Alabama coronavirus exposure notification app to be released in July, early August – WAAY

Alabama's coronavirus exposure notification app is set to be released sometime in July or early August as part of the "Stay Safe Together" platform.

The app uses technology from Apple and Google, and lets you know if you've come in contact with someone who tests positive for coronavirus.

"Human behavior is fundamentally at the foundation of this, but we're going to add all the tools possible to make this future and our fall workable to our students, faculty and staff as well as our business community across the state of Alabama," Dr. Selwyn Vickers, the Dean of Medicine at the University of Alabama in Birmingham where the platform started, said.

The platform includes coronavirus health checks, so you can check your health and symptoms regularly, as well as the exposure notification app that'll alert you if you've been around someone who tested positive for coronavirus. It's all anonymous.

Vickers' team is working to make the Stay Safe platform available to all universities across the state as students return in the fall.

As of right now, universities aren't required to use the platform, but Vickers say it's best if they do.

"It's not required yet. We are going to highly recommend it because we think it's a powerful tool for allowing individuals to know when they've been in contact with individuals who are positive, and it's a tool to support our state's effort for traditional contact tracing," he said.

One student told WAAY 31 he hopes schools plan to use it, so that students can come back to campus.

"That's an amazing thing for students, and I know there are a lot of students trying to come back. They want to be around their friends and get back in class and all this stuff," Elijah Oshin-Banjo, a college student, said.

The launch is expected in July or early August.

It was first launched at UAB in April for testing.

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Alabama coronavirus exposure notification app to be released in July, early August - WAAY

The US isn’t in a second wave of coronavirus the first wave never ended – Huron Daily Tribune

(The Conversation is an independent and nonprofit source of news, analysis and commentary from academic experts.)

Melissa Hawkins, American University

(THE CONVERSATION) After sustained declines in the number of COVID-19 cases over recent months, restrictions are starting to ease across the United States. Numbers of new cases are falling or stable at low numbers in some states, but they are surging in many others. Overall, the U.S. is experiencing a sharp increase in the number of new cases a day, and by late June, had surpassed the peak rate of spread in early April.

When seeing these increasing case numbers, it is reasonable to wonder if this is the dreaded second wave of the coronavirus a resurgence of rising infections after a reduction in cases.

The U.S. as a whole is not in a second wave because the first wave never really stopped. The virus is simply spreading into new populations or resurging in places that let down their guard too soon.

To have a second wave, the first wave needs to end

A wave of an infection describes a large rise and fall in the number of cases. There isnt a precise epidemiological definition of when a wave begins or ends.

But with talk of a second wave in the news, as an epidemiologist and public health researcher, I think there are two necessary factors that must be met before we can colloquially declare a second wave.

First, the virus would have to be controlled and transmission brought down to a very low level. That would be the end of the first wave. Then, the virus would need to reappear and result in a large increase in cases and hospitalizations.

Many countries in Europe and Asia have successfully ended the first wave. New Zealand and Iceland have also made it through their first waves and are now essentially coronavirus-free, with very low levels of community transmission and only a handful of active cases currently.

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In the U.S., cases spiked in March and April and then trended downward due to social distancing guidance and implementation. However, the U.S. never reduced spread to low numbers that were sustained over time. Through May and early June, numbers plateaued at approximately 25,000 new cases daily.

We have left that plateau. Since mid-June, cases have been surging upwards. Additionally, the percentage of COVID-19 tests that are returning positive is climbing steeply, indicating that the increase in new cases is not simply a result of more testing, but the result of an increase in spread.

As of writing this, new deaths per day have not begun to climb, but some hospitals intensive care units have recently reached full capacity. In the beginning of the outbreak, deaths often lagged behind confirmed infections. It is likely, as Anthony Fauci, the nations top infectious-disease specialist said on June 22, that deaths will soon follow the surge in new cases.

Different states, different trends

Looking at U.S. numbers as a whole hides what is really going on. Different states are in vastly different situations right now and when you look at states individually, four major categories emerge.

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Places where the first wave is ending: States in the Northeast and a few scattered elsewhere experienced large initial spikes but were able to mostly contain the virus and substantially brought down new infections. New York is a good example of this.

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Places still in the first wave: Several states in the South and West see Texas and California had some cases early on, but are now seeing massive surges with no sign of slowing down.

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Places in between: Many states were hit early in the first wave, managed to slow it down, but are either at a plateau like North Dakota or are now seeing steep increases like Oklahoma.

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Places experiencing local second waves: Looking only at a state level, Hawaii, Montana and Alaska could be said to be experiencing second waves. Each state experienced relatively small initial outbreaks and was able to reduce spread to single digits of daily new confirmed cases, but are now all seeing spikes again.

The trends arent surprising based on how states have been dealing with reopening. The virus will go wherever there are susceptible people and until the U.S. stops community spread across the entire country, the first wave isnt over.

What could a second wave look like?

