Stories
Slash Boxes
Comments

SoylentNews is people

posted by martyb on Monday May 04 2020, @02:12PM   Printer-friendly

2020-05-03 Roundup of COVID-19 (SARS-CoV2, Coronavirus) Stories

total_count 3,565,120
total_deaths 248,245
total_recovered 1,153,956
active_count 2,162,919
active_mild_count 2,112,878(98%)
active_serious_count 50,041(2%)
closed_outcome 1,402,201
closed_deaths_count 248,245(18%)
closed_recovered_count 1,153,956(82%)

Biologists Invent a New Way to Fight Viruses with Llama Blood and Molecular Super Glue

Biologists invent a new way to fight viruses with llama blood and molecular super glue:

For more than 20 years, researchers have tried with limited success to engineer antibodies into new treatments for bacterial and viral infections. Now, a team of scientists has come up with a new approach: fastening together tiny antibodies from llama blood with a type of bacterial super glue. The interconnected antibodies protect mice from two dangerous viruses, and they could subdue other pathogens.

The new work has been able to bypass a lot of the hurdles that stymied previous attempts, says protein engineer Jennifer Maynard of the University of Texas, Austin. I think this will be a very general technology that will be useful for infectious diseases and for cancer.

[...] The study shows that the small antibody approach is possible and gives new opportunities to optimize it, Wichgers Schreur says. Researchers still need to answer several questions before they can think about testing the strategy in people, he says, such as whether they can produce sufficient amounts of the linked antibodies. He adds that the approach could work against other types of viruses, but it probably won't be ready in time to fight the coronavirus causing the current pandemic.

Original Submission

First Drug Known to Work Against SARS-CoV-2 Imaged in Action

First drug known to work against SARS-CoV-2 imaged in action:

Just this week, we had the first promising report of a drug that appears to improve the recovery time of patients suffering from COVID-19. Hot on the heels of that announcement, a scientific journal has released a paper that describes how the drug interferes with the virus. While there's no real surprises in what has been revealed, it provides key details of how SARS-CoV-2 can be blocked.

[...] Remdesivir, which saw a large clinical trial produce promising results, is a drug that's designed to target one of these virus-specific vulnerabilities. The coronavirus genome is encoded using the chemical RNA, as opposed to the DNA used for our genome. In fact, there's nothing about our cells that requires them to make an RNA copy of an RNA molecule. As a result, the coronavirus genome encodes proteins that do this RNA-to-RNA copying, called an RNA-dependent RNA polymerase. Remdesivir was designed to look like one of the building blocks of RNA in the hope that it would bind to an RNA virus' polymerase and inhibit it.

That said, this drug was designed with the intention of inhibiting the polymerase of a different virus (Ebola), so it wasn't guaranteed to work against coronavirus. And our cells need to make RNA copies of DNA, a process that's similar enough that remdesivir could interfere with that, too.

Still, tests in cells had been promising enough to drive testing in humans. While that testing was starting, a group of Chinese scientists decided to look into how remdesivir actually works. To do so, they decided to figure out how the drug interacted with the coronavirus RNA polymerase at the atomic level. And that requires a technique to determine where all the atoms in the protein and drug are.

Original Submission

NIH Abruptly Cuts Coronavirus Research Funding, Alarming Scientists

NIH abruptly cuts coronavirus research funding, alarming scientists:

Researchers expressed alarm this week after the National Institutes of Health abruptly cancelled funding for a long-standing research project by US and Chinese scientists to examine how coronaviruses leap from bats to humans, potentially causing devastating pandemics such as the one we are currently experiencing by a coronavirus genetically linked to those found in bats.

The funding cut could set back critical research into preventing such disease spread, scientists say. They also expressed dismay that the decision was prompted by unfounded conspiracy theories and what some see as a wider attempt by the Trump administration to deflect criticism of its handling of the pandemic by blaming China for unleashing the disease.

The NIH has not provided a clear explanation for its move to cancel the funds, which occurred April 24 and was first reported by Politico Monday, April 27. However, in emails exchanges published April 30 by Science magazine, it is clear that the NIH was motivated by conspiracy theories that allege without evidence that the virus was somehow released by Chinese researchers in Wuhan, the central Chinese city where the pandemic began.

The grant that is now going unfunded is titled Understanding the Risk of Bat Coronavirus Emergence, and it was written by EcoHealth Alliance, Inc., a non-profit based in New York that collaborates with a leading Chinese researcher who studies bat coronaviruses in Wuhan. The NIH initially funded the work in 2014, providing $3.1 million for five years. The NIH then renewed the grant in 2019 after the work received an outstanding peer-review score, according to Science.

Original Submission

Florida Man Stalks Beach as Grim Reaper to Protest Reopening Amid Pandemic

Florida man stalks beach as Grim Reaper to protest reopening amid pandemic:

Florida's governor, Ron DeSantis, announced on Friday that state parks will soon reopen, even as the coronavirus pandemic continued and Death himself stalked the beaches of the Sunshine state.

In fairness, the Grim Reaper in question was actually Daniel Uhlfelder, a lawyer and campaigner for public beach access who put on a cowl and wielded a scythe in an attempt to alert Floridians to the dangers of reopening their economy too soon.

