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Unfortunately the Coronavirus is not going to kill tens of millions of people worldwide (I wish something would)… But it’s here to stay… Now a symbiotic part of human life!

Bad news, it’s not going to kill millions, tens of millions… hundreds of millions, of human beings, as first imagined.

(I know, I’m as upset as you are! 😢)

Good news! It’s here to stay… as a seasonal winter virus. Humans will adapt and grow an ‘immunity’ to it… May kill a few thousand each year, but the common flu kills more, so?

Chances are, you already had a coronavirus of some kind, may not have even known it… So have a Corona on us!

(taught the Chinese a lesson)

VIRUSES ARE A FASCINATING SUBJECT! The history of them, what they are, how little we know about them, our symbiotic relationship to them… They may have been the first lifeforms on Earth! We may have all evolved from a virus! An extraterrestrial virus at that.

(two life forms we know of, that purposely destroy their own environment… Viruses… And? HOMOSAPIENS! 😎… Viruses are clever enough to leave most of the hosts alive, and are able to then infect another)

“And people are worried about the future of designer babies! Fuck me, Hellfire Club… you people have noooo fucking idea!” 😎

The Urgent Questions Scientists Are Asking About Coronavirus

Let’s start with what we don’t know.

By Gabriel Leung

Dr. Leung is an infectious disease epidemiologist and dean of medicine at the University of Hong Kong.

  • Feb. 10, 2020
A technician doing diagnostic testing for the new coronavirus in Wuhan, China, last week.Credit…CHINATOPIX, via Associated Press

GENEVA — Around the world and around the clock, scientists are trying to figure out what must be done to end the global health emergency unleashed by the new coronavirus. As the outbreak accelerates and spreads, dozens of countries have deployed increasingly stringent measures to try to contain the epidemic. Almost as quickly, in a herculean effort, an international network of researchers at data and wet laboratories has started gathering and analyzing data to unmask and disarm this perplexing new disease.

In magnitude, scale and velocity, this coronavirus, known as 2019-nCoV, is too big a problem for any one team to solve. On Monday, China reported its largest single-day death toll, 97, pushing the total reported dead worldwide to 910, with more than 40,500 people infected on four continents.

On Tuesday, I’m joining my fellow scientists at the World Health Organization headquarters for an urgent meeting to piece together, like a giant jigsaw puzzle, our findings so far. We need to get a clear view of the contagion and plug the holes in our understanding of the disease to inform public health decisions that affect hundreds of millions of lives. Science has a critical role to play in restoring calm.

Let’s start with what we know. The new coronavirus is a close cousin of viruses that infect bats. It jumped from an unconfirmed wild source (most likely bats) to an intermediate host, possibly pangolins or other small mammals, being sold as food at a market in Wuhan, a transportation and commercial hub in central China. The infected people unknowingly spread it to others, setting off the outbreak’s deadly journey. We now estimate that it takes about five to six days — possibly upward of 14 days — for someone to show symptoms after becoming infected.ADVERTISEMENT

What do we most need to know next? For epidemiologists who track infectious diseases, the most pressing concerns are how to estimate the lethality of the disease and who is susceptible; getting detailed information on how it spreads; and evaluating the success of control measures so far.

No. 1 is the “clinical iceberg” question: How much of it is hidden below the surface? Because the outbreak is still evolving, we can’t yet see the totality of those infected. Out of view is some proportion of mildly infected people, with minor symptoms or no symptoms, who no one knows are infected.

A fleet of invisible carriers sounds ominous; but in fact, an enormous hidden figure would mean many fewer of the infected are dying. Usually, simple math would determine this “case fatality” ratio: divide the total number of deaths by the total number of people infected. In an emerging epidemic, however, both numbers keep changing, and sometimes at different speeds. This makes simple division impossible; you will invariably get it wrong.

In 2003, during the early days of the SARS outbreak, the medical community got the math wrong. At first, we believed that case fatality hovered between 2 percent and 3 percent. It took two pages of longhand algebra, written in Oxford, England, coded into a computer in London and then applied to data from Hong Kong, to get it right. The actual case fatality for Hong Kong was staggering: 17 percent.ADVERTISEMENT

That’s not to suggest we’re facing as dire a scenario now. Several groups, including mine, are each using our own methods to calculate a preliminary estimate of the new virus’s lethality. If there’s near agreement among our findings, expected within the week, we’ll be more confident in describing the new coronavirus. Does it resemble the seasonal flu, SARS or one of the largest plagues in human history, the 1918-19 “Spanish flu” pandemic?

Knowing the number of people likely to die, or who get seriously sick or have zero symptoms, will help health authorities determine the strength of the response required. They can better estimate how many isolation beds, heart-lung machines and medicines, among other things, are needed.