It is possible though at this point it seems unlikely that the U.S. could control the virus before a vaccine is developed. If that happens, it would be time to start thinking about a second wave. The question of what it might look like depends in large part on everyones actions.

The 1918 flu pandemic was characterized by a mild first wave in the winter of 1917-1918 that went away in summer. After restrictions were lifted, people very quickly went back to pre-pandemic life. But a second, deadlier strain came back in fall of 1918 and third in spring of 1919. In total, more than 500 million people were infected worldwide and upwards of 50 million died over the course of three waves.

It was the combination of a quick return to normal life and a mutation in the flus genome that made it more deadly that led to the horrific second and third waves.

Thankfully, the coronavirus appears to be much more genetically stable than the influenza virus, and thus less likely to mutate into a more deadly variant. That leaves human behavior as the main risk factor.

Until a vaccine or effective treatment is developed, the tried-and-true public health measures of the last months social distancing,universal mask wearing, frequent hand-washing and avoiding crowded indoor spaces are the ways to stop the first wave and thwart a second one. And when there are surges like what is happening now in the U.S., further reopening plans need to be put on hold.

This article is republished from The Conversation under a Creative Commons license. Read the original article here: https://theconversation.com/the-us-isnt-in-a-second-wave-of-coronavirus-the-first-wave-never-ended-141032.

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The US isn't in a second wave of coronavirus the first wave never ended - Huron Daily Tribune

Cebuanos complacent and stubborn? – The Freeman

Cebuanos complacent and stubborn?

Among the reasons that PRRD gave for sending former general Cimatu to Cebu last week to help in the COVID-19 pandemic was that Cebuanos are complacent and stubborn. This is a generalization that was debated and contested by many people in main and social media, and an issue worth digging deeper into, not just for Cebuanos, but for all Filipinos and people in general. There are Americans, Europeans, Asians, and all kinds of people all over the world who are not really following the suggested precautions of wearing face masks, physical distancing, crowding, and staying at home.

Human behavior in crisis situations like a pandemic has been studied as an extension of many behavior studies by many sociologists, political scientists and economists. This is important because social studies have no controlled laboratories, but use the open social environment as their laboratories to test theories on human behavior. While it is difficult to arrive at a predominant human reaction or behavior in a given situation, the objective is to get the most probable/possible behavior of the majority or the average person, the average person being an artificial construct representing 70%/80% of the people. Economists also use this concept of the average rational man to determine consumer behavior.

There are actually many factors that affect human behavior and are as varied as there are locations. Geography, environment/climactic conditions, economics, demographics, education levels, and politics are some of them. Hot and cold weather affects peoples temperament, the stage of economic development/wealth distribution/poverty levels are catalysts for extreme behavior, and the young, educated, and uneducated react differently. The prevailing national and local politics which depends on the credibility and capability of the leaders are also major factors in the eventual behavior or misbehavior of people during pandemics.

To effectively and efficiently influence human behavior in this pandemic or in any other situation, the above factors are the givens/backdrops that have to be known, as these cannot be changed in the short term. The authorities have to make a plan, organize, implement, and control, given these prevailing conditions. These are the management and governance parameters. The inadequacy of Cebu and the national government in managing the COVID-19 pandemic is a management and governance issue. There was enough information on the different environments and even the favorable fiscal and monetary conditions of the country at the outset of the pandemic, but the planning, implementing, and control were wanting. The government and Cebu City in particular, is not organized to handle the pandemic. The implementors who are the barangay leaders were far but directly under the mayor, the councilors were not utilized, and the City Hall departments were not properly empowered and coordinated. Planning could also be faulted due to the dearth of available competency as the new mayor had to scout for willing and able staff with the deficiency of the political structure. As a consequence, there was an absence in the control mechanism. The available and generated data before and during the pandemic were inadequate and faulty compounding the management problem. You cannot manage what you cannot measure.

While it is difficult to define or there may not be an average Cebuano or person, there is a normal distribution of personal characteristics/temperaments which can be represented in a normal curve or a Poisson distribution. Most people would fall under 80% to 90% of the curve, while 10% to 20% would be in the fringes, depending on the steepness of the curve. Good governance and good management flatten this distribution curve, (also the COVID-19 infection curve), leaving the complacent and stubborn in the fringes.

Cebuanos, are not more complacent and stubborn than other Filipinos, they were just not as well-managed as those in other areas. Look at Pasig, Marikina, Baguio, and Valenzuela.

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Cebuanos complacent and stubborn? - The Freeman

The Anthropause: How the Pandemic Gives Scientists a New Way to Study Wildlife – WIRED

But with the fishers, the behavioral change in the anthropause happened waaaaay too fast to be genetic. Instead, it could be a change driven by choices made by individuals or groups of animals. You see that personalities differ, says Wikelski. There may be now a selection for certain personalities to enter cities, and that may be propagated through their culture.

The global experiment on the transmission and retention of information in animal societies is just unbelievably beautiful, Wikelski adds.

