”
Some of these dynamics were clear during the West African Ebola outbreak, in which misinformation and paranoia circulated faster than the actual virus (in part because of the man who now sits in the White House). If anything, the threat of misinformation is now worse, as false reports readily cascade through channels that amplify extreme messages over accurate ones. At a time when researchers are faster than ever at filling the information gaps that escort a new disease, those gaps can also fill just as quickly with bunk.
Hoaxes and half-truths are huge problems during epidemics. The worried well can overwhelm health-care facilities, and make it harder for medical providers to find and treat actual cases. Confused citizens might forgo sensible measures such as hand washing in favor of inefficient ones like panicked mask buying. And misinformation tends to intensify the xenophobia that emerges during epidemics. As diseases spread, “individuals find people to blame based on their prejudices, or make themselves feel less at risk by finding points of discrimination between themselves and others,” says Alexandra Phelan, who studies legal and policy issues related to infectious diseases at Georgetown University. Gay men suffered stigma and discrimination when HIV first emerged. Ebola became a stand-in for “any combination of ‘African-ness,’ ‘blackness,’ ‘foreign-ness,’ and ‘infestation’” during the West African outbreak, my colleague Hannah Giorgis once wrote. And now, as was the case with SARS in 2003, anti-Asian racism is rampant.
[ Read: How to misinform yourself about the coronavirus SEE TIMELINE]
In recent years, the world has seen a rise in anti-immigration rhetoric and isolationist politics, all of which are evident in the reactions to the 2019-nCoV outbreak. The State Department issued its highest-level travel advisory, warning Americans not to travel to China. Citizens who have recently returned from Hubei province are being quarantined. Noncitizens who have recently been to China will be denied entry. Such measures might seem intuitively sensible, but border screenings and travel bans have historically proved ineffective and inefficient at controlling diseases. If anything, they can make matters worse. “People will find a way to get where they want to go, but you lose the opportunity to provide them with information, and you drive them away from public health services,” Phelan says. “Measures that try to carve a country off from the rest of the world are deeply rooted in the protectionist approaches that have proliferated in politics. I think they make the world less safe.”
Bans can also break the fragile bonds of international trust that are necessary for controlling diseases, which is why the WHO advised against them when it declared a PHEIC. If countries know that they’ll be cut off during an epidemic, with all the economic repercussions that entails, they may be less likely to report future outbreaks, leading to costly delays. “The U.S. is a country with considerable normative weight internationally,” Phelan says. “And if a country knows that the U.S. is going to react like this, are they really going to come forward?” If China pays the price for transparency with 2019-nCoV, what lesson will it learn for the next epidemic?
And there will be a next epidemic. A new disease was always going to rear its head to test the world’s mettle, and more almost certainly will in the future. As I argued in 2018, the world isn’t ready. There has assuredly been progress—vaccines can be produced faster, global cooperation is tighter, basic research is nimbler—but supply chains are stretched, misinformation is rife, and investments in preparedness always fall into neglect once panic subsides. “Every year, things get more and more connected,” Inglesby says. “Epidemics like this show that all of it can be relatively quickly put at risk.”
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I PREPARED FOR EVERYTHING, BUT NOT CORONAVIRUS ON A CRUISE SHIP
Last year, I published a thriller set on a cruise. A few weeks ago, I found myself quarantined on the Diamond Princess.
By Gay Courter | Published February 27, 2020 6:00 AM ET | The Atlantic | Posted February 27, 2020 |
ome bad outcomes, you half expect: This time the mammogram will detect an abnormality; this time the cop will notice you were 10 miles over the speed limit; this time the IRS is serious about a total audit. But you don’t expect that your luxury cruise from Japan will harbor a killer virus, resulting in your being returned to the U.S. in a cargo plane that lands at a remote Air Force base where you are ordered into federal quarantine for a minimum of two weeks, leaving you without rights, without agency, and on the wrong side of a heavily guarded fence.
At least, I didn’t expect any of this, even though I wrote a thriller set on a cruise ship—or perhaps in part because I wrote a thriller set on a cruise ship, and figured my imagination was more fevered than reality. I had imagined a murder mystery with medical clues, but I had not imagined this. I had prepared for everything, but I had not prepared for this.