As footage of a socially distanced interview with a TV reporter at Miramar Beach in Walton county went viral, Uhlfelder told CNN: "We aren't at the point now where we have enough testing, enough data, enough preparation for what's going to be coming to our state from all over the world from this pandemic.

"I know how beautiful and attractive our beaches are. But if we don't take measures to control things, this virus is going to get really, really out of control."

Original Submission

Dossier Lays Out Virus Case Against China

Dossier lays out virus case against China:

China deliberately suppressed or destroyed evidence of the coronavirus outbreak in an assault on international transparency that cost tens of thousands of lives, according to a dossier prepared by concerned Western governments on the COVID-19 contagion.

The 15-page research document, obtained by The Saturday Telegraph, lays the foundation for the case of negligence being mounted against China.

It states that to the endangerment of other countries the Chinese government covered-up news of the virus by silencing or disappearing doctors who spoke out, destroying evidence of it in laboratories and refusing to provide live samples to international scientists who were working on a vaccine.

Original Submission

Surviving COVID-19: A Disease Tolerance Perspective

There is an interesting editorial in the most recent release of the journal Science Advances questioning the heavy virus-focused approach in attacking the COVID-19 virus outbreak. I know there are some who frequent this site who are much smarter about these things than I, and I thought it would be an interesting topic for discussion.

The editorial is written by Janelle Ayres of the Salk Institute for Biological Studies. She describes the race to find new antiviral solutions to combat this virus and she notes that should an effective solution be found, it will be effective for the fraction of infected patients that develop mild cases of COVID-19 by shortening their length of infection and for reducing transmission to other hosts. However, for those whom progress along the downward spiral (pneumonia, respiratory failure, etc.), their fate depends upon how their body responds to the virus. The need here is to keep them alive until their body can work through the infection. While hospitals are scrambling to find respirators, beds, and other equipment to keep patients alive, the scientists are focusing on antivirals and not on the drugs that promote physiological function during the infection.

There is no scientific or public health reason for why we have not developed such therapeutics. It was described more than a decade ago that the infection defense response relies on essential mechanisms for survival that limit damage to the host and promote physiological function, rather than targeting the pathogen. These mechanisms are called disease tolerance mechanisms encoded by the host's cooperative defense system and are essential for survival following infections and operate to achieve the same goal as supportive care. The cooperative defense system also encodes antivirulence mechanisms that neutralize pathogen and host-derived pathogenic signals that cause damage.

One of the advantage therapeutics has is that there is less of a chance for drug resistance to occur because the therapeutics target the host and not the virus.

The simple explanation for this disconnect is that the perspective for combating infectious diseases shared by scientists is incomplete. The fields of immunology and microbiology have focused on understanding strategies to kill the infection, which has provided us with some of the most important innovations for global health: vaccines and antimicrobials. However, while this perspective is valuable, it is not enough. Instead of asking "how do we fight infections?", we might start asking "how do we survive infections?". To understand the answer to this question, we must approach infectious diseases at the molecular, cellular, organ, physiological, and organismal levels. We have an understanding of the mechanisms of disease pathogenesis for COVID-19 related pathologies, and now, we need to understand the mechanism that restore normal function in the body and how we can drug these pathways for COVID-19 treatment.

Journal Reference:
Janelle S. Ayres, Janelle S. Ayres. Surviving COVID-19: A disease tolerance perspective [open], Science Advances (DOI: 10.1126/sciadv.abc1518)

Original Submission

"They're Writing COVID on All the Death Certificates": NYC Funeral Directors Doubt Legitimacy

"They're Writing COVID On All the Death Certificates": NYC Funeral Directors Doubt Legitimacy of Deaths Attributed to Pandemic. - Global Research:

Project Veritas today released another video featuring conversations with funeral home directors and their staff throughout New York City questioning the number of deaths officially attributed to the COVID-19 pandemic.

In late April, a Project Veritas reporter spoke with Michael Lanza, the director of Staten Island's Colonial Funeral Home.

To be honest with you, all of the death certificates are writing COVID on it, they re writing COVID on all the death certificates, Lanza said.

Lanza said DeBlasio might see inflated COVID death tallies as a way to bring more money to New York City.

Whether they had a positive test or didn't, so I think again this is my personal opinion, I think like the mayor and our city they re looking for federal funding and the more they put COVID on the death certificate the more they can ask from the federal funds.

The Staten Island funeral director said it did not add up to him.

I think it's political, so, I m going to turn around and say: You know, like, not everybody that we have here that has COVID on the death certificate died of COVID. Can I prove that? No, but that is my suspicion.

Original Submission

South Korean Scientists Doubt COVID-19 Reinfections

There have been worrying signs that it is possible to have COVID-19 reinfection, such that getting sick with the disease and recovering might not confer subsequent immunity to the disease as with other similar diseases. This would make controlling the spread of the disease much more difficult. However, further studies by Korean infectious disease experts seem to show that these reports of reinfection may be due to false positives, since the PCR tests South Korea uses for diagnosing COVID-19 infections also detect remnant RNA strands of the virus, which can persist in the body of a previously infected person for months without causing further disease. The Korea Herald reports:

South Korea's infectious disease experts said Thursday that dead virus fragments were the likely cause of over 260 people here testing positive again for the novel coronavirus days and even weeks after marking full recoveries.