Scientists can watch such rapid, dramatic behavioral shifts thanks to increasingly sophisticated monitoring equipment. Tracking collars of course map an animals movement, but some now come equipped with inertial measurement units, or IMUs, the same sensors that let you shift your phone around to control a game. This allows researchers to determine if a wild animal has suddenly accelerated, indicating that it might have been startled. An even more sophisticated monitoring device might detect the animals heart rate or listen with a microphone to its interactions with its peers.

It's the Fitbit for animals, says Wikelski. Are they sick? Are they fine? Are they interacting? How quickly are they moving? Are they getting up at the right time, at the same time as before? Are they active differently during the night, during the day?

During the anthropause, researchers can marry this data that tracks animal behavior with data that tracks human behavior, particularly traffic, to show whether a species might be exploiting our absence or going about its business as usual in the wild. As the anthropause continues and eventually wanes, scientists will be able to watch how a species adapts, answering questions that would have been impossible to tackle if not for the pandemic.

Researchers have been trying to solve one of these riddles for decades: Are animals afraid of our built environmentroads, buildings, and other infrastructureor are they afraid of us? We suddenly didn't have humans in many areas, says ecologist Matthias-Claudio Loretto of the Max Planck Institute of Animal Behavior and University of Konstanz, coauthor on the anthropause paper. So, he says, if animals will visit these places during the pandemic shutdown, they're obviously just normally afraid of humans.

On the other hand, if a particular species didnt penetrate a populated area even with humans gone these past few months, that might be an indication that its the built environment keeping them away. But conservation biologists can look at the species that did traipse through an area and note the paths they took.

The riddle gets more nuanced in urban places where the restrictions on movement havent been particularly strict. Maybe a city has allowed residents to go for walks, so animals are still avoiding public parks, but are instead turning up in places that are entirely shut down to people. Some cities may have restricted driving, while others didntresearchers can look at both traffic and animal data to see how species in different areas adapted.

The anthropause is bringing scientists a unique opportunity to study how animals move through built environments; this knowledge could inform new modifications to urban areas to provide safe passage for animals. For example, maybe if we learn that a development or freeway has sliced a species habitat and population in two, we could reunite them to encourage genetic diversityisolated populations, after all, tend to inbreed. It's not good enough that managers tell animals where to go, says Wikelski. Animals should tell us where they need to go, where they want to go. It's the animal-defined corridor that we need.

But not every animal species has benefited from the freedom of having fewer humans around. The generalists among them, like coyotes, rats, and wild boar, may comfortably move about city streets, taking any food they can. But theres nothing for a mountain lion in downtown San Franciscoits prey, like deer, remain in the hilly regions to the south of the city.

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The Anthropause: How the Pandemic Gives Scientists a New Way to Study Wildlife - WIRED

Coronavirus in Ohio: No single number captures the pandemic. But watch this one. – The Cincinnati Enquirer

Cincinnati Enquirer Published 6:23 a.m. ET June 30, 2020 | Updated 4:16 p.m. ET June 30, 2020

There are "four C's" to help keep you safe from coronavirus. Get to know what those are. Cincinnati Enquirer

Back in April, health experts warned Kaiser Health News, a leading provider of health news and information, that a one-day peak in cases would not signal that the tide had turned against the new coronavirus.Two months later, what's clear in Hamilton County is that the trend here is sharply up and there's no clear sign of a peak.

On June 18, the county recorded at least 100 new COVID-19 positive patients for the first time. Since then, seven more days (including Sunday, the last day for which data are available) have exceeded 100 cases.

Scientists use averages to figure out the ups and downsof infectious diseases such as the virus. With the coronavirus, they oftenuse one of three different averages to track trends in new cases.

State officials feature the 21-day moving average on Ohio's coronavirus dashboard. It accounts for the 10 to 14 days that it takes for many people to display symptoms once they've been infected by the virus. (Except that the Centers for Disease Control and Prevention estimates 35% of the infected never show symptoms, a number lower than found in some studies.)

Twenty-one days ago, Hamilton County's21-day average of cases was 38, according to an Enquirer analysis of data from the Johns Hopkins University COVID-19 tracking project. On June 18, that first date of 100-plus cases, the 21-day average was 45. By June 22, when the county had a single-day record of 191 new positive results, the average was 61. A week later, on June 28, it was 89.

With new case totals over 100 foreach of the last five days, the 21-day averagewill keep going higher this week with no plateau, much less a decline, on the horizon.

The average of new cases sometimes is expressed in other ways.

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The seven-day average is used by the Associated Press and other news organizations. Hamilton County's seven-day average is 138 cases, nearly double from the level on June 18 (when that first 100-plus count was reported). The White House coronavirus task force used the 14-day average, keeping in mind the virus' incubation period, when it set up criteria for reopening businesses, schools and the like. The county's 14-day average is 115 cases, more than twice the reading on June 18.

Bottom line: All three averages have risen sharply at the end of this month.

The result: State and even federal officialsare worried we haven't seen a peak in Hamilton County. The county was among the hot spots nationally discussed by Ohio Gov. Mike DeWine in a conference call with Vice President Mike Pence, head of the Trump administration's coronavirus task force.