My husband, Phil, and I had planned the trip meticulously for more than a year as an indulgence, an escape. My sister brags about traveling with only carry-on luggage, but my approach is to pack everything I might ever need—and then some. Phil grumbles about the lugging, but he knows me: It’s against my principles to travel light. Our plan was to spend a week in Tokyo, visiting trendy art installations and sampling the best of Japanese cuisine, from ramen and tofu treats to Wagyu beef and haute sushi.
In mid-December, a worrywart friend, who knew that our itinerary included a stop in Hong Kong, started sending me stories about a SARS-like coronavirus disease. “Might you postpone?” he asked.
“Not going to China, let alone Wuhan,” I replied.
“Hong Kong is China,” he reminded me.
“Only going to be there one day!”
I watched as the numbers in Wuhan began to rise and as the Chinese government imposed draconian measures to keep residents within the city’s borders—but without a frisson of concern, I finished packing city gear for metros, walking, rain, and moderate winter temperatures, plus layers for cold and snow for our winter excursion after the cruise. I added dressy pantsuits for three formal nights on the ship and showy but inexpensive necklaces to match. The stops in Vietnam and Okinawa called for a few summery outfits. I had stuffed everything into one large suitcase, along with two folding bags for the inevitable treasures we would find.
We took our long-anticipated first-class flight, wore the airline’s designer PJs, slept in the cushy bed, and dined on foie gras, abalone, and other delicacies, accompanied by glasses of champagne. Once we arrived, we were wowed by the Prince Gallery hotel’s soaring views of Tokyo, cutting-edge electronics, and plumbing wizardry, and we were impressed by how one of the most populous cities in the world manages to be so clean and easy to navigate. We enjoyed learning to make washi paper from slurry and visiting a whole building dedicated to origami.
Then we traveled to Yokohama, boarded the Diamond Princess, and looked forward to spending the lunar new year in Hong Kong and visiting Vietnam, Taiwan, and then several other Japanese ports.
By the time we arrived in Hong Kong, on January 25, the combined concerns over the political protesters and the virus had caused the city to cancel all the new-year festivities. Still, we went into town for a dim sum lunch, tram ride to Victoria Peak, market shopping spree, and Peking-duck feast. It was the vacation of a lifetime.
On the last night of the cruise, the captain’s voice came over the speaker in our room, announcing that a passenger who had not returned to the ship in Hong Kong had tested positive for the novel coronavirus—so novel it had not yet been named—and that Japanese authorities would not let us off the ship until everyone on board filled out a questionnaire, ominously delivered by the quarantine division, and had our temperatures checked. We slept fitfully, awaiting the knock on the door.
That was three weeks ago. It soon became clear that we would be confined to our rooms for at least 14 days. Unlike some others staying in windowless rooms, we had a small suite with a balcony. Meals for the 2,666 people on board were delivered three times a day. There was no butter, no salt, as this post-cruise fare was meant to satisfy only hunger, not the palate. Our decadent vacation was very much over. Out came a mini-salt shaker that I keep with my toothpaste in case I need a saltwater gargle for a sore throat. I dug into my stockpile of Earl Grey and the mountain oolong I had purchased in Taipei. After talking with several doctor friends, we decided to take Tamiflu prophylactically. I always pack it during flu season. I opened my cold-prevention packet of high doses of vitamin C, zinc, and echinacea to boost our immune systems. A friend needed something for a feminine itch, and was surprised I had both the cream and suppository versions of the medication she needed, to her great relief.
I mention these details knowing they’re wildly out of keeping with the situation. What’s unsalted food when you’re stuck on a boat and more than 600 of your fellow passengers have tested positive for a deadly virus, and some of them have died? But the fact that I had a solution for the tasteless food kept me sane; it kept me feeling somewhat in control when I utterly lacked control.
Now that we’re in a drafty room during a cold spell in San Antonio, the heating pad with an extension cord that I expected to use while sleeping on tatami mats has made up for the thin Red Cross blanket. The mini shampoo and conditioner bottles from the Tokyo hotel filled in when my calculated one-month supply from home ran out. My emergency snacks—nuts, Kind bars, and cookies—came in handy after 23 hours on buses and the bare-bones cargo plane we flew on during our “extraction process” by the U.S. government.