Oh Myoung-don, who leads the central clinical committee for emerging disease control, said the committee members found little reason to believe that those cases could be COVID-19 reinfections or reactivations, which would have made global efforts to contain the virus much more daunting.

The tests detected the ribonucleic acid of the dead virus, said Oh, a Seoul National University hospital doctor, at a press conference Thursday held at the National Medical Center.

He went on to explain that in PCR tests, or polymerase chain reaction tests, used for COVID-19 diagnosis, genetic materials of the virus amplify during testing, whether it is from a live virus or just from fragments of dead virus cells that can take months to clear from recovered patients.

Original Submission

Top Chinese Cyber Spy Crashes Australian Press Conference to Defend Chinese COVID Origins

A Chinese official who was a cyber spy hijacked a press conference to defend China's position in the midst of Australia calling for an independent inquiry into the source of the COVID-19 virus. The Chinese official, Long Zhou, stated that "there is no absolute freedom in this world" while denying China had launched Cyber attacks. Australian officials have responded to this event by cancelling events with "Twiggy" Forrest and stating the costs for purchasing all medical equipment procured by the billionaire would be reimbursed. The fallout from Twiggy's decision to allow China to gatecrash a major media event is he will now find himself out in the cold with a source from Canberra saying Twiggy will find the door to Canberra is closed .

Original Submission

First Bit of Success from a Randomized Trial of a COVID-19 Treatment [UPDATED]

First bit of success from a randomized trial of a COVID-19 treatment [UPDATED]:

Update, 5:40pm ET, April 29: Additional data on remdesivir's effects from a separate study are described below the original article.

Today, Dr. Anthony Fauci announced the first potential treatment for COVID-19 had emerged from a randomized clinical trial sponsored in part by the National Institutes of Health. The drug, remdesivir, significantly shortened the recovery time for patients with COVID-19, triggering an ethical clause that allowed the placebo group to receive the real drug. Unfortunately, that cut the trial short before a significant effect on mortality was clear.

Fauci made the announcement while speaking to the press with President Donald Trump in the White House.

Remdesivir was originally developed to target a different virus: Ebola. It works by binding to the enzyme that copies the RNA genome of the Ebola virus. Since our cells don't need to make copies of RNA, the hope has been that we can find drugs that target the viral enzyme but not any that our own cells need. Testing had already indicated it was safe for general use, suggesting that remdesivir was successful in this regard. Unfortunately, it didn't clearly work against the Ebola virus, leaving it the very large collection of drugs that are safe but ineffective.

With the onset of the SARS-CoV-2 pandemic, remdesivir received renewed interest, given that the new virus also has an RNA genome and enzymes dedicated to copying it. While the drug wasn't designed specifically to bind these proteins, the overlapping biochemical needs of the Ebola and SARS-CoV-2 enzymes meant that there was a chance that the drug would be effective, leading to some early anecdotal reports of its use.

This appears to be the first report of a non-anecdotal test of the drug. Fauci said that the trial, conducted in the United States and various European countries, had enrolled 1,090 patients. Those participants were randomly assigned to receive the drug or placebo, and the primary measure of success was time to recovery—how quickly the patients could be discharged from the hospital or resume normal activities. By this measure, remdesivir was a significant success; those receiving the drug took an average of 11 days to recover; those on the placebo took 15 days. That's a 30 percent faster recovery, a result that's statistically significant given the size of the trial population.

[...] On the same day that Anthony Fauci announced the positive results of a large clinical trial of the antiviral drug remdesivir, the research journal The Lancet released a smaller randomized study of the same drug from China. In this study, the researchers had planned on a large-enough population of patients for their study design to have a high probability of producing significant results. But the severe restrictions in place in Wuhan cut the number of patients in their hospitals that met the study's selection criteria, leading to its termination with a small population (only 237 patients). Potentially confusing matters, the participants were allowed to continue some other untested treatments, including anti-virals and immune-system modulators.

[...] None of the results were statistically significant, but the researchers saw a result consistent with what Dr. Fauci announced today: those taking remdesivir reached clinical improvement faster than those in the placebo group. Had the trial involved more patients, it might have found a significant improvement here. Since the total number of people needing ventilators was even smaller, there was no chance of a significant result here.

Original Submission

First Randomized Trial of Remdesivir Suggests Antiviral Drug is Not Associated with Significant Clinical Benefits

First randomized trial of remdesivir suggests antiviral drug is not associated with significant clinical benefits, more research needed:

Although their study is the first randomised controlled trial (considered the gold standard for evaluating the effectiveness of interventions) of remdesivir, the authors caution that interpretation of their findings is limited because the study was stopped early after they were unable to recruit enough patients due to the steep decline in cases in China*. They conclude that more evidence from ongoing clinical trials is needed to better understand whether remdesivir can provide meaningful clinical benefit.

In the absence of any known treatment for COVID-19, remdesivir is one of a handful of experimental drugs undergoing clinical trials worldwide. It has only been available to patients with COVID-19 on compassionate grounds (the use of unapproved drugs when no other treatment is available). In the trial, all patients received standard care including lopinavir-ritonavir, interferons, and corticosteroids.