1. A measure of the coronavirus that's based in part on community spread is flashing red in Hamilton County, as well asin Butler, Kenton and Warren counties.

The measure is the R0 (spoken asR-naught, pronounced AHR-nawt)or reproductive number. Data from the Health Collaborative, a consortium of hospitals in the Cincinnati area, show the virus' R0 in the four counties is above one.The R0indicatesthe number of people, on average, that one infected person will subsequently infect. Any reading above one indicates infections are rising. But it's worth noting that the R0 is an estimate anddifficult to calculate (in part because it measures human behavior, which can change abruptly).

2. Infection rates are highest among younger people in the region, with the positive test rate for those ages 20-30 at over 10%.

The Health Collaborative data show the positive rate in this age group rose in the second half of June to above 10% even as the positive rate fell in all other age groups.

The local data mirrors a national trend. People under 45 made up 42% of cases before Memorial Day weekend but 55% of cases reported since then, USA TODAY analysis has found.

The trend holds in places where new cases are surging and in those that are not, according to the analysis of data from 25 states and the Centers for Disease Control and Prevention.

3. Local hospitals have room but beds are filling

Hospitalizations are rising across the Cincinnati region.The number of COVID-19 patients in Hamilton County's hospitals has doubled from a low of 65 people on June 11 to more than 130 this weekend, DeWine said at his Monday news conference.

The Health Collaborative's dashboard showed the region's hospital and ICU beds just under 80% occupancy on Sunday. So there's room for more patients, but not the surplus of space that existed inearly May, as the pandemic was easing.

In addition, more young people are ending up in the hospital with COVID-19, an Enquirer analysis of state data shows. People under 40 accounted for 11% of Hamilton County hospitalized cases in March and April. But that rose to 19% in May and stands at 37.4% so far in June.

Kaiser Health News and USA TODAY contributed.

Read or Share this story: https://www.cincinnati.com/story/news/2020/06/30/coronavirus-ohio-no-single-number-captures-pandemic-watch-one-hamilton-county/3283338001/

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Coronavirus in Ohio: No single number captures the pandemic. But watch this one. - The Cincinnati Enquirer

US Facebook Advertising Boycott to Expand Internationally – VOA Learning English

American organizers of a Facebook advertising boycott say they are seeking support in Europe to push the social media service to do more to remove hate speech.

The Stop Hate for Profit campaign has received support from more than 160 companies. They include American corporations like Coca-Cola, Levi Strauss & Company, Patagonia and The Hershey Company.

The companies united to stop buying advertising on Facebook, the worlds largest social media company. The boycott, which includes Facebook-owned Instagram, was launched following the death of George Floyd in Minneapolis, Minnesota.

Floyd, a 46-year-old black man, died on May 25 after a white police officer kneeled on his neck for several minutes. The incident was caught on video. Floyds death led to widespread protests across America aimed at police and racial inequality.

Anger over Floyds death also led to public demonstrations in cities across the world. Some corporations also released statements denouncing racism in society.

The Stop Hate for Profit campaign is supported by several U.S. civil rights groups and non-profit media organizations.

One group is the Anti-Defamation League (ADL). The ADL said in a recent open letter that Facebooks hate speech, incitement, and misinformation policies are inequitable.

The group said Facebooks efforts to find and remove hateful material are not effective. It added that a companys ad can appear on Facebook next to hateful or divisive material. The ADL also criticized the company for failing to remove false information appearing in advertisements or published by users.

Critics have said that Facebook reported receiving $70 billion in advertising money in 2019, while earning about $18 billion in profit.

One campaign supporter is the group Free Press. It said that even with such high advertising profits, the company has repeatedly failed to meaningfully address hate, incitement to violence and disinformation across its products.

The Stop Hate for Profit campaign has created a set of demands for Facebook.

Among them are the establishment of a new process to help users targeted with ads based on race and other identifiers. The groups are pushing Facebook to release more information about the number of hate speech reports it receives. They also want the company to stop making money from ads linked to harmful content.

Jim Steyer heads the media education group Common Sense Media. He recently told the Reuters news agency that the campaign will start calling on major companies in Europe to join the boycott.

The next frontier is global pressure, said Steyer. He added that he hopes the campaign will lead regulators in Europe to reexamine policies covering the social media company. Earlier this month, the European Commission announced new guidelines for technology companies to report monthly how they are attempting to reduce misinformation about the new coronavirus.

Steyer said the campaign will urge major international advertisers like Unilever and Honda - which have already stopped buying U.S. ads - to halt all Facebook ads worldwide.

Campaign organizers say they also plan to keep urging more U.S. companies to take part in the boycott. Jessica Gonzalez is co-leader of the group Free Press. Gonzalez told Reuters she recently contacted big U.S. telecommunications and media companies to ask them to join.