When we were “processed” in an airplane hangar last week, we were handed paperwork that read: “Under Section 361 of the Public Health Service Act based on the scientific evidence collected concerning the outbreak of 2019 Novel Coronavirus (COVID-19), the disease meets the definition of ‘severe acute respiratory syndromes’ as specified under Executive Order 13295, as amended by Executive Orders 13375 and 13674.” The paperwork ordered us into quarantine—the first in the U.S. in 60 years—with violation penalties of a criminal fine and up to one year in jail.
Everyone on the other side of the fence is dressed in uniform. If they have to cross over to interact with us, they must be in full protection regalia and we must be wearing masks. They stand as far back as possible, taking our temperatures with an outstretched arm. We feel dehumanized, like pariahs, scum, outcasts. I use this heightened language because this is a heightened situation.
I used to think that if I carried the right accoutrements, I would have something on hand for any emergency or change of plans. I had something for almost every need, even anti-anxiety meds in case of a crisis—which indeed this was.
But I had forgotten the ruby slippers. There was nothing to click to send us home. My debit card, which works in any ATM in the world, cannot unlock the fence around the perimeter of this stockade. All the airline points in the world cannot purchase a single ticket home.
Technically, we are not allowed out of our rooms. After seeing some other cruisers in their N95 masks walking outside, we asked how we could win the same privilege. “We do not recommend you leave your room for your own safety,” the yellow-suited guard with no name tag said, “but we can’t stop you.”
So here I stand, against advice, gulping fresh air through the mask’s fiber, watching soldiers in Army drab and Air Force blue drilling and chanting. I wake to the bugle playing reveille at 5:30 a.m. and hear taps at what must be a soldier’s bedtime. At precisely 5:30 p.m., there’s another bugle alert called “retreat.” We open the door and see members of our “support team” on the better side of the fence. They have stopped in their tracks and placed their right hands over their hearts while the “Star-Spangled Banner” is played. Everyone stares in the same direction, where presumably a flag is being lowered. Every day a few more of us quarantined cruisers put on our face masks and do the same. They brought us home for one reason only: Because we were Americans in harm’s way. Someday—hopefully—we will be on the same side of the fence.
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GAY COURTER is a writer and the author of five books, including The Midwife.
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#trump administration#u.s. news#politics#president donald trump#politics and government#us politics#public health#health#health & fitness#coronavirus#corona virüsü#virus corona vũ hán#china coronavirus#covid2019#covid19#covid 19#covidー19#worldtraveler#world travel#worldpolitics#world news#financial world#top news#top stories google news#news
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Dangerous Diseases Pass on By Rats
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How to find the next pandemic virus before it finds us
More than 100 years ago, a deadly flu virus circled the globe. It caused the influenza pandemic of 1918-1919. Before it was over, this disease had sickened an estimated 500 million people. That was one-third of everyone alive at that time. Some 20 million to 50 million people died.
Flash forward to the 1970s. People in a small Central Africa village fell ill with a mystery disease. It caused bleeding that would not stop. Soon, this Ebola virus would spread to other villages.
Explainer: What is a coronavirus?
What do these famous viral outbreaks have in common with the new coronavirus disease known as COVID-19? Scientists believe animals initially carried the viruses that cause all three. Such diseases are known as zoonoses (ZOH-wuh-NO-sees). That means they started in animals and later spread to people.
Flu likely came from birds. Researchers think that bats may have been the source of the Ebola virus and of COVID-19. “Roughly 75 percent of global pandemics and disease outbreaks caused by new viruses come from wild animals,” says Tracey Goldstein. She’s a virus detective at the University of California, Davis. She hunts for new viruses among the wild animals of Africa.
When viruses pass from wildlife to people, it’s called a spillover. Fortunately, spillovers that affect more than a handful of people are rare. But big spillovers do seem to be happening more often, Goldstein and others observe.
To prevent the next big outbreak, researchers around the world are scouting the role of wild animals in the emergence of new human diseases. Scientists want to understand which groups of animals or viruses pose the biggest risks. What they learn could help us all.
Virus hunters turn to bats
Viruses are tiny, infectious particles. They “live” but aren’t technically alive. They can reproduce only within the cells of a living host. That host can be an animal, plant, bacterium or fungus.