"Unfortunately, our trial found that while safe and adequately tolerated, remdesivir did not provide significant benefits over placebo," says Professor Bin Cao from China-Japan Friendship Hospital and Capital Medical University in China, who led the research. "This is not the outcome we hoped for, but we are mindful that we were only able to enroll 237 of the target 453 patients because the COVID-19 outbreak was brought under control in Wuhan. What's more, restrictions on bed availability resulted in most patients being enrolled later in the disease course, so we were unable to adequately assess whether earlier treatment with remdesivir might have provided clinical benefit."

He continues: "Future studies need to determine whether earlier treatment with remdesivir, higher doses, or combination with other antivirals or SARS-CoV-2 neutralising antibodies, might be more effective in those with severe illness."

Remdesivir was originally developed to treat Ebola, and is designed to interfere with the way a virus reproduces, thereby stopping it from multiplying inside the body. It has been shown to successfully block SARS-CoV-2 from replicating in vitro, and had activity against other coronavirus infections like severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and COVID-19 in animal studies. Case studies have also reported benefit in some severely ill patients with COVID-19, but until now, there have been no clinical trials of remdesivir, so its efficacy against COVID-19 in patients is unknown.

Original Submission

Tests in Recovered Patients in S. Korea Found False Positives, Not Reinfections, Experts Say

Tests in recovered patients in S. Korea found false positives, not reinfections, experts say:

SEOUL South Korea's infectious disease experts said Thursday that dead virus fragments were the likely cause of over 260 people here testing positive again for the novel coronavirus days and even weeks after marking full recoveries.

Oh Myoung-don, who leads the central clinical committee for emerging disease control, said the committee members found little reason to believe that those cases could be COVID-19 reinfections or reactivations, which would have made global efforts to contain the virus much more daunting.

The tests detected the ribonucleic acid of the dead virus, said Oh, a Seoul National University hospital doctor, at a press conference Thursday held at the National Medical Center.

He went on to explain that in PCR tests, or polymerase chain reaction tests, used for COVID-19 diagnosis, genetic materials of the virus amplify during testing, whether it is from a live virus or just from fragments of dead virus cells that can take months to clear from recovered patients.

The PCR tests cannot distinguish whether the virus is alive or dead, he added, and this can lead to false positives.

PCR testing that amplifies genetics of the virus is used in Korea to test COVID-19, and relapse cases are due to technical limits of the PCR testing.

As of Sunday, 263 people in Korea tested positive for the disease again after being declared virus-free, of which 17 were minors or teens, the National Medical Center said.

Original Submission

A Close Look at the Frontrunning Coronavirus Vaccines as of April 28 (Updated)

A Close Look at the Frontrunning Coronavirus Vaccines As of April 28 (updated):

There's plenty of news on the coronavirus vaccine front, so let's have a look. If you need some details on the different sorts of vaccines in general, here's the background post, which should help this one make sense. This is a rapidly advancing field, with a huge number of programs. Some of the players are doing a lot more than they're talking about, while others (as is always the case) are talking much more loudly than their actions really justify. The signal/noise isn't great, but this will be an attempt to make sense of the landscape as of today.

Update: I should put in the links to the larger vaccine lists, as I did in the earlier post. Here's a good overview of the coronavirus vaccine world in a recent Nature Reviews Drug Discovery. The official WHO list is here, and at BioCentury they have constantly updated open-access summaries of the vaccines and other therapies that are in the clinic and the ones that are still preclinical. They ve also recently published this excellent overview of vaccine issues in this area.

[...] So by my count, the biggest and most advanced programs include two inactivated virus vaccines, three different adenovirus vector vaccines, two mRNA possibilities, a DNA vaccine, and a recombinant protein. That's a pretty good spread of mechanisms, and there are of course plenty more coming up right behind these. You cannot do the tiniest search for such information without being inundated with press releases about companies working on coronavirus vaccines — not complaining here — and moving on to smaller companies would make this post multiple times longer. I ll update as more news comes out and add in more companies and candidates.

Original Submission

Trump Admin Threatens to Sue States that Don't Lift Pandemic Orders

Trump admin threatens to sue states that don't lift pandemic orders:

The Trump administration is threatening to sue states and municipalities whose pandemic orders infringe on people's rights or cause "undue interference with the national economy."

"I am directing each of our United States Attorneys to also be on the lookout for state and local directives that could be violating the constitutional rights and civil liberties of individual citizens," US Attorney General William Barr wrote yesterday in a memo to all 94 US attorneys' offices. The Barr memo said that "even in times of emergency, when reasonable and temporary restrictions are placed on rights, the First Amendment and federal statutory law prohibit discrimination against religious institutions and religious believers." The memo is available at The Washington Post website.

Barr's memo is not just aimed at protecting members of religious groups. He continued:

Original Submission

Researchers Crack COVID-19 Genome Signature

Researchers crack COVID-19 genome signature:

Using machine learning, a team of Western computer scientists and biologists have identified an underlying genomic signature for 29 different COVID-19 DNA sequences.

This new data discovery tool will allow researchers to quickly and easily classify a deadly virus like COVID-19 in just minutes a process and pace of high importance for strategic planning and mobilizing medical needs during a pandemic.