Responding to demands for more action, Facebook has admitted the company has more work to do. It said it was working with civil rights groups and experts to develop more tools to fight hate speech. Facebook said its investments in artificial intelligence (AI) tools permit the company to identify about 90 percent of hate speech before users report it.

Im Bryan Lynn.

Sheila Dang reported this story for Reuters. Bryan Lynn adapted the report for VOA Learning English, with additional information from the Stop Hate for Profit campaign and online sources. Mario Ritter, Jr. was the editor.

We want to hear from you. Write to us in the Comments section, and visit our Facebook page.

________________________________________________________________

kneel v. to put one or both knees on the ground

inequitable adj. not fair

divisive adj. causing disagreements between people

address v. to discuss

content n. the information or ideas included in a book, film or on the internet

frontier n. the limits of what is known or what has been done before

regulator n. the prople or institutions that make rules or laws that control something

artificial intelligence n. the power of a machine to copy intelligent human behavior

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US Facebook Advertising Boycott to Expand Internationally - VOA Learning English

How Shelter-In-Place Orders Affected Atlanta’s Air Pollution | 90.1 FM WABE – WABE 90.1 FM

In Atlanta, its getting hot and traffic is coming back, which means air quality will go downhill.

Still, if it seemed like this spring the air was better while so many people were sheltering in place, thats because it was, at least in some respects.

In March, people started staying home because of the coronavirus. In April, it became mandatory statewide. And that had a dramatic effect on traffic.

On the Perimeter, for example, before the shutdown, there were about 217,000 vehicles a day, according to Christina Fuller, a public health and air pollution expert at Georgia State. After the governors shelter-in-place order, the number came down to about 133,000 a day, she said.

Thats almost a 40% decrease in cars and trucks that are on the highways, she said.

And that had an effect on particulate matter, a pollutant from tailpipes and smokestacks that can contribute to conditions including asthma and heart disease. Using data from air monitors in Atlanta, including along roads, Fuller said she could see that levels of particulate matter had dropped.

Theyve been consistently lower in the air, especially for the month of April, she said.

The change cant necessarily all be attributed to people not driving because weather can have an effect: rain can temporarily lower levels of particulate matter, while cooler temperatures can lead to an increase. So there will need to be more analysis to sort things out, Fuller said.

Pulling back, changes were apparent on a bigger scale, too.

NASA scientist Bryan Duncan, whos a Georgia Tech alumnus, uses satellites to study air quality. One pollutant in particular that he looks at is nitrogen dioxide, another one that affects peoples health.

It has a relatively short lifetime. Once its emitted, its around only for a matter of hours. So researchers can see hot spots where its coming from.

Over cities, over power plants, sometimes major highways. So its a great indicator of pollution in general, Duncan said.

In March and April, he said, nitrogen dioxide levels over a lot of the East Coast, including Atlanta, decreased by about 30% to 40%.

Like Fuller, he cautioned that there has to be more analysis to figure out exactly what happened where, and to sort out whats because of changes in human behavior versus the weather.

Still, he said, Its absolutely dramatic.

But theres a lot of different kinds of pollution out there, and not everything is so clear.

Ozone, for instance, is more complicated to untangle.

Ozones a really neat pollutant, said Ted Russell, a professor of environmental engineering at Georgia Tech, where he studies air quality.

During the spring, ozone levels are typically lower in Atlanta. And its not a pollutant that comes directly from cars or industrial sources. Instead, its a result of emissions from those sources but also from trees reacting to sunlight.

A recent analysis by NPR found that even though traffic has been down around the country, ozone hasnt dropped nearly as much as expected. Russell said thats not surprising, since ozone doesnt come directly from traffic and its so affected by season and weather.

When I look at the air quality data for ozone, its not that clear at all, and in part because the meteorology plays such a big role, he said. So for ozone, we really cant tell if its the meteorology thats making the biggest difference day to day or the emissions.

All these pollutants particulate matter, ozone and nitrogen dioxide are things that affect peoples health, not the greenhouse gases that contribute to climate change.

With carbon dioxide which also comes from tailpipes and smokestacks its harder to see local effects. There is a lot of it, and its long-lived. So its all just muddled in the atmosphere, not at certain hot spots. Nationwide, carbon emissions have gone down, but like the other pollutants are likely to come back up.

Still, Duncan said maybe pollution wont bounce back quite as much. Hes learned he likes telecommuting, and he hopes to continue doing it a couple days a week.

And I think other people may realize that, too, he said.

People may also get new insight into the connection between their cars and air quality, said Fuller.

Because it may be difficult for people to think, Oh, when Im driving my car, then what does that do? How much can I contribute? But we see that as a group, it really does make a big difference, she said.

She said that if people want to keep seeing cleaner air going forward, there are going to have to be bigger changes in policy and in planning.