“Humans carry lots of viruses,” notes biologist Kevin Olival. He works for a group called the EcoHealth Alliance. Based in New York City, it tries to protect people and wildlife from new diseases. Measles and common skin warts are examples of viral diseases. But not all viruses are harmful, Olival notes. Some seem to have no effect on the body. It all depends on the virus and the host.
Scientists Say: Outbreak, Epidemic and Pandemic
“All mammals carry viruses,” Olival says. “But there’s something about bats that might be a little different or unique.” That’s why he has made bats — and the viruses they carry — a focus of his research.
Bats are thought to be the host for a number of relatively new viruses that can sicken people. Among them are the Ebola virus, Marburg virus, Nipah virus and SARS-CoV-2. That last one is the coronavirus responsible for COVID-19. In 2002, another coronavirus from bats caused a massive outbreak of SARS (severe acute respiratory syndrome) in China. Highly contagious, SARS showed some similarities to COVID-19.
Olival and his colleagues at EcoHealth Alliance have been studying the coronaviruses hosted by bats. In China alone, they found 400 different strains of these viruses. Most of them probably wouldn’t sicken people, he says. To figure out which can, researchers will have to perform tests. That will involve taking human cells and infecting them with each virus in the lab, he explains.
See all our coverage of the new coronovirus outbreak
Or, researchers could survey people living near the bats and sample their blood. Olival’s colleagues at EcoHealth Alliance were part of a research team that did just that. They worked in rural Chinese villages. And there they found signs that mini coronavirus spillovers have been underway.
The researchers surveyed 1,585 people. They collected blood from 1,497 of them. Of these, 265 (almost one in every six people) reported some symptoms in the past year of a SARS- or flu-like disease. Nine people also tested positive for SARS-like coronaviruses that had previously been found in area bats. None of these nine remembered having any interactions with bats. However, the people who had reported SARS-like or other severe respiratory infections did say they had been exposed to wildlife and livestock.
This suggests that there may be zoonotic illness in these populations. And, the researchers add, the novel bat-linked viruses in the blood of some of these villagers offers “evidence for bat-borne coronavirus transmission to people.” Hongying Li of the EcoHealth Alliance and her colleagues reported their findings in the September 2019 Biosafety and Health.
Why bats?
Researchers don’t know precisely why bats are a good host for many deadly viruses. But they have some ideas. Bats are the only mammals that fly. (Other “flying” mammals don’t fly. They only glide.) Flying is hard work. A bat needs about twice as much energy for its flight muscles as a similar-sized rodent needs to run on the ground. Putting all their energy into flying could leave bats with less energy to fight off sickness or injury. But that doesn’t happen. Scientists think that flight may have led bats to evolve stronger immune systems than other mammals.
Judilee Marrow collects a saliva sample from a rodent in Gabon, Africa. She and her colleagues at Smithsonian’s National Zoo take these samples to the lab where they will be investigated for viruses.C. Whittier
A unique immune system might mean a unique response to viruses. For instance, one recent study showed that bats’ bodies can limit the ability of a virus to trigger dangerous inflammation. That response may push viruses to evolve in ways that let them rapidly spread from cell to cell. And if that altered virus now spreads to a species without such a strong immune system, the new victim might get super-sick — and quickly.
Olival’s work has mainly taken him to Malaysia. This Southeast Asian nation has more than 100 bat species. He wants to better understand how viruses there might spread between different groups of bats. So he collects genetic information from bats and bat viruses. He uses that to build computer models. These computer programs predict which bat viruses could cause real harm in people and other animals, he explains.
Explainer: What is a computer model?
Some, such as the Nipah virus, can infect a wide range of animals. Several species of fruit bats in Southeast Asia carry that virus without getting sick. But in 1999, Nipah virus triggered a deadly outbreak among Malaysia’s pigs and pig farmers.
Goldstein’s team performed similar work with bats in Sierra Leone. That’s a country in West Africa. Her group had suspected local bats carried the Ebola virus. It was not a wild guess. In 2014 and 2015, an Ebola outbreak killed nearly 4,000 West Africans. And in January 2015, researchers linked the start of that outbreak to a two-year old boy in Guinea. He liked to play in a hollow tree where insect-eating bats used to live.