The study also supports the scientific hypothesis that COVID-19 (SARS-CoV-2) has its origin in bats as Sarbecovirus, a subgroup of Betacoronavirus.

The findings, Machine learning using intrinsic genomic signatures for rapid classification of novel pathogens: COVID-19 case study, were published today in PLOS ONE.

The "ultra-fast, scalable, and highly accurate" classification system uses a new graphic-based, specialized software and decision-tree approach to illustrate the classification and arrive at a best choice out of all possible outcomes. The entire method uses a new graphic-based, specialized software to illustrate a best choice out of all tested possible outcomes.

Original Submission

Doctor's Note: Why Do We Get Fevers?

Doctor's Note: Why do we get fevers?:

One of the most prominent symptoms of COVID-19 is fever. So, if you are running a temperature, you should stay at home and self-isolate. When we get a fever, we usually respond by trying to bring our temperature down - usually by taking paracetamol.

But evidence suggests that a fever may be part of your body's strategy for fighting an infection rather than just a by-product of the infection.

What is a fever?

It is normal for your body's temperature to fluctuate throughout the day, and it is often highest in the evenings and lowest in the mornings.

A fever is usually defined as a temperature above 37.5 degrees Celcius (99.5 degrees Fahrenheit), but the temperature you read can vary depending on where you take it from.

When taken in the mouth, the average body temperature is usually between 36.5C (97.7F) and 37.2C (98.96F) but, taken in the armpit, it can be 0.2C to 0.3C (0.36F-0.54F) lower.

During the pandemic, there has been a shortage of thermometers, and without one, it can be difficult to determine whether you have a fever.

To assess whether you might have a fever without the use of a thermometer you can use the back of your hand to feel your forehead, check in the mirror for a flushed face, observe for chills, muscular aches and weakness and assess for dehydration from a fever by checking for darker, more concentrated urine.

Original Submission

Anti IL-6 for Coronavirus Patients: Does It Work, or Not?

Anti IL-6 For Coronavirus Patients: Does It Work, or Not?:

It's been looking for some time as if these coronavirus infections need a biphasic approach to therapy an antiviral approach earlier on, and for those in serious trouble, perhaps a shift to immune modulation as the body's reaction to the virus starts doing even more harm. That post goes into some detail on possible therapies targeting IL-6 for this purpose, and today we finally have some clinical data on the idea. Prepare yourself, if you are one of the many people who haven t had experience with investigational therapies but are watching to see how things play out with the pandemic. Because this is another one of those cases that will make you wonder what's going on.

There's an antibody against the IL-6 receptor from Roche/Genentech, tocilizumab (brand name Actemra), and this morning came preliminary word from France that the CORIMUNO-TOCI trial had produced positive results. This was in patients who had moderate to severe disease but were not in the ICU: 65 got standard of care, and 64 got standard of care plus tocilizumab (but note: the trial, although it has a control group, was open-label). The press release says that both deaths and the need for later ventilator support were significantly reduced in the treatment group, with no more adverse effects than in the control group.

The French team is also studying tocilizumab in patients in intensive care, and they re looking at another approved antibody to the IL-6 receptor as well, sarilumab (brand name Kevzara) from Sanofi and Regeneron. These two drug are both given for rheumatoid arthritis, with the same mechanism of action, but every antibody is a different beast. For example, tocilizumab is given i.v. and sarilumab is subcutaneous, so they have different pharmacokinetics right from the start.

And those results are certainly going to be interesting, because we have the results of a separate study on sarilumab this morning where it was shown to be almost completely ineffective. There had been an earlier report from China of efficacy for the drug, albeit in a small trial without a control group and if there's one thing that people should take away about drug discovery from this whole pandemic experience, it's that small uncontrolled trials cannot prove anything. All they can do is to point to something that might be interesting to study for real, and you should be ready for most such signals to turn out to be noise.

Original Submission


Original Submission

 
This discussion has been archived. No new comments can be posted.
Display Options Threshold/Breakthrough Mark All as Read Mark All as Unread
The Fine Print: The following comments are owned by whoever posted them. We are not responsible for them in any way.
  • (Score: 5, Informative) by Anonymous Coward on Monday May 04 2020, @03:08PM (28 children)

    by Anonymous Coward on Monday May 04 2020, @03:08PM (#990238)

    The censored doctors [washingtontimes.com] did a straight numerical comparison of the totals for flu and covid-19 without adjusting for the timeline. Covid-19 deaths for a month already equal seasonal flu deaths for a year, at the very least it's 12x more deadly.

    To avoid non covid-19 deaths we need to reopen wearing masks and with social distancing in place. I don't understand what the problem is here, there's no legal "right" to expose someone to a potentially fatal pathogen (it may only be a misdemeanor in CA [cnn.com]).

    Starting Score:    0  points
    Moderation   +5  
       Interesting=2, Informative=3, Total=5
    Extra 'Informative' Modifier   0  

    Total Score:   5  
  • (Score: 2) by JoeMerchant on Monday May 04 2020, @03:32PM (27 children)

    by JoeMerchant (3937) on Monday May 04 2020, @03:32PM (#990252)

    Covid-19 deaths for a month already equal seasonal flu deaths for a year, at the very least it's 12x more deadly.