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Dragons of immunology | Opinion – Chemistry World

Since everyone is being forced these days to think about immunology, lets consider it in terms of chemistry and drug discovery. You can get two very different perspectives based on where you stand. From one view, inflammation and immune response might look like a wonderfully productive area for small molecules. Aspirin, dexamethasone, ibuprofen, hydrocortisone there are classic drugs that work on and near these pathways and have been used successfully by uncounted millions of patients. In the modern era, the list of best-selling prescription drugs prominently features antibodies and fusion proteins aimed at immunologic targets such as TNF-alpha and CD20, as treatments for inflammatory diseases from rheumatoid arthritis to cancer.

But from another vantage point, the whole field is full of trap doors, dead ends, and irritable dragons. Dexamethasone and other such steroids have such powerful effects (and powerful side effects) that they have to be administered carefully and for short periods. Thats why compounds such as ibuprofen were hailed as being anti-inflammatories that (good news!) werent steroids. The list of potential side effects for those antibodies is also long and impressive. To pick a particularly dramatic example that many will recall, a 2006 attempt by TeGenero to create a super-agonist for the T-cell receptor CD28 led to catastrophic effects in the Phase 1 volunteers, many of whom barely survived the initial dose.

Thats what the immune system has to offer: tremendous power, but power that can be aimed in all sorts of directions. And because immunology itself is so wildly, insanely complicated, there are a bewildering number of potential targets to think about. Were looking at hundreds of millions of years of evolutionary tinkering; there are layers upon layers of tangled, interlocking signaling pathways and mechanisms. Theres the innate immune system always on but rather nonselective and the adaptive system that features a gigantic combinatorial chemical library of antibodies that we all carry around with us for our entire lives slower to get going, but capable of feats of recognition that we still have trouble matching in the laboratory. Those aeons of evolution have been a walk down the narrow path between too little activity, opening the door to fatal infections, and too much, leading to autoimmune syndromes and responses to an infection that are worse than the disease itself. Its little wonder that the systems are encrusted with regulatory loops, flywheels, and gear-shifting mechanisms.

As usual, most of what drug discovery has to offer is an assortment of grit, sand, and spanners to throw into this apparatus. We are far, far better at shutting particular enzymes and receptors down than we are in turning any particular signal up. When you do see a drug mechanism that enhances some sort of activity, odds are good that it works by inhibiting something else that was in turn suppressing the desired target. A great number of interesting ideas in the field dont seem to be amenable to small-molecule manipulation at all, which is where those antibodies come in. The requisite binding sites can be too large and the selectivity needed to target them may be too great for anything other than a good-sized protein to have a chance.

Thats meant that immunology has been a proving ground for new therapeutic ideas and new modes of action. Monoclonal antibodies and fusion proteins are just the beginning. Mechanisms targeting protein expression, intra- and extracellular localisation, degradation, and the intricate varieties of post-translational modification are all highly relevant to immune and inflammation pathways. Add in the number of genetic immunological problems that can occur in the population, which would be targets for gene therapy or RNA mechanisms, and you have the whole range of cutting-edge drug research being brought in.

Most of these are too early in the process to be of likely use against the Covid-19 pandemic, of course. But we are learning a great deal about immunology very quickly under these conditions, with the huge efforts going into characterising the pathogen; treating the overactive immune response to it; and developing antibodies and vaccines against it. Well come out of this, and well come out of it with more tools and more knowledge than when we went in all acquired at a faster pace than we ever would have achieved otherwise. Lets take the benefits where we can find them!

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Dragons of immunology | Opinion - Chemistry World

What’s the answer to slowing the spread of COVID-19 for older adults? – Aspen Times

Theres a lot of stupid floating around out there.

Thats what South Carolina Gov. Henry McMaster said during a recent news conference in which he pleaded with the public to make better decisions to slow the spread of COVID-19.

Thats the best quote ever its how you explain the recent surge (in cases), said Dr. Michael Schmidt, PhD, a professor of microbiology and immunology at the Medical University of South Carolina.

Dr. Schmidt is the guest host of an upcoming webcast, How Colorado Can Work Smarter to Slow the Spread of COVID-19 in Older Adults, presented by Renew Senior Communities. Renew CEO Lee Tuchfarber is co-hosting.

This is a plague for which the human race has a choice, Dr. Schmidt said. We already know how to stop this virus dead in its tracks.

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Much of the discussion will focus on how we can do our part as a society to slow the spread, but Dr. Schmidt will also discuss promising light at the end of the tunnel. From the potential that oral polio vaccines can safely and cheaply protect the U.S. population to excitement over bluetooth technology expanding the efficiency of contact tracing, Dr. Schmidt said various stop-gap measures could make a big difference until theres a COVID-19 vaccine.

The only thing more infectious than this virus is hope, he said.

Personal responsibility

The way we control the virus is really straightforward, Dr. Schmidt said its hygiene.

Wearing a mask to protect others, washing your hands and keeping a physical distance of at least six feet from other people are the most effective safety precautions.

If weve learned one thing, there are a lot of folks out there who are infected and dont know it, he said. The mere act of speech actually can spread the virus. So, if youre out carrying your business and talking, wear a mask.

Physical distancing is your only hope if youre not wearing a mask. The hope being that the virus dissipates in the air before smashing into your face.