Last month, to start understanding the severity of this illness, my team assisted Chinese experts in analyzing the initial 425 confirmed cases of infection. We learned that 65 percent of people had neither visited a market nor been exposed to another person showing pneumonialike symptoms, which implied, among other things, the possibility that some infected people don’t suffer from obvious symptoms — meaning the illness isn’t always severe.

Along with getting a grasp on the level of severity is figuring out susceptibility, or who is most at risk for infection. The data so far indicates that this would include older adults, the obese and people with underlying medical conditions. There are few reports of children becoming infected. But are they not showing symptoms, or are they immune? And could they infect others as silent carriers? We must study those under 18 to find out; the answers could help us fine-tune public health measures. For example, should schools in China and Hong Kong remain closed?ADVERTISEMENT

Returning to the big picture, we must also refine what we know about how the new coronavirus is passed between people. Even as the outbreak appears to keep escalating, we believe the rapid — sometimes necessarily draconian — response of governments and health authorities has made a dent in transmission. In another recent study, we estimated how many people could get infected if there were no drastic public health interventions. Our goal with this report was to sound the alarm over what could be, so that it wouldn’t be.

Scientists are working toward quantifying effectiveness of the response. We need to find out if the virus’s basic reproductive number, the R0 or R-naught, has dropped. While our earliest estimates showed that typically every person infected by the new coronavirus passes it to 2 to 2.5 others, it’s still too early to know if measures have reduced the number to below the critical threshold of 1.

Simultaneously, we’re closely watching the rest of the world for any large, sustained outbreaks that might resemble ground zero in Wuhan. We expect more clarity within days or weeks. As of Monday, the largest concentration of infected patients in a single location outside mainland China, at more than 130 people, is on a cruise ship, the Diamond Princess, quarantined at Japan’s Yokohama port.ADVERTISEMENT

Finally, scientists need to appraise the control, or social distancing, measures deployed since the outbreak began. The challenge involves trying to quantify how many infections were actually prevented through measures such as wearing masks, closing schools and locking down cities. One possible approach to this assessment in China could involve using location services data from cellphones.Opinion | Dan WerbTo Understand the Wuhan Coronavirus, Look to the Epidemic TriangleOpinion | David QuammenWe Made the Coronavirus EpidemicOpinion | Howard MarkelWill the Largest Quarantine in History Just Make Things Worse?

As we determine research priorities at the World Health Organization headquarters in Geneva this week, the hope is that the science being urgently coordinated will also fight the crisis on other fronts. It could help battle the emerging “infodemic,” the cacophony of real news, fake news and pseudoscience that feeds uncertainty and breeds panic.

And it could help roll back some measures seemingly fueled by populism and nativism. The travel advisories, outright travel bans, immigration controls and xenophobic treatment of people from different places are doing significant harm.

The goal is to stay at least a couple of steps ahead of the epidemic curve. Scientists must prepare health authorities to catch any subsequent waves of infections and prepare for the possibility that this particular virus could reappear seasonally — and maybe one day it could be only as bad as the common cold.

I’ve seen record-breaking outbreaks before and witnessed the world rally. If we all play our roles and remain on guard, then chances are we will defeat the new coronavirus, too. This is the best way to honor Dr. Li Wenliang, one of the first doctors in Wuhan to warn the world about the disease — the very one that killed him last week, at age 34.

Gabriel Leung (@gmleunghku), an epidemiologist who studied SARS and managed the response to the swine flu pandemic in Hong Kong, is founding director of the World Health Organization Collaborating Center for Infectious Disease Epidemiology and Control and dean of medicine at the University of Hong Kong. He is an adviser to the Hong Kong and Chinese governments on the new coronavirus.

Experts envision two scenarios if the new coronavirus isn’t contained

By SHARON BEGLEY @sxbegle

FEBRUARY 4, 2020

crowd of people
ADOBE

With the new coronavirus spreading from person to person (possibly including from people without symptoms), reaching four continents, and traveling faster than SARS, driving it out of existence is looking increasingly unlikely.

It’s still possible that quarantines and travel bans will first halt the outbreak and then eradicate the microbe, and the world will never see 2019-nCoV again, as epidemiologist Dr. Mike Ryan, head of health emergencies at the World Health Organization, told STAT on Saturday. That’s what happened with SARS in 2003.

Many experts, however, view that happy outcome as increasingly unlikely. “Independent self-sustaining outbreaks [of 2019-nCoV] in major cities globally could become inevitable because of substantial exportation of pre-symptomatic cases,” scientists at the University of Hong Kong concluded in a paper published in The Lancet last week.

