Study connects specific genes with defective social behavior – Harvard Gazette

Animals rely on group behavior to survive, whether its fish swimming together to avoid predators or humans sharing knowledge with each other. But despite the importance of such social interactions, scientists do not have a good understanding of the biological processes that guide collective behavior.

In a new study published in iScience, researchers at Harvard University and the Max Planck Institute of Animal Behavior developed a new way to study how genes influence collective behavior. Using zebrafish as a model, they set out to establish the connection between genetic mutations and behavior.

We are interested in answering a fundamental biological question: why do animals live in groups? said Mark Fishman, Harvard professor of stem cell and regenerative biology. To search for genes that affect collective behavior, we focused on genetic mutations that are associated with psychiatric diseases that have a social behavior component, including autism and schizophrenia.

The team observed that in fish with specific genetic mutations associated with human psychiatric disease, group behavior was altered. The findings pave the way for a new generation of research into neuropsychiatric conditions such as bipolar disorder, autism, and depression.

The researchers tested 90 different genes to see if they affect zebrafish social behavior, using gene editing to mutate one gene at a time. For each genetic mutation, the researchers put the edited fish together in a large tank to see how they interacted with each other.

We used computer vision to track individual fish and analyze their interactions, said Fishman. By documenting how interactions change among the fish whether they get out of each others way, or whether they align with each other we could see how the overall pattern of group behavior changes.

The researchers found several genetic mutations that had a distinctive effect on fish group behavior. Normally, zebrafish spend much of their time in dynamically moving groups, called schools when all moving together in a coordinated fashion, and shoals when in less directed groups. Some mutations affected these groups, for example causing the fish to be scattered throughout the tank, or huddling together in one location.

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Study connects specific genes with defective social behavior - Harvard Gazette

Why do dozens of diseases wax and wane with the seasonsand will COVID-19? – Science Magazine

People seeking help for pandemic influenza in Brazil in July 2009, when cold weather boosted the spread of the disease.

By Jon CohenMar. 13, 2020 , 7:41 PM

On a December afternoon, 13 days before the winter solstice, six men and women checked into the Surrey Clinical Research Facility, part of the University of Surrey in the United Kingdom. After having their noses swabbed to check for 16 different respiratory viruses, they walked into their own temperature-regulated rooms and, for 24 hours, each person stayed in a semirecumbent position in dim light. Nurses placed a cannula into a vein of each persons arm, allowing easy sampling of blood that flowed through a tube to portals in the wall. The six subjects could press buzzers for bathroom breaks, where the stool and urine were collected, but otherwise, they were alone in the near-dark.

None of these people were sick. And although the shortest day of the year was approaching, their ritual had nothing to do with pagan rites, Yuletide traditions, or the annual hippie gathering at nearby Stonehenge to celebrate the rebirth of the Sun. Instead, they were paid volunteers in a study led by infectious disease ecologist Micaela Martinez of Columbia University to investigate a phenomenon recognized 2500 years ago by Hippocrates and Thucydides: Many infectious diseases are more common during specific seasons. Its a very old question, but its not very well studied, Martinez says.

Its also a question that has suddenly become more pressing because of the emergence of COVID-19. With SARS-CoV-2, the virus that causes the disease, now infecting more than 135,000 around the globe, some hope it might mimic influenza and abate as summer arrives in temperate regions of the Northern Hemisphere, where about half of the worlds population lives. U.S. President Donald Trump has expressed that hope repeatedly. Theres a theory that, in April, when it gets warmhistorically, that has been able to kill the virus, Trump said on 14 February. But whats known about other diseases doesnt offer much support for the idea that COVID-19 will suddenly disappear over the next few weeks.

Different diseases have different patterns. Some peak in early or late winter, others in spring, summer, or fall. Some diseases have different seasonal peaks depending on latitude. And many have no seasonal cycle at all. So no one knows whether SARS-CoV-2 will change its behavior come spring. I would caution over-interpreting that hypothesis, Nancy Messonnier, the point person for COVID-19 at the U.S. Centers for Disease Control and Prevention, said at a press conference on 12 February. If the seasons do affect SARS-CoV-2, it also could defy that pattern in this first year and keep spreading, because humanity has not had a chance to build immunity to it.

Even for well-known seasonal diseases, its not clear why they wax and wane during the calendar year. Its an absolute swine of a field, says Andrew Loudon, a chronobiologist at the University of Manchester. Investigating a hypothesis over several seasons can take 2 or 3 years. Postdocs can only get one experiment done and it can be a career killer, Loudon says. The field is also plagued by confounding variables. All kinds of things are seasonal, like Christmas shopping, says epidemiologist Scott Dowell, who heads vaccine development and surveillance at the Bill and Melinda Gates Foundation and in 2001 wrote a widely cited perspective that inspired Martinezs current study. And its easy to be misled by spurious correlations, Dowell says.

Despite the obstacles, researchers are testing a multitude of theories. Many focus on the relationships between the pathogen, the environment, and human behavior. Influenza, for example, might do better in winter because of factors such as humidity, temperature, people being closer together, or changes in diets and vitamin D levels. Martinez is studying another theory, which Dowells paper posited but didnt test: The human immune system may change with the seasons, becoming more resistant or more susceptible to different infections based on how much light our bodies experience.

Beyond the urgent question of what to expect with COVID-19, knowing what limits or promotes infectious diseases during particular times of year could point to new ways to prevent or treat them. Understanding seasonality could also inform disease surveillance, predictions, and the timing of vaccination campaigns. If we knew what suppressed influenza to summertime levels, that would be a lot more effective than any of the flu vaccines we have, Dowell says.

At least 68 infectious diseases are seasonal, according to a 2018 paper by Micaela Martinez of Columbia University. But theyre not in sync, and seasonality varies by location. In this graphic, based on U.S. federal and state health records, each bubble represents the percentage of annual cases that occurred in each month. (The data are old because many diseases declinedin some cases to zeroafter introduction of vaccines.)

(GRAPHIC) N. Desai/Science; (DATA) Project Tycho

Martinez becameinterested in seasonality when, as an undergraduate at the University of Alaska Southeast, she had a job tagging Arctic ringed seals, doing skin biopsies and tracking their daily and seasonal movements. While working on her Ph.D., her focus on seasonality shifted to polio, a much-feared summer disease before the advent of vaccines. (Outbreaks often led to the closing of swimming pools, which had virtually nothing to do with viral spread.) Polio seasonality in turn made her curious about other diseases. In 2018, she published The calendar of epidemics inPLOS Pathogens, which included a catalog of 68 diseases and their peculiar cycles.

Except in the equatorial regions, respiratory syncytial virus (RSV) is a winter disease, Martinez wrote, but chickenpox favors the spring. Rotavirus peaks in December or January in the U.S. Southwest, but in April and May in the Northeast. Genital herpes surges all over the country in the spring and summer, whereas tetanus favors midsummer; gonorrhea takes off in the summer and fall, and pertussis has a higher incidence from June through October. Syphilis does well in winter in China, but typhoid fever spikes there in July. Hepatitis C peaks in winter in India but in spring or summer in Egypt, China, and Mexico. Dry seasons are linked to Guinea worm disease and Lassa fever in Nigeria and hepatitis A in Brazil.