Many medical folks are wearing face shields because the virus can come in from your tear ducts, Dr. Schmidt said.

As for hand hygiene, simple soap and water is all you need. The Centers for Disease Control and Prevention recommends washing hands for at least 20 seconds.

Strict safety protocols have proven to work at Renew Senior Livings two communities in Aurora and Glenwood Springs. Tuchfarber said all residents at both communities have remained COVID-free while a great number of the senior living facilities in Colorado have experienced outbreaks.

Renew put various safety measures in place for staff before they enter the building, and theyve even provided staff with meals to take home to their families to decrease their need to go to the grocery store. Much of this decision-making is data-driven, with various phases of safety measures implemented depending on the R-naught (Ro), which is the estimate of the number of people to whom each infected person spreads the virus.

Theres an inherent spreadability of the virus itself, but theres also an environmental factor, Tuchfarber said. So behavior can really affect the Ro.

What: How Colorado Can Work to Slow the Spread of COVID-19 for Older Adults, a webcast talk series presented by Renew Senior Communities.

When: Wednesday, July 1, 3 to 4 p.m.

Where: Register for free at renewsenior.com.

Featured co-host: Dr. Michael Schmidt, PhD, is a professor of microbiology and immunology at the Medical University of South Carolina. He is a well-published expert in the area of

infectious disease control and pandemics. He ran the American Society for Microbiology

and set its research priorities for vaccines and testing. He hosts a podcast called, This

Week in Microbiology. Dr. Schmidt is an advisor to MicrogenDx, the second largest next

generation testing lab in the U.S.

Testing

Testing serves a vital role in understanding and controlling the spread of COVID-19, Dr. Schmidt said. He points to data from Taiwan, a densely populated island that has managed to keep its number of confirmed cases of COVID-19 to date to less than 450 thanks to aggressive testing and contract tracing.

Going forward, given that we know there is significant asymptomatic and presymptomatic transmission of the virus, pre-emptive testing may be a way we help slow the spread of the virus in areas that have suddeningly seen a surge in an increase in new cases, he said. Simply, local areas may wish to routinely screen random members within their community looking for an up-turn in the number of cases. Such a program will be especially important to companies with public-facing employees, so that they can ensure that their employees and customers are as safe as possible.

Renew is working on a strategy for preemptive testing rather than waiting for a positive case and then reacting to it. Tuchfarber said Renew should be implementing that new protocol very soon.

Preemptive testing of all staff on a regular basis, unprompted by a positive test result, is presently a rarity in our industry, but is an important measure to assure safety. We are preparing to integrate this program in our COVID-19 safety regimen, Tuchfarber said. This is an extra measure of safety that we feel strongly about taking.

Facilitating a global response

In an effort to facilitate a global response, scientists are looking at three strategies: diagnostics, therapeutics and vaccines.

Diagnostics essentially look at how we can slow the spread faster and better, while therapeutics focus on the use of drugs.

If were going to restart the economy, we need two to three drugs so the virus doesnt adapt to the drugs like it did with HIV and hepatitis C in the 1980s, Dr. Schmidt said.

Vaccines are the area for which Dr. Schmidt is truly excited. There are more than 90 candidate vaccines currently being studied, with microbiologists, structural biologists, physiologists and others all pulling in the same direction.

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What's the answer to slowing the spread of COVID-19 for older adults? - Aspen Times

Cause of Common Autoinflammatory Disease May Have Protected Ancestors From Plague – Technology Networks

Researchers have discovered that Mediterranean populations may be more susceptible to an autoinflammatory disease because of evolutionary pressure to survive the bubonic plague. The study, carried out by scientists at the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health, determined that specific genomic variants that cause a disease called familial Mediterranean fever (FMF) may also confer increased resilience to the plague.

The researchers suggest that because of this potential advantage, FMF-causing genomic variants have been positively selected for in Mediterranean populations over centuries. The findings were published in the journal Nature Immunology.

Over centuries, a biological arms race has been fought between humans and microbial pathogens. This evolutionary battle is between the human immune system and microorganisms trying to invade our bodies. Microbes affect the human genome in many ways. For example, they can influence some of the genomic variation that accumulates in human populations over time.

"In this era of a new pandemic, understanding the interplay between microbes and humans is ever critical," said Dr. Dan Kastner, NHGRI scientific director and a co-author on the paper. We can witness evolution playing out before our very eyes.

One such microbe is Yersinia pestis, the bacterial agent responsible for a series of well-documented bubonic plague(link is external) epidemics that led to over 50 million deaths.

FMF, like the plague, is an ancient disease. It is the most common periodic fever syndrome, and symptoms of FMF include recurrent fevers, arthritis, rashes and inflammation of the tissues that line the heart, lungs, and abdominal organs. FMF may also lead to renal failure and death without treatment. The disease appears across the Mediterranean region and mostly affects Turkish, Jewish, Armenian and Arab populations.

