UPDATED: @WHO Recs for national #SARSCoV2 testing strategies *Testing is critical to the overall #COVID19 prevention & control strategy & must be linked to public health actions* Details re types of tests, prioritization when capacities are stretched ⬇️ www.who.int/publications/i/item/WHO-2019-nCoV-lab-testing-2021.1-eng pic.twitter.com/ms2OxBeLmK
"#Misinformation on social networks during the novel #coronavirus pandemic: a quali-quantitative case study" bmcpublichealth.biomedcentral.com/articles/10.1186/s12889-021-11165-1 Themes: - Facebook (76%) - Often a "real-life stories" (47%) - Fabricated content (53%) & false connections (34%) - Negative tone #ScienceUpFirst pic.twitter.com/kfoiygvdTR
On Monday the number of cases are usually lower than on other days... so 22,868 today is quite high and concerning. COVID-19: UK reports 22,868 new coronavirus cases and a further three deaths news.sky.com/story/covid-19-uk-reports-22868-new-coronavirus-cases-and-a-further-three-deaths-12344064 pic.twitter.com/snh1AALuR2
DC reports 28 new coronavirus cases over the past three days.
It’s another exhausting twist in an outbreak defined by them. Before delta was detected in India and dubbed B.1.617.2, new versions of the coronavirus had been worrisome but manageable despite their faster spread.
Rapid-fire research had demonstrated our immune systems are sturdy and that a full course of COVID-19 vaccines could shield us against the early mutants. Even partial vaccination or immunity built up after infection with the original strain—SARS-CoV-2 classic—provided protection.
But studies this month from the United Kingdom shift the immunity narrative. According to the latest findings from Public Health England, one dose of COVID-19 vaccine—specifically Pfizer and AstraZeneca—cannot withstand the delta variant.
When it comes to preventing symptomatic cases of the delta variant, the vaccine effectiveness after one dose drops to 35%. Compare that against 79% with two doses. For hospitalization, a single dose offers 80% effectiveness, while two shots give 96%.
What does all of this mean for U.S. areas with relatively solid rates of COVID-19 vaccination, such as New York? The worry isn’t that people are skipping second shots. Nearly nine out of 10 Americans complete their two-dose vaccines courses, according to data from New York City and the Centers for Disease Control and Prevention.
Researchers say the real problem is that one-dose recipients offer a preview of what happens to people who live on the margins of solid immunity. If you got infected and recovered, banking on your natural defenses might no longer ward off the delta variant. A shot is needed.
“If you're unvaccinated, you will get infected, and you will have a higher probability of ending up in the hospital,” said Dr. Theodora Hatziioannou, a virologist at Rockefeller University in New York City. “The vaccinated people might get infected too, but they will deal with this a lot better.”
The unvaccinated—particularly younger adults and grade-school children—now appear to be at higher risk for cases and hospitalization than when the dangerous alpha variant (B.1.1.7) sprouted in the U.K. There, delta rose to become the dominant variant of coronavirus there in nine weeks. It now makes up 95% of British cases, primarily consisting of unvaccinated people under 50 years old.
“We seem to be following the pattern with the delta variant, with a doubling time of about two weeks,” Dr. Anthony Fauci, chief medical adviser to the president, said June 22nd during a White House briefing.
Places with the best vaccination rates are starting to see resurgences, too. New York City data show the delta variant accounts for nearly a quarter of analyzed cases, up from 5% the week prior. Similar jumps have been recorded across the Northeast and out west in California. Israel is witnessing fresh outbreaks because of the delta variant despite 84% of adults being fully inoculated. In New York City, that rate is only 60%.
“Our healthcare leadership believes that the best answer to the variant is just keep deepening the vaccination effort,” Mayor Bill de Blasio told the Brian Lehrer Show on Friday. “But Brian, we're going to watch it carefully. There's no evidence at this moment that it changes the trajectory. But if anything occurs, when we have to make adjustments, we will make them quickly.”
But while the vaccines are still expected to prevent serious illness caused by the delta variant in healthy immune systems, more harm will likely come in senior citizens or people with weakened immunity due to pre-existing conditions. In the U.K., deaths are rising among older adults who are fully vaccinated. Israeli officials are reinstating some mask mandates for those who’ve taken shots, a policy recommendation echoed by the World Health Organization.