    Love your math. Flu is seasonal, as we suspect COVID also is. Both numbers should tail off significantly (in the northern hemisphere) until late October.

    My interpretation of your data is that COVID-19 is something less than 12x more deadly, not 12x at the very least.

    --
    🌻🌻 [google.com]
    • (Score: 4, Interesting) by HiThere on Monday May 04 2020, @04:03PM (6 children)

      by HiThere (866) Subscriber Badge on Monday May 04 2020, @04:03PM (#990265) Journal

      There's no particular reason to suspect that COVID is seasonal. I suppose there could be in some places, if, e.g., people huddled together in air-conditioned hives to avoid the heat, or heated hives to avoid the cold. But that's about the limit of the reason we have.

      The predictions of an especially bad fall/winter is because that's also the flu season, and getting both at once would be exceptionally unpleasant.

      --
      Javascript is what you use to allow unknown third parties to run software you have no idea about on your computer.
      • (Score: 2) by JoeMerchant on Monday May 04 2020, @04:56PM (2 children)

        by JoeMerchant (3937) on Monday May 04 2020, @04:56PM (#990302)

        There's no particular reason to suspect that COVID is seasonal.

        Here's one: https://www.health.com/condition/infectious-diseases/coronavirus/does-sunlight-really-kill-covid-19-heres-what-doctors-say [health.com]

        It’s true that UV light can decrease the viability of viruses (including the new coronavirus) on surfaces

        --
        🌻🌻 [google.com]
        • (Score: 2) by HiThere on Monday May 04 2020, @10:30PM (1 child)

          by HiThere (866) Subscriber Badge on Monday May 04 2020, @10:30PM (#990464) Journal

          Yes, but...how much light has how much effect? IIUC, it isn't by a significant amount. There *is* a reasonable argument that if the surfaces are hot, the particles won't stay infectious very long. And it *MAY* be true. But how much of the spread is via surfaces rather than some other means? Most statements seem to concentrate on particles floating in the air.

          --
          Javascript is what you use to allow unknown third parties to run software you have no idea about on your computer.
          • (Score: 2) by JoeMerchant on Monday May 04 2020, @11:20PM

            by JoeMerchant (3937) on Monday May 04 2020, @11:20PM (#990487)

            Most statements are politically-motivated rather than science-based; we'll find out when the seasons change.

            --
            🌻🌻 [google.com]
      • (Score: 1) by khallow on Monday May 04 2020, @05:08PM (2 children)

        by khallow (3766) Subscriber Badge on Monday May 04 2020, @05:08PM (#990311) Journal

        There's no particular reason to suspect that COVID is seasonal.

        Aside from variations in covid infections by climate (with cooler climates tending to have a faster rate of infection than warmer climates)? And knowing that covid survives better in the colder, drier conditions of winter than it does in the warmer, more humid conditions of summer. To the contrary, there's plenty of indication that covid is seasonal.

        • (Score: 2) by HiThere on Monday May 04 2020, @10:33PM (1 child)

          by HiThere (866) Subscriber Badge on Monday May 04 2020, @10:33PM (#990467) Journal

          Well, Georgia is performing an experiment to tell whether you are correct or not.

          --
          Javascript is what you use to allow unknown third parties to run software you have no idea about on your computer.
    • (Score: 4, Insightful) by Immerman on Monday May 04 2020, @04:12PM (8 children)

      by Immerman (3985) on Monday May 04 2020, @04:12PM (#990273)

      > Flu is seasonal, as we suspect COVID also is.
      Do we? I understand the southern continents have been having problems with it to, and they've been in summer. It does seem to be less contagious there, but it's so contagious to begin with that "less contagious" is still comparable to the flu during flu season.

      • (Score: 2) by JoeMerchant on Monday May 04 2020, @04:59PM (7 children)

        by JoeMerchant (3937) on Monday May 04 2020, @04:59PM (#990306)

        Just because something is seasonal does not mean it falls to zero in the off season - seasonal variations can mean the difference between epidemic and mild to moderate nuisance. Also, pre-lockdown those southern hemisphere cities were just as connected by air travel to the rest of the world as everybody else...

        Anyone who takes "sunlight kills viruses on surfaces and in the air" to mean "I'm gonna go sunbathe and cure my COVID" deserves the Darwin award they may be receiving.

        --
        🌻🌻 [google.com]
        • (Score: 2) by Immerman on Monday May 04 2020, @06:26PM (6 children)

          by Immerman (3985) on Monday May 04 2020, @06:26PM (#990365)

          It usually means it falls pretty close though.

          Flu isn't usually a problem because flu season ends just as its exponential growth is starting to really build momentum. If it didn't we could expect most people to catch it every year, instead of averaging around 5%, And we could expect 10-20x as many total people (600+ thousand Americans/year instead of the usual 30-60k). It still spreads in the off season, but environmental conditions make it less contagious so that the contagion rate drops from about 1.5 new infections per contagious individual, to well under 1. And once you fall below 1 you no longer have exponential growth, and the total number of active cases rapidly trends toward 0.