Seasonality is easiest to understand for diseases spread by insects that thrive during rainy seasons, such as African sleeping sickness, chikungunya, dengue, and river blindness. For most other infections, theres little rhyme or reason to the timing. Whats really amazing to me is that you can find a virus that peaks in almost every month of the year in the same environment in the same location, says Neal Nathanson, an emeritus virologist at the University of Pennsylvania Perelman School of Medicine. Thats really crazy if you think about it. To Nathanson, this variation suggests human activitysuch as children returning to school or people huddling indoors in cold weatherdoesnt drive seasonality. Most viruses get transmitted between kids, and under those circumstances, youd expect most of the viruses to be in sync, he says.

Nathanson suspects that, at least for viruses, their viability outside the human body is more important. The genetic material of some viruses is packaged not only in a capsid protein, but also in a membrane called an envelope, which is typically made of lipids. It interacts with host cells during the infection process and helps dodge immune attacks. Viruses with envelopes are more fragile and vulnerable to adverse conditions, Nathanson says, including, for example, summertime heat and dryness.

A 2018 study inScientific Reportssupports the idea. Virologist Sandeep Ramalingam at the University of Edinburgh and his colleagues analyzed the presence and seasonality of nine virusessome enveloped, some notin more than 36,000 respiratory samples taken over 6.5 years from people who sought medical care in their region. Enveloped viruses have a very, very definite seasonality, Ramalingam says.

In a study in New York and New Jersey, Micaela Martinez hopes to find out how artificial lighting affects the immune system.

RSV and human metapneumovirus both have an envelope, like the flu, and peak during the winter months. None of the three are present for more than one-third of the year. Rhinoviruses, the best-known cause of the common cold, lack an envelope andironicallyhave no particular affinity for cold weather:The study found them in respiratory samples on 84.7% of the days of the year and showed that they peak when children return to school from summer and spring holidays. Adenoviruses, another set of cold viruses, also lack an envelope and had a similar pattern, circulating over half the year.

Ramalingams team also studied the relationship between viral abundance and daily weather changes. Influenza and RSV both did best when the change in relative humidity over a 24-hour period was lower than the average (a 25% difference). Theres something about the lipid envelope thats more fragile when the humidity changes sharply, Ramalingam concludes.

Jeffrey Shaman, a climate geophysicist at Columbia, contends that what matters most is absolute humiditythe total amount of water vapor in a given volume of airand not relative humidity, which measures how close the air is to saturation. In a 2010 paper inPLOS Biology, Shaman and epidemiologist Marc Lipsitch of the Harvard T.H. Chan School of Public Health reported that drops in absolute humidity better explained the onset of influenza epidemics in the continental United States than relative humidity or temperature. And absolute humidity drops sharply in winter, because cold air holds less water vapor.

Why lower absolute humidity might favor some viruses remains unclear, however. Variables that could affect the viability of the viral membrane could include changes in osmotic pressure, evaporation rates, and pH, Shaman says. Once you get down to the brass tacks of it, we dont have an answer.

Will SARS-CoV-2, which has an envelope, prove fragile in spring and summer, when absolute and relative humidity climb? The most notorious of the other coronavirus diseases, SARS and Middle East respiratory syndrome (MERS), offer no clues. SARS emerged in late 2002 and was driven out of the human population in the summer of 2003 through intensive containment efforts. MERS sporadically jumps from camels to humans and has caused outbreaks in hospitals, but never widespread human-to-human transmission like COVID-19. Neither virus circulated for long enough, on a wide enough scale, for any seasonal cycle to emerge.

If we knew what suppressed influenza to summertime levels, that would be a lot more effective than any of the flu vaccines we have.

Four human coronaviruses that cause colds and other respiratory diseases are more revealing. Three have marked winter seasonality, with few or no detections in the summer, molecular biologist Kate Templeton, also at the University of Edinburgh, concluded in a 2010 analysis of 11,661 respiratory samples collected between 2006 and 2009. These three viruses essentially behave like the flu.

That does not mean COVID-19 will as well. The virus can clearly transmit in warm, humid climates: Singapore has more than 175 cases. Two new papers published on preprint servers this week come to opposite conclusions. One, co-authored by Lipsitch, looked at COVID-19 spread in 19 provinces across China, which ranged from cold and dry to tropical, and found sustained transmission everywhere. The second study concludes that sustainedtransmission appears to occur only in specific bands of the globe that have temperatures between 5C and 11C and 47% to 70% relative humidity.

In the final analysis, theres a balancing act between environmental factors and a populations immune system. The other coronaviruses have long been around, so a certain part of the population has immunity, which may help exile those viruses under unfavorable conditions. But thats not true for COVID-19. Even though there might be a big seasonal decline, if enough susceptible people are around, it can counter that and continue for a long time, Martinez says. Lipsitch doesnt think the virus will go poof in April either. Any slowdown is expected to be modest, and not enough to stop transmission on its own, he wrote in a recent blog post.

In Surrey, Martinez is investigating a different factor that might eventually affect COVID-19 incidence. Her subjects have returned to the clinic repeatedlyat the winter and summer solstices and again at the spring and autumn equinoxesso the researchers can evaluate how their immune system and other physiology change over the course of the day and from season to season.

She doesnt expect to show that our immunity is, say, weaker in the winter and stronger in the summer. But by counting different immune system cells, assessing metabolites and cytokines in the blood, deciphering the fecal microbiome, and measuring hormones, Martinezs team hopes to find that the seasons may restructure the immune system, making some types of cells more abundant in certain locales, and others less, in ways that influence our susceptibility to pathogens.

Animal studies support the idea that immunity changes with the seasons. Ornithologist Barbara Hall from the University of Groningen and her colleagues, for example, studied European stonechats, small songbirds that they caught and then bred in captivity. By taking multiple blood samples over the course of 1 year, they found that the birds ramp up their immune systems in the summer, but then tamp them down in the autumn, the time they migrate, presumably because migration is a big drain on their energy.

Melatonin, a hormone primarily secreted at night by the pineal gland, is a major driver of such changes. Melatonin keeps track of the time of day but is also a biological calendar for the seasons, says Randy Nelson, an endocrinologist at the University of West Virginia who specializes in circadian rhythms. When nights are long, more melatonin is released. The cells say, Oh, Im seeing quite a bit of melatonin, I know, its a winter night. In studies of Siberian hamsterswhich, unlike mice, are diurnalNelson and his co-workers have shown that administering melatonin or altering light patterns can change immune responses by up to 40%.

Seasonal changes in humidity, temperature, and other factors may affect the viability of viruses in droplets produced when people sneeze or cough.

The human immune system, too, seems to have an innate circadian rhythm. For instance, a vaccine trial in 276 adults by researchers at the University of Birmingham randomly assigned half to receive an influenza vaccine in the morning and the other half in the afternoon. Participants in the morning group had significantly higher antibody responses to two of the three flu strains in the vaccine, the researchers reported in 2016.

Theres evidence of seasonal variation in the actions of human immune genes as well. In a massive analysis of blood and tissue samples from more than 10,000 people in Europe, the United States, Gambia, and Australia, researchers at the University of Cambridge found some 4000 genes related to immune function that had seasonal expression profiles. In one German cohort, expression in white blood cells of nearly one in four genes in the entire genome differed by the seasons. Genes in the Northern Hemisphere tended to switch on when they were switched off south of the equator, and vice versa.

Just how these massive changes affect the bodys ability to fight pathogens is unclear, however, as immunologist Xaquin Castro Dopico and colleagues explain in a 2015 paper describing the findings. And some changes could be the result of an infection, instead of the cause. The team tried to eliminate people who had acute infections, but of course a seasonal infectious burden likely plays a part, says Dopico, who now is at the Karolinska Institute. And seasonal immunity changes could not explain all the complex variation in seasonality that diseases show. Theyre all out of sync with each other, Nathanson points out. Hes also skeptical that seasonal immune system changes could be large enough to make a difference. It would have to be pretty markedly different.