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Researchers are therefore asking what seems like a defeatist question but whose answer has huge implications for public policy: What will a world with endemic 2019-nCoV — circulating permanently in the human population — be like?Related: 

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“It’s not too soon to talk about this,” said Dr. Amesh Adalja, an infectious disease specialist at the Johns Hopkins Center for Health Security. “We know that respiratory viruses are especially difficult to control, so I think it’s very possible that the current outbreak ends with the virus becoming endemic.”

Experts see two possibilities, each with unique consequences:

Just another coronavirus

2019-nCoV joins the four coronaviruses now circulating in people. “I can imagine a scenario where this becomes a fifth endemic human coronavirus,” said Stephen Morse of Columbia University’s Mailman School of Public Health, an epidemiologist and expert on emerging infectious diseases. “We don’t pay much attention to them because they’re so mundane,” especially compared to seasonal flu.

Although little-known outside health care and virology circles, the current four “are already part of the winter-spring seasonal landscape of respiratory disease,” Adalja said. Two of them, OC43 and 229E, were discovered in the 1960s but had circulated in cows and bats, respectively, for centuries. The others, HKU1 and NL63, were discovered after the 2003-2004 SARS outbreak, also after circulating in animals. It’s not known how long they’d existed in people before scientists noticed, but since they jumped from animals to people before the era of virology, it isn’t known whether that initial jump triggered widespread disease.

OC43 and 229E are more prevalent than other endemic human coronaviruses, especially in children and the elderly. Together, the four are responsible for an estimated one-quarter of all colds. “For the most part they cause common-cold-type symptoms,” said Richard Webby, an influenza expert at St. Jude Children’s Research Hospital. “Maybe that is the most likely end scenario if this thing becomes entrenched.”Support STAT: STAT is offering coverage of the coronavirus for free. Please consider a subscription to support our journalism. Start free trial today.

All four, in particular HKU1, can cause pneumonia, and sometimes death. It is rare enough that researchers do not have good estimates of its prevalence or virulence, but two of the others have been better studied. In one of the few close looks at OC43 and 229E, researchers measured their infection rates during four winters (1999-2003) in Rochester, N.Y., among 2,897 healthy outpatients, adults with cardiopulmonary disease, and patients hospitalized with acute respiratory illnesses.

They identified 398 coronavirus infections (four people had both OC43 or 229E). Infection rates ran from 0.5% among healthy elderly adults to 15% among healthy young adults (where “healthy” means they had no viral symptoms), with the highest rates coming in the winter of 2000-2001, for no obvious reason — suggesting that coronavirus infection rates will rise and fall unpredictably, much like seasonal flu, and that its consequences will also be similar: some serious illness, some mild, and a lot of asymptomatic infections.

The most common symptoms were runny nose, cough, and congestion, for about 10 days; no one even ran a fever. All told, 35% of infections with 229E and 18% with OC43 were asymptomatic. “Asymptomatic infection … [meaning] without respiratory symptoms was fairly common,” the authors concluded. A new type of coronavirus is responsible for the outbreak of respiratory illnesses that began in Wuhan, China December 2019. While experts are still unclear how exactly these viruses are transmitted, coronaviruses such as those that caused the SARS and MERS outbreaks in years past offer clues.ALEX HOGAN AND HYACINTH EMPINADO/STAT

But sometimes symptoms were nothing to sneeze at. There were 96 coronavirus infections among the 1,388 hospitalized patients. OC43 caused more severe disease than 229E, requiring intensive care for 15% of those infected. About one-third of the patients admitted to the hospital with either coronavirus developed pneumonia; one of the 229E patients and two of the OC43 patients died.

On the bright side, if a coronavirus infects enough people regularly there will be greater business incentive to develop a vaccine and other countermeasures. That never happened with SARS because it died out, leaving no market for such products.

On the decidedly darker side, a fifth endemic coronavirus means more sickness and death from respiratory infections.

Odds: Moderate. “I think there is a reasonable probability that this becomes the fifth community-acquired coronavirus,” Adalja said, something he expanded on in his blog. Webby agreed: “I have a little bit of hope that, OK, we’ll put up with a couple of years of heightened [2019-nCoV] activity before settling down to something like the other four coronaviruses.”

2019-nCoV returns repeatedly like a bad seasonal flu

The “seasonal” reflects the fact that viruses can’t tolerate high heat and humidity, preferring the cool and dry conditions of winter and spring, Webby said. That’s why flu, as well as the four coronaviruses, are less prevalent in warm, humid months. If the new coronavirus follows suit, then containment efforts plus the arrival of summer should drive infections to near zero.