To gauge what might happen going forward, let’s break down how the delta variant could affect New Yorkers based on their vaccine status. The COVID-19 vaccine rollout has undoubtedly dropped cases and hospitalizations to all-time lows. But due to sizable gaps in coverage, the question is whether the Empire State can sustain its progress everywhere now that life has reopened.
To comprehend just how fast that is, let’s hit reset on the COVID outbreak in the Bronx.
Say this borough of 1.4 million people had never experienced the pandemic. There was no vaccine campaign, and no one was wearing masks or social distancing. The whole population and their immune systems were unacquainted with SARS-CoV-2 or its variants. Until one day, 10 people with the disease show up.
The delta variant would hit the Bronx harder and faster than its predecessors—as judged by the standard model for recreating outbreaks. The delta outbreak would peak after about two months, with more than 67,000 cases in a single day. By comparison, an alpha epidemic would take three months to hit full steam, amassing about 47,000 infections during its worst day. The classic strain is way behind, summiting with 26,000 cases at around four and half months.
“It's really important to build these types of models because it's often difficult to grasp how something like this is going to play out in reality,” said Dr. Patrick Wedlock, a senior research analyst with the Public Health Computational and Operations Research (PHICOR) team at The City University of New York.
This simple model doesn’t precisely tell us how the delta variant will spread through the Bronx this summer, given 41% of the borough has been fully inoculated as of June 27th. Although that’s the lowest vaccination rate in the city, it’s been enough to blunt the Bronx’s pandemic this year. But even the delta variant could thrive in this environment:
“Those who are unvaccinated have the greatest risk of becoming seriously ill, which is why the New York State Department of Health urges all eligible New Yorkers to get vaccinated as soon as they are able,” a state health department spokesperson said in a statement to WNYC/Gothamist.
Part of this transmission equation also centers around the strength of human immunity and how long it lasts. Thanks to a staggering amount of research, scientists have a sense of how these defenses work during the first 6-12 months after an infection or vaccination.
“What we have learned in a short timespan is amazing,” Dr. Nathaniel Landau, a virologist at New York University’s Grossman School of Medicine who studies mammalian immune systems. “It's been incredible to see how the biomedical research community has come together to answer questions and to learn about the virus and to develop vaccines.”
Recent experiments from his lab and others show that the variants spread faster in part because their mutations allow the virus to stick more firmly to ACE2, the protein doorway coating our cells. These genetic changes also make it harder for our immune systems to spot and defend against the variants.
Antibodies and T cells tend to dominate this conversation around our immune defenses. Both turn on within days of infection or vaccination, but each shield comes with its own capabilities. Antibodies scan the surface of germs but can only recognize familiar features, such as parts of coronavirus’s spike protein. T cells are immediately more versatile.
“T cells have the ability to see more than just the spike protein, so they can see all the internal parts of the virus,” Landau said. “Whereas the antibodies can only see the thing that's sticking out of the virus.”
The limited scope of antibodies becomes key when distinguishing between run-of-the-mill immunity after infection versus the extra oomph offered by vaccination. Merely catching the coronavirus produces a less consistent antibody response, when researchers look from patient to patient. T cells, so far, show sturdier protection against the virus and its variants, both after infection or vaccination.
“What we know is that following infection, the neutralizing antibody titers vary greatly between individuals,” said Hatziioannou from Rockefeller University. “Some have quite strong responses, but others have really, really low responses.”
In a study published June 14, Hatziioannou and her colleagues show the antibodies aren’t static early on but are consistently refining themselves to thwart the coronavirus better. Their team and others found that just one dose of vaccine can enhance this process, widening the antibodies’ scope. Their results help explain why health officials recommend shots even for people who’ve been previously infected with the coronavirus.
“You just have greater quality antibodies being produced at greater levels. You have neutralizing antibody titers that are really exceptionally high,” Hatziioannou said. “And they are able to neutralize not only the parental viruses that circulated but also all the variants that we looked at. They're really remarkable.”
Why does this matter? Antibodies are the major players in whether you’ll get reinfected. They halt the virus as soon as it comes into contact with our organs. T cells are powerful, but they’re more involved with clearing the virus after it’s already arrived and preventing symptoms.
“There have been a few rare cases of reinfection, but the large majority of people are protected by the antibodies from becoming reinfected,” Landau said. “We see antibodies in a vaccinated person are about five times stronger than the antibodies that you get from the natural infection.”