Martinez, however, says she has found intriguing hints. Early analyses from her Surrey study, which ended collecting data in December 2019, dont reveal anything about seasonality yet, but they do show that specific subsets of white blood cells that play central roles in immune system memory and response are elevated at certain times of day. She hopes to firm up the finding by launching a similar but larger study next year.

Martinez cautions, however, that artificial light may play havoc with the circadian rhythms that have evolved, with unpredictable effects on disease susceptibility. To explore possible impacts, Martinez has a separate study underway, with Helm, in both urban and rural parts of New York and New Jersey. They have installed light sensors on trees and poles and outfitted participants with devices that monitor light exposure and body temperature. The fact that people really are just kind of washing out the rhythms in light exposure can be problematic, she says.

Experiments of naturecould also offer insights into the factors affecting disease seasonality, Dowell suggested in his 2001 paper. People from the Southern and Northern Hemispheres who have adapted to different seasons regularly mix on cruise ships or at conventions, where they are confronted by the same pathogens. Witness the massive COVID-19 outbreak on thePrincess Diamond, which was docked and quarantined in Yokohama, Japan, for 2 weeks last month: Researchers could potentially analyze whether they were infected at different rates.

Whatever the answers, they might eventually bring important public health benefits, Martinez says. For example, If we know how best to administer vaccines, in terms of what time of year and the best time of day to take advantage of our immune systems, then we can get a lot more bang for our buck, she says.

The global COVID-19 emergency may bring more attention to the research and help speed discoveries, she says. But for now, no one knows whether rising humidity, the lengthening days, or some as-yet-unsuspected seasonal effect will come to the rescueor whether humanity must confront the pandemic without any help from the seasons.

Time will tell.

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Why do dozens of diseases wax and wane with the seasonsand will COVID-19? - Science Magazine

Trivially Speaking: Go back to 1976 to trace the origin of the meme – Loveland Reporter-Herald

Once in a while its not very often I encounter a new word. My English background and reading habits limit this meeting to only a few opportunities.

Recently, I did stumble on one that I first thought was simply a misspelling of memo. The word was meme.

In my prior gainful employment I read many memos and even wrote a few. As you would know, memo is just the short version of memorandum (from the Latin, It must be remembered).

Most of them even the ones I wrote werent of the must be remembered variety. I always believed that the Latin word was just in the wrong order; it should have been random memo. However, I digress.

Anyone who has held a job in a company, school district or government knows what a memo is (but Ill bet cant quote one from memory).

So when I went resource-fishing for meme I netted something entirely different.

If youre familiar with memes, hold up your hand and you can be excused from the rest of this column.

A meme is an idea, behavior or style that spreads by imitation from person to person within a culture.

This is where it gets tricky. Often the meme has the aim of carrying a particular theme or meaning. The meme is the vehicle for transmitting ideas, practices or symbols from one brain to another through writing, gesture, ritual or other imitable act with a mimicked theme.

Meme is a new word born in my 37th year.

The word had its birth in Richard Dawkins 1976 book The Selfish Gene.

Dawkins cited the work of three ologists as his inspiration. They were an anthropologist, an ethologist and a geneticist. The studies led him into the conclusion that evolution depended on the existence of a self-replicating unit of transmission in the case of biological evolution, the gene.

Thus to Dawkins, the meme was a self-replicating unit with relevance to explaining human behavior and cultural evolution.

He did coin the word meme and developed his meme theory, although the possibility that ideas were subject to similar pressures of evolution as were biological characteristics was noted during Darwins time.

Richard may have had some help in his choice of words.

Meme could be a shortening of mimeme, ancient Greek havent the modern Greeks made any contributions? for imitated thing.

Prior to its being identified as a meme we can consider the graffito, Kilroy Was Here! as qualifying. It became extremely popular in the 1940s, especially in the military. Then it existed under various names in other countries. Today its seen as one of the first widespread memes in the world.

Some observers have likened the transmission of memes to the spread of contagions.

The internet and its vehicles have eased the distribution of memes and many days one or two pop up in communications that pass by Trivially Speaking.

Even Twoey has picked up on memes. As he takes his constitutionals, he pauses to leave his version of Kilroy was here for other wandering canines.

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Trivially Speaking: Go back to 1976 to trace the origin of the meme - Loveland Reporter-Herald

Coronavirus: What we need to learn from the 1918 flu epidemic – Los Angeles Times

Its hard to believe weve devoted so little of our memory to something that killed 50 million people. Once in a while, the 1918 flu epidemic pops up like a plot point in the period TV drama Downton Abbey. But in an age before instant communications, and in the midst of that vast man-made meat grinder of death called World War I, our exhausted species buried the epidemic along with its dead. Yet with the coronavirus now on the move around the world, its worth resurrecting the 1918 pandemic to study ourselves then, know how we reacted to it, how we learned and didnt learn from it.

Laura Spinney is a science journalist whose book Pale Rider: The Spanish Flu of 1918 and How It Changed the World, gives us what we have forgotten or never knew about this illness that killed almost three times the 18 million victims of World War I. Many millions caught the Spanish flu but survived: the king of Spain, paradoxically; Mohandas K. Gandhi; Franklin Delano Roosevelt; and Walt Disney. When you think of our alternative history had they not survived, you get a sense of how life-altering this death tsunami was for the world.

*****

Are we seeing deja vu all over again for what was called the Spanish flu?

The Spanish flu is one of the worst, if not the worst, pandemics that humanity has ever known. And I think we should hope that this one is not that bad. Weve had many other pandemics, both of flu and of other diseases, that were not nearly as bad as the Spanish flu of 100 years ago.

So, yes, there are parallels, but I think we need to keep it within perspective.

What are some characteristics that we see in every one of these, about human behavior, human psychology, the disruptions to society and to economies?

An epidemic of infectious disease is something that brings us right down to earth. It kind of makes a mockery of all the ways that human beings like to divide themselves up, by class, by wealth, by color, by religion, because everybody is vulnerable.

For example, borders borders dont coincide with geographical frontiers, with oceans or mountains. Theyre lines on a map. Theyre ideas that some politician had. And viruses have no idea what that means, and they just walk across them.

What about our individual psychology?

Theres a lot of fear and some of that is reasonable. This is a disease that we dont yet understand. It looks to be more lethal than seasonal flu, and perhaps more contagious.

But I think that a big important issue here is information. And people will act sensibly and appropriately and proportionately if theyre properly informed. And we dont seem to be able to manage that information dimension of pandemic very well.

In 1918, for example, there was a big problem of wartime censorship, which blocked information getting out there.

And today we have a very different problem, which sort of comes to the same thing in the end, which is fake news. I think its a big problem in trying to inform people about this current outbreak and how best to manage it and behave in it.

As a lot of young people have pointed out to me, information tends to be locked behind paywalls these days, whereas fake news is free. And this is the attitude of people whove grown up with the internet: They dont expect to pay for their information. And so they get deluged with a lot of bad information. And I think that a lot of the kind of disproportionate behavior stems from that fact.

Information, weve learned, is absolutely crucial to managing an epidemic. You want people to comply with your public health measures voluntarily, because we know that mandatory health measures tend to be counterproductive. Theyre only going to do that if, A, they trust you, and B, you give them correct information. We have a massive problem of fake news, and that is going to be a major obstacle this time around.