Genomic variants in the MEFV gene cause FMF. MEFV encodes a protein called pyrin. In healthy people, pyrin plays a role in the inflammatory response of the body. Pyrin is activated when there is an immune response (for example, in the event of an infection). Pyrin increases inflammation and the production of inflammation-related molecules.

In contrast, FMF patients produce abnormal pyrin because of genomic variants (mutations) in the MEFV gene. Mutated pyrin does not need an infection or other immune trigger to be activated; rather, it is able to directly predispose people to seemingly unprovoked episodes of fever and inflammation.

The MEFV mutations also have other usual properties. Researchers have discovered that people with only one copy of a MEFV genomic variant that causes FMF do not get the disease. Also, prior to effective treatment, those with two copies have high mortality rate by the age of 40, but usually live long enough to have children.

Despite the lower survival rate, almost 10% of Turks, Jews, Arabs and Armenians carry at least one copy of an FMF-causing genomic variant. If chance were the only factor, that percentage would be much lower.

The researchers proposed that this higher percentage was a consequence of positive natural selection, which is an evolutionary process that drives an increase in specific genomic variants and traits that are advantageous in some way.

"Just like sickle cell trait is positively selected for because it protects against malaria, we speculated that the mutant pyrin in FMF might be helping the Mediterranean population in some way," said Jae Jin Chae, Ph.D., senior author of the paper and a staff scientist in NHGRI's Metabolic, Cardiovascular and Inflammatory Disease Genomics Branch. "The mutant pyrin may be protecting them from some fatal infection."

The team turned to Yersinia pestis, the infamous bubonic plague-causing bacterium, as a possible candidate for driving the evolutionary selection for FMF mutations in the Mediterranean population.

It turns out Yersinia pestis contains a particular molecule that represses the function of pyrin in healthy individuals. In doing so, the pathogen suppresses the body's inflammatory response to the infection. This way, the body cannot fight back.

"Inflammation is a process in which white blood cells protect the body from infection. From the host's point of view, inflammation helps us survive. From the bacteria's point of view, inflammation is something to be evaded by any means available," said Daniel Shriner, Ph.D., staff scientist in the Center for Research on Genomics and Global Health at NHGRI.

Researchers were struck by the fact that Yersinia pestis affects the very protein that is mutated in FMF. They considered the possibility that FMF-causing genomic variants may protect individuals from the bubonic plague caused by Yersinia pestis.

The idea that evolution would push for one disease in a group to fight another may seem counterintuitive. But it comes down to what is the least bad option.

The average mortality rate of people with bubonic plague over centuries has been as high as 66%, while, even with a carrier frequency of 10%, less than 1% of the population has FMF. Theoretically, the evolutionary odds are in the latter's favor.

But first, the team had to verify if two of the genomic variants that cause FMF had indeed undergone positive selection in Mediterranean populations.

For this, they performed genetic analysis on a large cohort of 2,313 Turkish individuals. They also examined genomes from 352 ancient archaeological samples, including 261 from before the Christian era. The researchers tested for the presence of two FMF-causing genomic variants in both groups of samples. They also used population genetics principles and mathematical modeling to predict how the frequency of FMF-causing genomic variants changed over generations.

"We found that both FMF-causing genomic variants arose more than 2,000 years ago, before the Justinian Plague and the Black Death. Both variants were associated with evidence of positive selection," said Elaine Remmers, Ph.D., associate investigator in NHGRI's Metabolic, Cardiovascular and Inflammatory Disease Genomics Branch.

Researchers then studied how Yersinia pestis interacts with FMF-causing genomic variants. They took samples of particular white blood cells from FMF patients. In addition, they took samples from people who carry just one copy of the genomic variants (hence, do not get the disease).

The team found that Yersinia pestis does not reduce inflammation in white blood cells acquired from FMF patients and people with one copy of FMF-causing genomic variants. This finding is in stark contrast to the fact that Yersinia pestis reduces inflammation in cells without FMF-associated mutations.

The researchers thought that if Yersinia pestis does not reduce inflammation in people with FMF, then perhaps this could potentially increase patients' survival rate when infected by the pathogen.

To test this hypothesis, the researchers genetically engineered mice with FMF-causing genomic variants. They infected both healthy and genetically engineered mice with Yersinia pestis. Their results showed that infected mice with the FMF-causing genomic variant had significantly increased survival as compared to infected healthy mice.

These findings, in combination, indicate that over centuries, FMF-causing genomic variants positively selected in Turkish populations play a role in providing resistance to Yersinia pestis infection. Whether the same is true for other Mediterranean populations remains to be seen. The study offers a glimpse into the unexpected and long-lasting influence of microbes on human biology.

ReferencePark, Y.H., Remmers, E.F., Lee, W. et al. Ancient familial Mediterranean fever mutations in human pyrin and resistance to Yersinia pestis. Nat Immunol (2020). https://doi.org/10.1038/s41590-020-0705-6.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Cause of Common Autoinflammatory Disease May Have Protected Ancestors From Plague - Technology Networks