Reinfections appear to be mercifully rare among the fully vaccinated, with only 13 cases detected out of 10,000 screened in the latest iteration of Britain’s SIREN study. Landau said he wouldn’t be surprised if reinfections are more prevalent among inoculated people but are simply asymptomatic and overlooked. But that could ultimately be a healthy thing.
“The immune system needs to be in good shape, just like an athlete. It needs to stay in practice. When you do have such a low-level infection, it strengthens your immune response and will protect you for longer,” Landau said. “What's happening in real life all the time is that we are getting infected by viruses in an asymptomatic way. So you don't know that you're getting infected, but your T-cell response, as a result, gets strengthened.”
COVID-19 has taught us the value of stopping disease before it gains momentum. This lesson applies on a national level as well as to our immune systems. The difference between a severe or mild case can depend upon whether a person’s defenses respond slowly or softly.
The COVID-19 vaccines reinforce the body, ensuring that everyone starts on a stronger footing if the virus shows up. With the shots, weaker immune systems become stout, and the sturdy becomes ironclad. This armory can definitely last for months—but potentially for years.
But the variants are tearing at the margins. Public Health England has recorded about 92,000 delta cases as of June 25th. These infections and their overnight hospitalizations are twice as common in unvaccinated people, most of whom are younger than 50. Schools appear to be the primary drivers of these new outbreaks, bucking the longstanding trend with the coronavirus.
“The Imperial College of London did a study in over 100,000 homes and found that youth were driving the U.K. surge,” Fauci said during the briefing, “with a fivefold higher positivity among children (5 to 12) and young adults (18 to 24) versus people older than 65.”
And among those with COVID-19 shots, deaths are occurring more often in adults over 50, an age bracket where immune systems are more likely to be weaker before vaccination.
The clear message is to get vaccinated with a full course of COVID-19 vaccine as soon as you can. Two doses of Moderna are expected to offer solid protection against the delta variant, given it is an mRNA vaccine like Pfizer.
The jury is still out on the Johnson & Johnson vaccine, despite comments from a former FDA commissioner who claimed it is only 60% effective against the delta variant, based on findings with the AstraZeneca shot.
While Johnson & Johnson and AstraZeneca use similar biotechnology platforms, “the antigen is presented slightly differently by the two vaccines,” said Hatziioannou from Rockefeller University. “The antibody response from the Johnson and Johnson would be more similar to the mRNA vaccines than the one from AstraZeneca.”
Dr. Céline Gounder, an infectious disease specialist and epidemiologist at the NYU Grossman School of Medicine and Bellevue Hospital, agrees that more data are needed for the average person who has taken Johnson & Johnson’s single shot. But the calculus will likely be different for someone at very high risk for severe disease, senior citizens, immunosuppressed individuals and people with underlying medical conditions.
“If you are at increased risk for not responding to the vaccine or have an increased risk of severe disease,” Gounder said at the WNYC 2021 Health Convening, “in those people, I would recommend getting an mRNA vaccine, a second dose after your Johnson and Johnson. But that second dose should be either Moderna or Pfizer.”
Read full article at Gothamist
28 June, 2021 - 11:07am
28 June, 2021 - 11:07am
Since the early phases of the global coronavirus disease (COVID-19) pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), national and regional lockdowns have been instrumental in controlling the spread of the virus in many parts of the world. In most cases, those countries that were able to implement lockdowns early on in the pandemic were better able to manage the spread of SARS-CoV-2 among their populations.
New research by scientists in Brazil and the USA suggests that three primary factors have influenced the early macro-geographical dynamics of the COVID-19 pandemic in Brazil.
The study’s findings suggest that if a lockdown had been imposed earlier on in superspreader cities like São Paulo, mandatory road traffic restrictions had been enforced, and intensive care unit (ICU) beds had been allocated more equitably across geographical regions, Brazil’s experience of the COVID-19 pandemic might have been mitigated.
The team has published their study in the Nature Scientific Reports journal.
Although international airports served as main entry points for SARS-CoV-2, the factors that drove COVID-19's uneven geographical spread and deaths in Brazil remain unclear.
On March 27, 2929, Brazil announced a temporary ban on foreign air travel, and state governments imposed quarantine orders to prevent viral spread. Though the first COVID-19 case was reported on January 28, 2020, it was not until May 2020 that the number of cases reached more than 100,000. From there, the case continued to rise.