Does peoples behavior alter, or are we at heart the same scared, selfish creatures weve been for thousands of years?

I think were the same inconsistent creatures weve been for thousands of years. In Europe, 40,000 people will probably die from seasonal flu this winter. Nobody is panicking about that. And in a sense, thats understandable, because we know a lot more about the flu. Theres a flu season every year. We sort of know what to expect.

Whereas we dont know what to expect from this coronavirus.

But in another way, it suggests that weve got things out of perspective. And I think that in some ways were very irrational and we react to the news cycle. If we could just draw back a little bit and see that HIV has been killing legions of people for decades. TB is on the rise because theres anti-microbial resistance, which means that the drugs arent working that well anymore. Childhood diseases are coming back largely because of vaccine hesitancy.

I mean, this could go very big, this coronavirus. But at the same time, its not the only problem, and we mustnt lose sight of the others.

What would it have been like to be alive and in your 20s in 1918 or 1919, when you were doing your daily business, whether it was going to the market or maybe going to the movies or taking a train to see a relative? How different did the world look with the flu afoot?

One thing that we cant overlook is that the world was at war. And so people in their 20s say, people between 20 to 40 were of conscriptable age and in many countries were active in the military.

The age group of 20 to 40 unfortunately was also very vulnerable to the Spanish flu for reasons that we only partly understand today. Daily life was rather traumatic at that time. Pregnant women were particularly vulnerable and had miscarriages in large numbers, and also died more commonly than people who werent pregnant and people in other age groups.

Everything I say has to come with the caveat that it depends where you were in the world, because this is a global phenomenon. But say were talking about the industrialized parts of the world: Those were the parts that were beginning to be used to the concept of public health campaigns, to the idea that governments could intervene in your private lives and tell you how to behave for the collective good of society. Wear a mask. Dont cough. Use a handkerchief.

Also it was a very much more obedient society in some ways. Doctors were far more paternalistic, and people were far more willing to do what the doctor told them without questioning it than they are today.

That was enhanced also by time of war. It was almost a patriotic duty to put your mask on and not shake hands and use a handkerchief and so on.

People were more likely to respond with mystical explanations in religion in 1918, to find religious explanations for what was happening to them. Psychologically, I think it was much easier even for people in supposedly advanced countries to try and find mystical explanations for this maybe divine punishment for this dreadful war.

Youre going to go to the church or the mosque, go to the synagogue and pray, which is probably not wise if it means that youre going into a crowd of other people. And indeed, you see that as were seeing in South Korea today, that gatherings in religious sects and so on in places of worship are accelerating the spread of the disease. And they did so in 1918 as well.

During the war, of course people would have had to sacrifice and pull together. Did that in any way prepare them to deal with this pandemic of flu? Because in your book, you write that your best chance of survival was to be selfish and guard your food and water and ignore all pleas for help, which seemed to work against the lets all pull together war effort of the previous four years.

What I was trying to say in the book was that logically, rationally, the best way to bring a pandemic or epidemic to an end quickly with the minimum number of casualties is that everybody isolate themselves because then the virus cant spread and it dies out.

But actually, and in some ways heartwarmingly though not very rationally, our instinct is to help each other. You see that very often people went to each others aid and not just family and friends, but also strangers.

Psychologists talk about something called collective resilience. They talk about the idea that when theres an external threat a disease of this kind, for example people start redefining themselves. The self is no longer the individual self. Its the collective self, because its everyone whos threatened by this external thing, and so people pull together as a collective self and they consider themselves all in the same boat.

And of course, it is antithetical to the idea of stopping the infection from spreading. But its a basic human instinct, for better or worse.

Over centuries, when diseases have appeared, blame has been assigned. Sometimes the Jews were blamed. Syphilis was called the French pox, if you werent French. In this case, the Spanish flu was not Spanish. This is an uglier aspect of disease and human nature.

It is the eternal human dilemma. Who is us and who is not us? Who is other and where is this threat coming from? And so the other side of human behavior that we tend to see in epidemics is this pointing of blame.

And were seeing it today with the coronavirus. There have been massive reports, spiking reports, of xenophobia directed at people of East Asian descent. During the plague outbreaks of the Middle Ages, Jews were very often blamed for poisoning the water in the wells, and expelled, and all sorts of other awful things happened to them.

This is a perennial and ugly side of human nature.

After the flu epidemic there were world-shaking political consequences.

When 50 million people die, or 2.5% of the human population, which is what were talking about, that is not negligible. That is going to have an impact.

If you take the example of South Africa, there were already the stirrings of what would become apartheid. There had been talk of segregating towns along color lines, but nothing had been translated into law. And you see that translation into law happening from the 1920s.

One of the arguments I made in my book, for which I think theres pretty good evidence, is that the epidemic gave a big spur to that legislation because white people blamed very explicitly black people for bringing in the disease without any evidence whatsoever. In fact the black population suffered much worse than the white population in terms of percentages in South Africa.

In India, when the pandemic struck, it became absolutely blatantly clear to everyone how dismally the British colonial authorities had provided for the healthcare of the indigenous population. People were dying in droves and in the absence of any British doctors the British doctors there were, were very often at the front as well the hole was even more glaring.

The people who stepped into that [medical] breach tended to be the militants, the grassroots militant activists for independence who had already worked out how to cross caste barriers and work together for a different goal, i.e. independence.

Once the pandemic passed, emotion against the British was even higher than it had been before. And secondly, those people were far more united than they had been. And now they came together behind Gandhi. He found that suddenly, he had the grassroots support that he had been lacking until then.

What about social changes within the family or a society?

Huge demographic changes. Often it was the pillars of the community, the breadwinners, who were being taken out. The few studies there are suggest that old people went in droves into workhouses because they no longer had any way of supporting themselves.

There were also millions of orphans created. Even in the most advanced countries of that time, there was no real social welfare net, no organized system of adoption. And so these people kind of just vanish.

Another interesting observation is that were talking about a time when the biggest killer of human beings was infectious disease. What it did as a result was to leave behind a smaller but in many ways healthier population, which now began to reproduce at a higher rate. So what you see in the 1920s is a baby boom.

If you look at humanity at the population level, its recovering from this huge disaster very, very quickly in a way.

When it comes to medicine and its ability to cope and its advances, wed had four years of very heroic battlefield medicine, but those techniques were exactly the opposite or inadequate when it would come to dealing with a pandemic. What came out of this in terms of medicine and public health?

Virus was a relatively new concept when the Spanish flu exploded, and once it had receded, I think doctors took a long, hard look at what they knew or more importantly, what they didnt know.

You see from the 1920s, the field of virology takes off, also the field of epidemiology, and epidemiology is the cornerstone of good public health.

You see the discussion around socialized healthcare, the idea of a universal healthcare system thats free at the point of delivery, start. Theyd already been ongoing for a couple of decades, but now they really start coming together.

And then the other really important thing is, is a global health agency. The League of Nations had a health branch essentially the forerunner of the World Health Organization, which was created in 1946.

Of course, its the World Health Organization that is managing the global response to this current outbreak. But what I think is interesting is that these days, the World Health Organization has less sway than it had in the past. Its chronically underfunded by its member nations. And many of them have ignored its recommendations during this outbreak.

Weve forgotten a lot of the lessons that we learned after the Spanish flu and other pandemics, and we may be about to learn them again.