But also like flu viruses, that doesn’t mean it’s gone.

The “bad” reflects the fact that the number of 2019-nCoV cases and deaths so far suggests that the new coronavirus has a fatality rate around 2%. That’s almost certainly an overestimate, since mild cases aren’t all being counted. But even 2% is less than SARS’ 10% and nowhere near the 37%  of MERS (Middle East respiratory syndrome coronavirus). On the other hand, seasonal flu kills fewer than 0.1% of those it infects, though that’s still tens of thousands of deaths a year just in the U.S. The global disaster that was the 1917 “Spanish flu” pandemic killed 2.5% (though some estimates exceed 10%).Related: 

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“One scenario is that we go through a pandemic,” as the current outbreak may become, said Columbia’s Morse. “Then, depending what the virus does, it could quite possibly settle down into a respiratory illness that comes back seasonally.”

The toll that would take depends on how many people it infects and how virulent it is. Virulence reflects the viruses’ genetics.

The genome of the novel coronavirus consists of a single strand of RNA. Microbes with that kind of genome mutate “notoriously quickly,” said biologist Michael Farzan of Scripps Research, who in 2005 was part of the team that identified the structure of the “spike protein” by which SARS enters human cells.

But SARS has a molecular proofreading system that reduces its mutation rate, and the new coronavirus’s similarity to SARS at the genomic level suggests it does, too. “That makes the mutation rate much, much lower than for flu or HIV,” Farzan said. That lowers the chance that the virus will evolve in some catastrophic way to, say, become significantly more lethal.

The coronavirus “may not change [genetically] at all” in a way that alters function, said biologist Andrew Rambaut of the University of Edinburgh, who has been analyzing the genomes of the 2019-nCoV’s from dozens of patients. “It is transmitting quite well already so it may not have to ‘evolve’ to be endemic.”

Any evolution that does take place in an endemic coronavirus, including one that spikes seasonally, might well be toward less virulence. “It doesn’t want to kill you before you transmit it,” Farzan said. “One would therefore expect a slow attenuation” of virulence if the virus becomes like seasonal flu. Dead people don’t transmit viruses, “and even people sitting in their beds and shivering” because they are seriously ill “don’t transmit that well,” he said.

The toll of a seasonal-flu-like coronavirus also depends on immunity — which is also scientifically uncertain. Exposure to the four endemic coronaviruses produces immunity that lasts longer than that to influenza, Webby said, but not permanent immunity. Like respiratory syncytial virus, which can re-infect adults who had it in childhood, coronavirus immunity wanes.Related: 

With coronavirus, as with AIDS and Ebola, we must move beyond the fear

“Everyone, by the time they reach adulthood, should have some immunity to some coronavirus,” said Tim Sheahan, a coronavirus researcher at University of North Carolina’s Gillings School of Global Public Health. But because it doesn’t last, older people can get reinfected. The elderly also have a higher death rate from coronaviruses such as SARS and MERS, a pattern 2019-nCoV is following.

“There is some evidence that people can be reinfected with the four coronaviruses and that there is no long-lasting immunity,” Dr. Susan Kline, an infectious disease specialist at of the University of Minnesota. “Like rhinoviruses [which cause the common cold], you could be infected multiple times over your life. You can mount an antibody response, but it wanes, so on subsequent exposure you don’t have protection.” Subsequent infections often produce milder illness, however.

The common-cold-causing coronaviruses are different enough that an infection from one won’t produce immunity to another. But the novel coronavirus overlaps enough with SARS that survivors of the 2002-3003 outbreak might have some immunity to the new arrival,  Sheahan said: “Is it enough to prevent infection? I don’t know.”

How widespread even limited immunity would be, and therefore how many people would become ill from the next go-round of 2019-nCoV, also “depends on how many people get infected the first time around,” Webby said. That number is certainly higher than the more than 20,000 identified cases, since people with no or mild symptoms escape the attention of health care systems.

Since 2019-nCoV is new, “this first wave will be particularly bad because we have an immunologically naïve population,” Adalja said. Future waves should pass by people who were exposed (but not necessarily sickened) this time around, Morse said, “but that assumes this virus doesn’t develop the tricks of flu,” which famously tweaks the surface molecules that the immune system can see, making itself invisible to antibodies from previous exposures.

Odds: Pretty good. What we may be seeing “is the emergence of a new coronavirus … that could very well become another seasonal pathogen that causes pneumonia,” said infectious disease expert Michael Osterholm of the University of Minnesota. It would be “more than a cold” and less than SARS: “The only other pathogen I can compare it to is seasonal influenza.”

Helen Branswell and Andrew Joseph contributed reporting.

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