Scientists perform lab work in Tanzania to look for new viruses from wild animals.USAID PREDICT
Villagers had burned the tree down. But insect-eating bats had been linked to earlier Ebola outbreaks. That made these animals the most likely suspects in the West African outbreak, explained Fabian Leendertz at the time. He works at the Robert Koch Institute in Berlin, Germany. His team described how its detective work led to this conclusion in the January 2015 EMBO Molecular Medicine.
“We wanted to see what other viruses were circulating in bats and other animals” in Sierra Leone, recalls Goldstein. That country shares a border with Guinea. Knowing what viruses the bats hosted might help researchers better understand their viral risks to people.
The bats in Sierra Leone carried Marburg virus, Goldstein’s team discovered. It’s a close relative to the Ebola virus. Marburg causes severe bleeding in people, just as Ebola does. But Marburg has not yet sickened anyone in Sierra Leone. The researchers found the disease in bats before any people got sick. But now Goldstein’s group knows that bats pose a Marburg risk there.
Protecting people and wildlife
Figuring out where potentially dangerous viruses come from is only part of the challenge. Research also needs to identify what activities put people at risk of exposure to animal viruses, note Goldstein and Olival.
These new viral diseases aren’t passing from wild animals to people because animals are going out of their way to mess with us. “It’s because we interfere with them,” says David Quammen. He’s a science journalist. And he researched the topic for a book he wrote eight years ago, Spillover: Animal Infections and the Next Human Pandemic.
Ecology is a branch of biology that explains how different living things interact with each other and their surroundings. And “humans are changing ecology,” observes Hellen Amuguni. She’s a veterinarian and infectious-disease researcher at Tufts University in North Grafton, Mass. People can alter ecology by cutting down trees in forests. Or they might build roads or cities through the landscape. Some might hunt down wild animals for pets or food, explains Amuguni. All of these activities can impact the local ecology in ways that scientists are just beginning to understand.
One new study backs that up. Christine K. Johnson of UC Davis and her colleagues published it April 8 in the Proceedings of the Royal Society B. They found that hunting, wildlife trade, habitat destruction and the spread of cities into areas that were previously wildlands all increase the risk of virus spillovers. Selling wild animals at markets or shrinking their natural habitat can jumble together species that wouldn’t normally meet.
Hongying Li visits a live-animal food market in China. All animals, including these, may harbor harmful viruses. Li’s team is surveying the types of wildlife and livestock that local consumers might encounter.EcoHealth Alliance
Scientists think that the new coronavirus might have come from a live animal market in China. The virus could have passed directly from a bat to a human. Or it could have passed from a bat to another animal that was touched by a human. Wild animals kept in cages come into close contact with people and other animals. That provides more chances for viruses to spill over from one species to another.
And these events can be just as bad for wildlife as for people, points out Christopher Whittier. He’s a veterinarian at Tufts who studies human diseases that spill over into wildlife. “Understanding what viruses are in wildlife can help us to protect wild animals, too,” he notes.
The human measles virus can sicken and even kill mountain gorillas. Researchers in Africa discovered this back in 1988. People would gather to watch the apes in Rwanda’s national parks. At the time, no one knew that someone’s sneeze can infect local primates with colds and other viral diseases. And there’s plenty of opportunity for that. Each year, park gorillas and chimps were exposed to more people — and their germs — than would visit the average person’s house over a lifetime.
After scientists realized that these wild animals could get sick, practices changed. Today, people visiting wildlife parks in Africa are asked to keep at least 7 meters (23 feet) away from apes to avoid spreading germs.
When you really think about it, human health, animal health and the environment are all connected, says Olival. Preventing the next pandemic will take the work of doctors, veterinarians and scientists. Each field contributes something different to the understanding of new zoonotic diseases. “If we all come together,” he says, “we can improve the health of humans and the planet.”
Chris Whittier and his colleagues in the Central African Republic collect blood and saliva samples from this western lowland gorilla. These great apes can become infected with human viruses, including measles. The researchers’ goal is to protect gorillas, such as this adult female, from human viruses. This sedated animal will be released once she wakes up. C. Whittier/WWF
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