When you watch the news, read the news, follow this, what are you watching for?

One of the things thats become clear about managing any epidemic is that they tend to grow very fast in the first weeks or months. You can think of it like a forest fire that initially, when it sparks is surrounded by dry wood and so it just takes off, and then it gradually burns up its fuel and it runs out of fuel and it slows down and gradually it burns itself out.

An epidemic is a little bit the same, in the sense that its initially surrounded by everybody susceptible. As it burns through those hosts, either kills them or leaves them to some extent immune, it runs out of hosts and so gradually burns out.

If you can slow down that initial pattern of growth, that initial period of growth, you can make a massive difference in terms of how many people will eventually suffer from this pandemic overall.

How are we doing?

In retrospect, I think the Chinese did an amazing job. We see now that the rate of new cases in China is slowed down dramatically. We shouldnt be complacent, but that is encouraging. That means that, OK, it took a certain authoritarian regime to enact it.

Did you have any episodes of this flu in your family history in 1918-19?

The grandfather of my stepdaughter. When he died, they renovated his farmhouse in the north of Sweden. They found a pack of love letters bricked up inside the wall. And it turned out they were love letters that hed written to his first wife, his beloved first wife, who died a few weeks after their marriage, in the summer of 1918, of the Spanish flu, and he ended up marrying her best friend, who was the grandmother of that whole branch of the family that survived.

It illustrates how to us, looking back, everything seems to have happened as it should have been. But there was a huge game of musical chairs that set in after the Spanish flu, and peoples families were rearranged. You didnt necessarily feel that you were married to the person you wanted to be or you were supposed to be. Life suddenly took a very different path and people had to adapt.

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Coronavirus: What we need to learn from the 1918 flu epidemic - Los Angeles Times

How to keep calm in a pandemic: Education, information and communication – The Japan Times

As the coronavirus crisis continues to unfold worldwide and with no vaccine in sight, one thing prevails: uncertainty.

That has sent thousands of shoppers in Japan and abroad into a grocery-hoarding frenzy, including panic-buying of toilet paper and brawls over face masks.

But fears over the pandemic can be managed and psychologists and human behavior experts are calling for policymakers to be more transparent to help the public cope with distress over the outbreak and offer tips for navigating anxieties.

Why do people hoard toilet paper in a health emergency?

Japan was one of the first countries, after Hong Kong and Singapore, to see the coronavirus scare spark a number of false rumors on social media suggesting that toilet paper is expected to run out, spurring a consumer rush to stock up.

The Japan Household Paper Industry Association earlier in March assured the public that 98 percent of the countrys products were made domestically and thus there was no paper shortage in Japan.

Kazuhiro Goda, the associations director, believes the situation should soon get back to normal as long as consumers remain calm. But at the moment, many stores and supermarkets are still rationing goods as eerily empty shelves greet consumers in need of toilet paper.

Goda said that excessive purchasing of goods over a short period of time resulted in an instant shortage of toilet paper at many stores.

But makers do have plenty of stock, operate 24/7 and ship their products regularly. The thing is that distributors dont catch up with higher demand and thus stores havent re-stocked their shelves yet, waiting for delivery, he assured in a telephone interview Thursday.

Steven Taylor, a psychologist who has studied behaviors in crises, said, I think whats happening is toilet paper has become a symbol, a symbol of safety for some people.

In an interview Wednesday, the author of The Psychology of Pandemics described the tendency as an attempt to protect oneself from the virus as everyday things like hand-washing or covering ones mouth when coughing, as recommended by health experts, dont seem like enough.

But Taylor points out that panic-buying may continue even after stores restock their toilet paper supplies.

There will be panic buying of other things, he said.

David Savage, associate professor of behavioral economics at The University of Newcastle, Australia, compares panic-buying to a rush at a bank where individuals feel that the institution may be unable to release the individuals money due to some speculation.

What we observe with panic buying is based on incomplete information, due to uncertainty and a lack of knowledge in local conditions, he wrote in an email. But just like the runs of the bank, once started they are virtually impossible to stop.

What frightens us?

Savage believes that the general public is also dealing with ambiguity.

People do not know what it is that they do not know! he wrote. They are uncertain if or when the virus will spread to the region, they do not know if they themselves will be infected, which also means they do not know if they need to go into isolation and need several weeks worth of supplies.

Mafumi Usui, professor of social psychology at Niigata Seiryo University Faculty of Social Welfare and Psychology, said that fears in Japan have heightened to the point where some people exposed to daily doses of news on the coronavirus crisis wish to get infected soon.Amid alarming levels of spread, the World Health Organization on Thursday declared the coronavirus a global pandemic. By Friday, the number of confirmed COVID-19 cases had exceeded 120,000 and more than 4,300 people had died after contracting the virus.

But Usui believes the word pandemic wont spark more fear than the virus already has.

He said, however, that the anxieties may be associated with cultural norms and governments handling of the crisis.

In Japan, causing trouble to others frightens as much as the virus.

Many (Japanese) people fear theyll be the first in the area where they live, or their workplace, to contract it, Usui said. People dont want to stand out as these cases make headlines. And if they were first, many people would feel ashamed (of causing trouble).

The names of companies and establishments the patients had visited are disclosed in Japan.

What I think is actually occurring is not panic, but we are succumbing to several other behavioural issues, specifically herd behaviour and loss aversion (regret), Savage wrote.

When we see others acting in a certain way we have historical makeup that wants us to conform with the group. Or at the very least we stop and think about the behaviour and wonder if we should also be doing that.

Meanwhile, Taylor, a professor and clinical psychologist at the Department of Psychiatry at the University of British Columbia, pointed out that the situation surrounding the coronavirus may have an impact on specific groups of the population.

Those unknowns, theyre particularly difficult for people with the pre-existing history of anxiety problems, people who have a great deal of difficulty tolerating uncertainty, he said Wednesday.

What can policymakers do to ease public concerns?

What experts agree on is that the world needs competent leaders capable of delivering appropriate messages to their communities.

Usui believes that: In times of a crisis, the government and (health) officials need to effectively communicate risks but a good dialogue is based on trust and the government should also make effort in gaining it.

Usui stressed that the government should offer more advice on how to follow ones daily routine safely to ease the citizens fears and help them make rational decisions.

Weve heard (officials) urge the public to self-control or refrain from doing many things, as well as warnings of potential risks but Id like to hear more about whats relatively safe, he said.

Savage sees uncertainty and a lack of information as the true enemy in regard to public behavior, and stressed that unknowns perpetuate fear and create bias.

The best solution may well be as simple as public education campaigns delivered in the simplest way possible and framed in a positive light rather than a negative, he said.

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How to keep calm in a pandemic: Education, information and communication - The Japan Times

Spending less time on Facebook could boost your well-being and happiness – The Jakarta Post – Jakarta Post

New European research has found that spending just 20 minutes less time on Facebook each day could increase our happiness and healthy lifestyle habits.

Carried out by a team of psychologists from Ruhr-Universitt Bochum (RUB), Germany, the new study looked at 286 participants who used Facebook for an average of an hour each day.

Of these participants, 140 were asked to reduce their Facebook use by 20minutes each day over a two-week period, which is about one third of the average usage time, while the remaining 146 participants acted as the control group and carried on using Facebook as usual.

The participants were asked to complete questionnaires recording their Facebook use, their well-being (such as depressive symptoms) and their lifestyle (such as physical activity and smoking habits) before the start of the study, one week into it, at the end of the two weeks, and one month and three months after the study had finished.