          As for international spread - that actually doesn't matter that much beyond the initial infection. Once you have a handful of unquarantined local cases of an infectious disease you're facing your own exponential growth curve, which tends to rapidly outpace the international flow.

          It's not like Australia was able to just ban international travel and they were fine - COVID was still spreading fast enough within their population to be an issue during the summer. But it did mean that their lockdown and other precautions were far more effective than in the northern hemisphere, where the base contagion rate has been much higher. Now we're seeing the seasons starting to change though - and if they don't manage to stamp it out completely before then, it'll start being a much worse problem, just as it has been for us in the north.

          Likewise, we in the north will be getting a bit of a respite - it's going to get a lot easier to control the spread, but if we stop taking precautions it's still going to spread like a bad flu season that never ends.

          • (Score: 2) by JoeMerchant on Monday May 04 2020, @07:47PM (5 children)

            by JoeMerchant (3937) on Monday May 04 2020, @07:47PM (#990407)

            It's all about the R value - if your R is greater than 1.0, you've got an exponentially growing pandemic, below 1.0 it tends to die out naturally. Seasonal flu hovers around the 1.0 mark, a bit over during cold season and a bit less in the warm months. It's not a big difference in infectious potential, but it's a highly significant one.

            --
            🌻🌻 [google.com]
            • (Score: 2) by Immerman on Monday May 04 2020, @09:22PM (4 children)

              by Immerman (3985) on Monday May 04 2020, @09:22PM (#990438)

              Right. And available evidence puts the best estimates of R-value for "summer COVID" far enough over 1 to be a problem, while "Winter COVID" is well over 2

              Technically that is seasonal variation, but while the flu varies between bad gone so that there's a "flu season", COVID will probably fluctuate between bad and worse - without precautions there will be no "COVID season", it'll be a year-round problem.

              • (Score: 2) by JoeMerchant on Monday May 04 2020, @09:31PM (3 children)

                by JoeMerchant (3937) on Monday May 04 2020, @09:31PM (#990444)

                And available evidence

                Available to whom? So much political posturing, distortion of the numbers in both directions for various motives - teasing the truth out of that is pretty well impossible.

                I do believe (most of) the trailing numbers like admissions, deaths, and they're showing pretty clear "past the peak" behavior now- not that we can't get a Denver bounce, but hopefully the vulnerable are taking care of themselves and mostly being taken care of when they can't to protect them from a bounce.

                The Georgia governor's message was a little muddled, but I believe the right thinking was behind it: "for 90%+ of the population life goes on as normal now, shelter in place if you're vulnerable." Who knows? it _might_ work.

                --
                🌻🌻 [google.com]
                • (Score: 4, Insightful) by Immerman on Monday May 04 2020, @10:25PM (2 children)

                  by Immerman (3985) on Monday May 04 2020, @10:25PM (#990460)

                  You're right that statistics are clouded by many factors, but it seems to me we have two groups - the public health experts saying it's serious, with an R0 value in the 2-3.5 range, and politicians and pundits saying it's not. I know which group I trust more.

                  >they're showing pretty clear "past the peak" behavior now

                  Right - in the face of dramatic efforts to artificially lower the R0 value. Remove the effort, the R0 value goes back up, and we're no longer past the peak.

                  • (Score: 2) by JoeMerchant on Monday May 04 2020, @11:18PM (1 child)

                    by JoeMerchant (3937) on Monday May 04 2020, @11:18PM (#990484)

                    The question is: are the efforts still being expended in the correct places for the elderly and otherwise vulnerable, time will tell.

                    --
                    🌻🌻 [google.com]
                    • (Score: 0) by Anonymous Coward on Monday May 04 2020, @11:54PM

                      by Anonymous Coward on Monday May 04 2020, @11:54PM (#990496)

                      are the efforts still being expended in the correct places for the elderly and otherwise vulnerable

                      What efforts? Suspending state nursing home inspections? Prohibiting family visits to conveniently hide problematic conditions inside? Judging by the numbers, the "efforts" aren't yielding any results to write home about. At least my state hasn't had to clean up an abandoned nursing home filled with dead and dying livestock yet.

    • (Score: 1, Informative) by Anonymous Coward on Monday May 04 2020, @04:25PM (9 children)

      by Anonymous Coward on Monday May 04 2020, @04:25PM (#990283)

      Love your math. Flu is seasonal, as we suspect COVID also is. Both numbers should tail off significantly (in the northern hemisphere) until late October.

      The first Spanish flu outbreak was in the Summer and there's limited and conflicting data for sars2 transmission.

      My interpretation of your data is that COVID-19 is something less than 12x more deadly, not 12x at the very least.

      It's not my data and you're overlooking that we've already slowed the transmission rate with social distancing and lockdowns. For reference, CDC estimates for seasonal flu over the last decade vary between 12,000 and 61,000 while NYC alone has reported around 25,000 Covid-19 deaths. The UK has an average of 17,000 yearly and recent record of 28,300 seasonal flu deaths in 2014/15 while their current hospital death toll from covid-19 28,700. All considered, where does your guesstimate now lie if we reopened tomorrow without taking any measures to reduce transmission?