The findings, published in the journalComputers in Human Behavior, showed that the participants who were told to reduce their Facebook usage time used the platform less, both actively and passively.

Read also: Spending money on experiences rather than possessions could bring you more happiness

"This is significant, because passive use in particular leads to people comparing themselves with others and thus experiencing envy and a reduction in psychological well-being," commented lead author Dr. Julia Brailovskaia.

In addition, those who used Facebook less were also significantly more physically active, smoked less, were significantly more satisfied with their life, showed significantly fewer symptoms of depression, and showed fewer symptoms of addiction to Facebook after the two weeks, compared to the control group. These positive effects could also still be seen three months after the study had ended.

"After the two-week period of Facebook detox, these effects, i.e., the improvement of well-being and a healthier lifestyle, lasted until the final checks three months after the experiment," said Dr. Brailovskaia, who added that the findings suggest that just reducing the amount of time we spend on Facebook each day could be enough to increase our well-being and prevent addiction.

"It's not necessary to give up the platform altogether," concludes Dr. Brailovskaia.

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Spending less time on Facebook could boost your well-being and happiness - The Jakarta Post - Jakarta Post

NIH researchers discover tooth-enamel protein in eyes with dry AMD – National Institutes of Health

News Release

Friday, March 13, 2020

Finding may lead to novel therapeutic target for blinding disease.

A protein that normally deposits mineralized calcium in tooth enamel may also be responsible for calcium deposits in the back of the eye in people with dry age-related macular degeneration (AMD), according to a study from researchers at the National Eye Institute (NEI). This protein, amelotin, may turn out to be a therapeutic target for the blinding disease. The findings were published in the journal Translational Research. NEI is part of the National Institutes of Health.

Using a simple cell culture model of retinal pigment epithelial cells, we were able to show that amelotin gets turned on by a certain kind of stress and causes formation of a particular kind of calcium deposit also seen in bones and teeth. When we looked in human donor eyes with dry AMD, we saw the same thing, said Graeme Wistow, Ph.D., chief of the NEI Section on Molecular Structure and Functional Genomics, and senior author of the study.

There are two forms of AMD wet and dry. While there are treatments that can slow the progression of wet AMD, there are currently no treatments for dry AMD, also called geographic atrophy. In dry AMD, deposits of cholesterol, lipids, proteins, and minerals accumulate at the back of the eye. Some of these deposits are called soft drusen and have a specific composition, different from deposits found in wet AMD. Drusen form under the retinal pigment epithelium (RPE), a layer of cells that transports nutrients from the blood vessels below to support the light-sensing photoreceptors of the retina above them. As the drusen develop, the RPE and eventually the photoreceptors die, leading to blindness. The photoreceptors cannot grow back, so the blindness is permanent.

Recently, researchers found a calcium-containing mineral compound called hydroxyapatite (HAP) in dry AMD deposits. HAP is a key component of tooth enamel and bone. Small balls of HAP filled with cholesterol, called spherules, were found only in drusen from people with dry AMD, and not in those with wet AMD or without AMD.

In this study, Wistows team discovered that if they starved RPE cells grown in transwells, a type of cell culture system, for nine days, the cells began to deposit HAP. They determined that the protein amelotin, encoded by the gene AMTN, is strongly upregulated after extended starvation and is responsible for the mineralization of HAP in their cell culture model. Blocking this pathway in their RPE cell line also blocked the production of these drusen-like deposits.

To verify that their cell culture model was accurately representing dry AMD, the researchers examined human cadaver eyes with dry AMD, wet AMD, or without AMD. They found HAP and amelotin only in the eyes with dry AMD, and not in the other eyes. While amelotin was found sometimes in areas of dry AMD without drusen, it was primarily present in soft drusen areas with large deposits of HAP.

Prior to this study, nobody really knew how the hydroxyapatite was accumulating in the dry AMD drusen, said Dinusha Rajapakse, Ph.D., the first author of the study. Finding this tooth-specific protein in the eye, this protein thats linked to hydroxyapatite deposition that was really unexpected.

Why RPE cells in dry AMD begin depositing these HAP spherules is unclear, but Wistow thinks it may be a protective mechanism gone awry. Its possible, he says, that these protein, lipid and mineral deposits may help damaged RPE cells block blood vessels from growing into the retina, a problem that is one of the key features of wet AMD. But when the mineral deposits get too extensive, they may also block nutrient flow to the RPE and photoreceptors, leading to retinal cell death.

Mechanistically, amelotin looks like a key player for the formation of these very specific hydroxyapatite spherules. Thats what it does in the teeth, and here it is in the back of the eye. Conceptually, you could see coming up with drugs that specifically block the function of amelotin in eye, and this might delay the progression of the disease. But we wont know until we try it, said Wistow.

Good animal models for testing dry AMD therapeutics are urgently needed. Based on the findings from this study, Wistow and his team are creating a new mouse model for the disease. Additionally, Wistow believes his cell culture model, which mimics features of dry AMD, could potentially be useful for high throughput drug screening to find molecules that slow or prevent the development of soft drusen.

RThis press release describes a basic research finding. Basic research increases our understanding of human behavior and biology, which is foundational to advancing new and better ways to prevent, diagnose, and treat disease. Science is an unpredictable and incremental process each research advance builds on past discoveries, often in unexpected ways. Most clinical advances would not be possible without the knowledge of fundamental basic research.

NEI leads the federal governments research on the visual system and eye diseases. NEI supports basic and clinical science programs to develop sight-saving treatments and address special needs of people with vision loss. For more information, visit https://www.nei.nih.gov.

About the National Institutes of Health (NIH):NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

NIHTurning Discovery Into Health

Rajapakse D, Peterson K, Mishra S, Fan J, Lerner J, Campos M, and Wistow G. Amelotin is expressed in retinal pigment epithelium and localizes to hydroxyapatite deposits in dry age-related macular degeneration. Translational Research. 2020. doi: 10.1016/j.trsl.2020.02.007

###

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NIH researchers discover tooth-enamel protein in eyes with dry AMD - National Institutes of Health

Tracking the pandemic means finding the ‘canaries in the coalmine’ – Yale News

Dr. Nicholas A. Christakis, Sterling Professor of Social and Natural Science at Yale, has devoted years to investigating how social networks affect our health and behavior. His work offers insight into how to track and address epidemics like the current coronavirus crisis.

Christakis a physician and social scientist who directs Yales Human Nature Lab and co-directs the Yale Institute for Network Science also studies human nature, a subject he examines in his latest bestselling book Blueprint: The Evolutionary Origins of a Good Society (Little, Brown Spark).

Christakis spoke with YaleNews about how, amid a pandemic, human nature can hurt us and how it could help. Interview edited and condensed.

Why is it useful to consider the effect of social networks on epidemics?

The networks we study in the Human Nature Lab are face-to-face networks theyre composed of the interactions we have with our family, friends, coworkers, and neighbors. Of course, people also have interactions with strangers on the street and in shops. You might shake hands with a delivery person, that sort of thing. These are the kinds of connections one can understand through social network analysis. And these networks form the highways along which viruses spread, from person to person to person.

Understanding the structure of these networks, and the virus behavior as it moves through them, gives us insight into how to interrupt the spread and defend ourselves. It also gives us opportunities to predict how the virus will spread.

How are social networks structured?

Imagine strings of Christmas tree lights. Every light represents a person and the wires are the connections between people within the network. Imagine the strings are knotted at the center with tendrils emanating out to the periphery. Thats sort of what a network looks like.

The people at the center of the network are the most likely to catch whatever is spreading, whether its the latest gossip or a dangerous virus. Theyll be the first to hear the gossip or catch the virus. The people on the edges of the network, those with few friends and contacts, are the least likely to hear the gossip or get sick. They might never catch the virus, but if they do, itll happen late in the course of the epidemic.

How can we use this insight to predict the spread of a virus?

We have developed what we call the network sensor method, which seeks to identify the individuals at the networks center, those with lot of friends and contacts, and passively monitor them. They could function as canaries in the coalmine because the virus will strike them before it reaches the wider population. This could provide an early warning system for epidemics and be useful in proactive planning for outbreaks.

Our research has proven that this method can work, during the H1N1 pandemic in 2009. My lab is now in the midst of updating these tools for the current environment, working with some Yale undergraduate and graduate students. Were developing a mobile app that uses the network sensor method to help people track flu cases in their cities.

What should individuals be doing to slow the virus spread?

We need to avoid social mixing both individually and collectively. Besides washing their hands, individuals need to keep a certain physical distance from others (about four feet) and avoid touching each other. People should work from home if they can, and avoid non-essential meetings and travel. These are prudent steps anyone can take on their own. This kind of social distancing can help flatten the curve, meaning it will lead to a more gradual rate of infection and thus prevent our healthcare systems from being overwhelmed.

How does human nature affect our ability to pull off social distancing?

Its in our nature to be social. It is very unnatural for us to avoid assembling in groups, to avoid seeing our friends, to stop shaking hands, or hugging each other. Doing all this doesnt feel normal to human beings. Yet, our natural social behavior is what the pathogen is exploiting.

There is a misconception among some people that the kind and brave thing to do is to shake peoples hands and behave as if things were normal. They want to demonstrate that theyre not afraid of the virus by interacting with others. In reality, the kind and altruistic thing to do is precisely the opposite of this. When you avoid unnecessary social contact right now, you are preventing the virus from using your body as a transmission vector. The virus is spreading and the more paths we can stop, the better off everyone will be.

Do people have innate tendencies that can help us fight the virus?

Absolutely. They include our natural tendency to cooperate, which the current situation certainly requires. Even as were encouraged to distance ourselves from one another, we need to band together to fight this pandemic. We also have an innate capacity for teaching. We are very unusual as animals in that we dont just learn from each other, we teach each other things. That affirmative ability to share knowledge is exactly the kind of thing we need right now.

What advice would you give to policymakers as they address the crisis?

Policymakers face challenging decisions about closing schools or cancelling large events. They also have to decide how to best allocate resources to support the public health. These arent easy decisions because they involve a mix of demands that implicate public health, the economy, and our freedom to move about and gather as we please. Policymakers should be considering the thresholds for closing schools and banning large gatherings.

The most critical need as the epidemic crashes upon us will be the availability of hospital beds and ventilators for our ICUs. We need to do our best to plan for this.

Policymakers dont need to reinvent the wheel. There is accumulated knowledge on how to respond to pandemics. We dont know for sure how severe this pandemic will be, but it looks like it could be very significant, so we should act as though it will be very significant.

Are you addressing the coronavirus crisis in any new research?

I have a project with a Chinese team in which were using big-data methods to develop what is, to my mind, an innovative idea that will allow us to forecast the pandemic in real time, in a useful way. That paper is under review right now.

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Tracking the pandemic means finding the 'canaries in the coalmine' - Yale News

Warm Summer Weather Will Worsen Coronavirus, Singapore and Australia Suggest – Interesting Engineering

When the deadly coronavirus started to sweep around the world this year, a common skeptical retort to emergency worry rested in the comparison of the COVID-19 outbreak to the ordinary flu which is also dangerous to some populations, but also not a real threat to the general public.

Some experts, however, still maintain hope the virus will behave like influenza by fading in the Spring. But cases in countries presently in warm climates suggest otherwise, reports CNN.

RELATED: LATEST UPDATES ON WUHAN'S DEADLY CORONAVIRUS

We know now the comparison of coronavirus to the common flu is, quite literally, dead wrong. Based on current data, the lowest estimated fatality rate for coronavirus is thought to be 1% to 2%, compared to the 0.1% of fatalities for winter influenza. Coronavirus also seems roughly just as infectious as the flu, and perhaps more so, especially since there is no specific treatment, seasonal vaccine, let alone a cure.

But the virus may taper off with the coming of Spring.

"This is a respiratory virus and they always give us trouble during cold weather, for obvious reasons," said Nelson Michael, a top U.S. military medical researcher, of the deadly virus last week, reports CNN. "We're all inside, the windows are closed, etcetera, so we typically call that the influenza or the flu season."

Influenza is at home in cold and dry conditions, which is why most of the northern hemisphere experiences flu season during winter. Differences in human behavior during winter may also affect the spread of viruses. According to Michael, the coronavirus could behave like the flu, giving the public "less trouble as the weather warms up," however, he warned, the virus might return when the temperature drops again.

The general hope is for new radical government and public action to decrease the currently soaring total of new cases, reducing the spread during more temperate weather and giving health systems a chance to play catch-up with the first wave of coronavirus patients, while also buying precious time to develop a crucial vaccine.

"This is why it's really important to understand that a lot of what we're doing now is getting ourselves ready for what we're calling the second wave of this," warned Michael.

However, the coronavirus might not behave like influenza. Instead, it could spread unrestrained despite warm weather, through all of 2020. More than 100 cases were confirmed in Singapore as of writing, where it's almost always hot and muggy. Likewise, Australia, Brazil, and Argentina are all in the middle of summer and have so far reported dozens of cases.

Whatever the future holds for the coronavirus crisis, there are known unknowns that could still prove to turn in our favor and help us collectively curb the rapid growth of the coronavirus outbreak. But, since this pandemic is new, the unknowns we don't know could outweigh the unknowns we do.

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Warm Summer Weather Will Worsen Coronavirus, Singapore and Australia Suggest - Interesting Engineering

How Does COVID-19 Compare with the Flu? – Tufts Now

The new coronavirus that causes COVID-19 in many ways is exactly the type of situation that has motivated Jonathan Runstadler, a professor in the Department of Infectious Diseases and Global Health at Cummings School, and his research team in their efforts to keep the world ahead of the next influenza pandemic.

Runstadler leads a team of Tufts researchers who sample animals in the wild and return to the lab to analyze the samples for influenza viruses. Their mission is to better understand the ecology and lifecycle of the fluas well as what strains are circulating in natureto help predict and prevent deadly, wholly new strains that arise every decade or so.

Given the many purported similarities between the novel coronavirus and influenza, Tufts Now asked Runstadler about how what we know about regular and pandemic flu might apply to this quickly evolving situation.

>>> For the latest Tufts University guidance on COVID-19, please visit coronavirus.tufts.edu.

Tufts Now: How do you expect this COVID-19 epidemic to unfold in the United States and across the globe?

Jonathan Runstadler: This situation is still very unpredictable. We dont know enough about the virus itself or how it spreads. The confirmed cases are slowly climbing in the U.S., and they seem to be pretty widely distributed. But they still represent a fairly low number on the scale of this epidemic.