      • (Score: 1) by khallow on Monday May 04 2020, @05:21PM (8 children)

        by khallow (3766) Subscriber Badge on Monday May 04 2020, @05:21PM (#990318) Journal

        The first Spanish flu outbreak was in the Summer

        And yet we have stuff like this [nih.gov]:

        It has never been clear, however, where this pandemic began. Since influenza is an endemic disease, not simply an epidemic one, it is impossible to answer this question with absolute certainty. Nonetheless, in seven years of work on a history of the pandemic, this author conducted an extensive survey of contemporary medical and lay literature searching for epidemiological evidence – the only evidence available. That review suggests that the most likely site of origin was Haskell County, Kansas, an isolated and sparsely populated county in the southwest corner of the state, in January 1918 [1]. If this hypothesis is correct, it has public policy implications.

        [...]

        That left the United States. Jordan [Dr. Edwin Jordan, editor of The Journal of Infectious Disease] looked at a series of spring outbreaks there. The evidence seemed far stronger. One could see influenza jumping from Army camp to camp, then into cities, and traveling with troops to Europe. His conclusion: the United States was the site of origin.

        A later equally comprehensive, multi-volume British study of the pandemic agreed with Jordan. It too found no evidence for the influenza's origin in the Orient, it too rejected the 1916 outbreak among British troops, and it too concluded, "The disease was probably carried from the United States to Europe [5]."

        Australian Nobel laureate MacFarlane Burnet spent most of his scientific career working on influenza and studied the pandemic closely. He too concluded that the evidence was "strongly suggestive" that the disease started in the United States and spread with "the arrival of American troops in France [6]."

        The Fall 1918 spread of an even more serious influenza strain was well documented. Again, typical seasonal behavior.

        • (Score: 0) by Anonymous Coward on Monday May 04 2020, @05:45PM (7 children)

          by Anonymous Coward on Monday May 04 2020, @05:45PM (#990334)

          The Fall 1918 spread of an even more serious influenza strain was well documented. Again, typical seasonal behavior.

          Summer flu is atypical [nih.gov] and Covid-19 isn't flu, we're using the comparison as something we are all familiar with. Seasonality is something we do not yet know [newscientist.com]

          • (Score: 1) by khallow on Monday May 04 2020, @05:59PM (6 children)

            by khallow (3766) Subscriber Badge on Monday May 04 2020, @05:59PM (#990348) Journal

            Seasonality is something we do not yet know

            Given that we already see seasonality differences of the expected sort and covid viruses are known to survive better under cooler, drier conditions, I think we have demonstrated seasonality.

            • (Score: 0) by Anonymous Coward on Monday May 04 2020, @06:34PM

              by Anonymous Coward on Monday May 04 2020, @06:34PM (#990371)

              Remember back when the idiots at the WHO declared multiple epidemics but refused to call it a pandemic? Multiple epidemics is how seasonality develops. [smw.ch] We've not yet reached that point and the virus may mutate or disappear before we do.

            • (Score: 3, Interesting) by Immerman on Monday May 04 2020, @09:27PM (4 children)

              by Immerman (3985) on Monday May 04 2020, @09:27PM (#990442)

              Except that seasonality typically implies a season when the number of cases starts diminishing because the virus can't spread as fast as people are recovering. And COVID has been spreading just fine in the summer. Not as fast as in the winter, but fast enough that it's not just going t go away like seasonal flu does.

              • (Score: 1) by khallow on Tuesday May 05 2020, @03:07AM (3 children)

                by khallow (3766) Subscriber Badge on Tuesday May 05 2020, @03:07AM (#990557) Journal

                And COVID has been spreading just fine in the summer.

                Far less fine than it was earlier in the year in the Northern latitudes. For example, there was a much faster spreading of the disease in Europe than in India despite the more aggressive control measures and better health care systems.

                • (Score: 2) by Immerman on Tuesday May 05 2020, @02:19PM (2 children)

                  by Immerman (3985) on Tuesday May 05 2020, @02:19PM (#990687)

                  Yes, in the "off-season" it's easier to control, but it still spreads without control attempts. That's a huge difference from seasonal diseases which basically go away on their on once their season is over.

                  My big complaint is that almost everyone trying to portray this as a seasonal disease is trying to pretend COVID will go away when its season is over, and things will go back to normal, despite all available evidence indicating that is *not* what will happen.

                  • (Score: 1) by khallow on Tuesday May 05 2020, @02:49PM

                    by khallow (3766) Subscriber Badge on Tuesday May 05 2020, @02:49PM (#990713) Journal

                    Yes, in the "off-season" it's easier to control,

                    That's seasonality right there.

                  • (Score: 1) by khallow on Tuesday May 05 2020, @02:59PM

                    by khallow (3766) Subscriber Badge on Tuesday May 05 2020, @02:59PM (#990719) Journal

                    My big complaint is that almost everyone trying to portray this as a seasonal disease is trying to pretend COVID will go away when its season is over

                    Not hearing that myself. I've heard multiple mentions to some sort of fall rebound - just like the 1918 influenza.

    • (Score: 0) by Anonymous Coward on Tuesday May 05 2020, @04:30PM

      by Anonymous Coward on Tuesday May 05 2020, @04:30PM (#990764)

      Did you consider that we might be in the off-season of COVID?