So the majority of the data we have on this virus and disease is still that from China, and its difficult to know or to understand how reliable that data is and how representative it is of what may occur in other parts of the world, such as in the U.S. Its too early to predict the course of this outbreak with any certainty, butgiven that it has already been detected in more than 100 locations internationally, including in the United States, where several states have declared a state of emergency and the virus does appear to be spreadingI wouldnt be surprised if were dealing with this virus for quite a while.

Do you feel the spread of the new coronavirus has taken the U.S. by surprise?

The U.S. seems to be behind in terms of available tests, protective equipment and other readiness measures. Ironically, I think that this delayed response may have been driven by what has previously happened with avian influenza, where there were local outbreaks or minor epidemics of different flu strains in parts of Asia that didnt ultimately blow up into a pandemic.

I wonder if that set a pattern that many people expected this new coronavirus to follow after its initial emergence in China. And now were seeing that its not following that recent experience at all and that were in a different situation altogether. This is a different virus that were much less familiar withand that may be all the difference.

Theres typically a somewhat regular flu season. Do we know at this point if COVID-19 likely will have some sort of seasonal aspect to itperhaps a spike before it burns out?

We dont know. COVID-19 is a very similar disease to influenza. This new coronavirus seems to cause similar symptoms and to progress in a similar way to flu. And, as a respiratory disease, COVID-19 likely is transmitted in a similar fashion to the flu, via direct contact with respiratory droplets.

So you might hypothesize that it would behave similarly to the influenza virus in other ways as well, and for flu, we know that it typically has a seasonality. There are things that can knock that timing out of whack, and there are some seasons that are exceptions to the norm, depending on how transmissible and how severe the circulating strains of seasonal flu are. In general, though, the seasonality of the flu is driven by the propensity of influenza viruses to like low humidity and moderate temperatures.

The coronavirus is from an entirely different family of viruses, so it very well could behave differently. And, to my knowledge, we have not done experiments to verify why flu viruses seem to do better in those conditions, so we cant know how differentand similarthese two viral families would be in that regard. Much of the seasonality to flu is also driven by human behavior in winter versus summer, but I think the idea that there will be a seasonal aspect to COVID-19 is more of a hope than an expectation at this point.

How sick does this new coronavirus tend to make people?

From the information that we have at this point, in some ways, COVID-19 has behaved similar to the flu, though perhaps its a bit more contagious in the right conditions. The caveat is that this assumption is based mostly on information from cases seen in the Chinese population. But from that data, it appears that for most people, COVID-19 is a mild diseaseprobably a little flu-like, but maybe even milder and more like a cold.

There are other coronaviruses that regularly infect people and cause a common cold. And for the most part, people never bother to seek medical attention for these more common coronaviruses because they do not make people as ill as the flu.

Thats why people in the scientific community are a little wary about interpreting the data coming out of China. Its likely that there many more cases of COVID-19 that have not been accounted for. Many people probably have been ill with a much milder disease for which no clinical help was sought and no diagnostics doneand recovered without ever being diagnosed with COVID-19.

However, we can expect immunocompromised people to be more susceptible to contracting the disease and to have more severe disease or worse clinical signs than the average person. The disease seems to much more severely affect both the elderly and people who have other diseases or general health conditions that make them immunocompromised.

These groups of people may typically represent only a relatively small percentage of the total population. But if COVID-19 becomes widespread in the U.S. and other parts of the world, that will still add up to many people getting exposed to the virus and a large number of people developing severe disease. And the same holds true for an expectation of a large number of people dying from infection.

Whats interesting is thataccording to the Chinese data and most of the other recorded infections around the worldthe new coronavirus doesnt appear to affect younger kids in the same way the flu does. The flu tends to have a severity profile that peaks in very young children as well as in the elderly, but we are not seeing this with coronavirus in kids under age five, which is great. So hopefully this disease may not be such a worry for younger kids, although they could still be spreaders of the virus.

If other coronaviruses are common and usually mild in humans, what makes this one so different or dangerous? Are there any parallels to flu?

Coronaviruses indeed infect lots of animals, including humans. The coronaviruses routinely circulating in any species tend to be well adapted to that host and dont usually spill over into new species. For example, human coronaviruses that cause the common cold to the best of our knowledge dont infect the dogs and cats that people live with. And vice versathe coronaviruses that infect dogs and cats typically dont infect their owners.

But this new coronavirus causing COVID-19 in people hasnt been in humans before. It appears to have recently spilled over from wildlife. We dont fully understand where it came from yet and what host it was in prior to spilling into humans, but our lack of prior exposure to this virus means none of us have had the chance to develop an immune response to protect against COVID-19. Thats the kind of situation we worry about as well with pandemic flus, which typically occur when one of the strains circulating in birds or in other animals makes the jump into people.

Once a virus spills over into a new species, it has to do several things in order to successfully replicate itself and be transmitted by the host that its infecting. The ability to keep reproducing and spreading is gained through small changes in the viruss genomeand that may take a long or a relatively short time. Viruses like coronavirus and flu, which are both RNA viruses, tend to be able to mutateor changemore rapidly than some other viruses and certainly some other pathogens.

Do you have a sense of how close we are to a vaccine? Is it easier to create a vaccine for this new coronavirus than for the flu, which seems to be a hit or miss endeavor every year?

There is some scientific debate that there could be multiple lineages of the new coronavirus, some of which cause perhaps more severe disease and some which are milder, but there isnt convincing evidence of that yet. Further epidemiology and analysis of the virus will come out the more things progress. For now, it appears the epidemic was started in a single spillover event, which emphasizes the importance of improving our understanding of the ecology of infectious pathogens in animal hosts and the human-animal interactions that result in spillover.

In terms of creating a vaccine for COVID-19, the immediate goal would be to create a vaccine against what appears to be for the most part a single strain or type of coronavirus. That target might be a little easier than creating a vaccination for the flu, a virus that is endemic and has different strains and different subtypes that can dominate and appear in different yearsmaking it very difficult to predict which will be the emerging flu viruses and costly to develop vaccines, which is why researchers are trying to develop one universal flu vaccine against all of them.

However, the process to develop a vaccine for COVID-19 is still potentially a difficult one. In general, its easy to create a vaccine, but harder to create an effective one, and maybe even harder still to create a vaccine that you can get to enough people in the right amount of time.

A vaccine is probably months away at a minimum, if some of the newest technologies and approaches prove successful. If we are using standard technology for developing a vaccine, we probably shouldnt expect a coronavirus vaccine until next year. And those timelines are just for the development of the vaccine itself. Its the rest of the process that really takes timemaking sure a vaccine is safe and effective, doing the human clinical trials, and then being able to produce it.

What are the best things people can do to keep both themselves personally safe from COVID-19 and to protect the most vulnerable people around us from this new coronavirus?

This coronavirus, to the best of our knowledge right now, does behave like most respiratory diseases. And so, the same advice that applies to illnesses such as influenza or the common cold applies here.

Pay attention to personal hygiene and follow all that advice youve been hearing about how frequently and thoroughly to wash your hands. Dont touch your face with your hands. Try to keep an advisable social distanceat least six feet, if possiblebetween you and anyone with symptoms of a respiratory illness. Avoid situations where you may likely encounter groups of people who could be sick.

If you or someone in your family is diagnosed with COVID-19, take all the precautions recommended by the CDC and your health provider to keep yourselves and others safe, including avoiding close contact with other people and pets. And if youre ill with flu-like or respiratory symptoms, contact your doctor for guidance if necessary and stay home until youre well so you dont pass this illness on to a senior or anyone else.

Genevieve Rajewski can be reached at genevieve.rajewski@tufts.edu.

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