To date, the number of confirmed cases in Brazil has topped 18.38 million, with over 512,000 deaths, making it the third country in the world with the highest number of cases.
During the first three months of the pandemic in Brazil, São Paulo initially accounted for more than 85% of the caseload. However, even though the main entry points of SARS-CoV-2 were monitored and the main coronavirus genotypes were immediately identified, the routes taken by the virus to reach the entire country are still unknown.
Understanding the geographical spread of infectious diseases requires analyzing several factors, including environmental factors, pathogen population traits, and the flow of people in the transportation network.
The researchers examined human-mediated processes that turned capital cities into SARS-CoV-2 "superspreaders" at the geographical scale in the current study. The team also aimed to shed light on the critical processes that accounted for the macro-geographical patterns of COVID-19 cases and deaths in Brazil.
To arrive at the study findings, the researchers came up with a mathematical model of epidemics. They did not only consider population density but other factors like complex transportation networks.
The team believed that transportation patterns might have influenced the uneven geographical distribution of COVID-19 deaths in the country. Thus, they identified the spreading cities and Brazilian federal roads that contributed to the definition of the geographical patterns of COVID-19 cases. Further, the team also shed light on how the distribution of intensive care unit (ICU) beds across the country influenced the uneven spatial distribution of COVID-19 deaths during the first six months of the COVID-19 pandemic.
The study findings showed that three major factors influenced the spread of COVID-19 in Brazil. These include having a super-spreading city, federal highways, and the country's ICU beds and facilities.
São Paulo initially accounted for more than 85 percent of the case spread in the whole country. By adding 16 other spreading cities, the team accounted for 98 to 99 percent of the cases during the first three months of the pandemic.
The team also added that federal highways played an imperative role in the viral spread. These accounted for about 30 percent of the SARS-CoV-2 spread. Lastly, the distribution of COVID-19 deaths started to correlate with the allocation of intensive care units (ICU).
The team thus suggests that if the country has imposed a lockdown in superspreading cities like São Paulo, the cases and the impact of COVID-19 would be lower. The team also notes that if mandatory road traffic restrictions had been imposed, and more equitable distributions of ICU beds were in effect, there would have been fewer cases – and ultimately fewer deaths – in the country.
Tags: Coronavirus, Coronavirus Disease COVID-19, Epidemiology, Infectious Diseases, Intensive Care, Pandemic, Pathogen, Research, Respiratory, SARS, SARS-CoV-2, Severe Acute Respiratory, Severe Acute Respiratory Syndrome, Syndrome, Virus
Angela is a nurse by profession and a writer by heart. She graduated with honors (Cum Laude) for her Bachelor of Nursing degree at the University of Baguio, Philippines. She is currently completing her Master's Degree where she specialized in Maternal and Child Nursing and worked as a clinical instructor and educator in the School of Nursing at the University of Baguio.
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28 June, 2021 - 05:38am
The team at Duke University in the US demonstrated that the easy-to-use and energy-independent device can reliably detect multiple COVID-19 antibodies and biomarkers simultaneously.
The researchers are working to see if the point-of-care device can be used to predict the severity of a COVID-19 infection or a person's immunity against variants of the virus.
The platform called 'D4 assay' can detect Ebola infections a day earlier than the gold standard polymerase chain reaction (PCR) test, the researchers have shown in a recently.
The results, published in the journal Science Advances on June 25, show how flexible the technology can be to adapt to other current or future diseases.
'The D4 assay took six years to develop, but when the WHO declared the outbreak a pandemic, we began working to compress all of that work into a few months so we could explore how the test could be used as a public health tool,' said Ashutosh Chilkoti, a professor at Duke.
'Our test is designed to be both adaptable and truly point-of-care, and this is clearly a scenario when a portable, fast and cost-effective diagnostic would be most useful,' Chilkoti said.
The technology employs a polymer brush coating that acts as a sort of non-stick coating to stop everything except the desired biomarkers from attaching to the test slide when wet.
The high effectiveness of this non-stick shield makes the D4 assay incredibly sensitive to even low levels of its targets, according to the researchers.
The approach allows researchers to print different molecular traps on different areas of the slide to catch multiple biomarkers at once, they said.
The current iteration of the platform also features tiny patterned tunnels that use the physics of liquids to draw samples through the channels without needing any electricity.
With just a drop of blood and a biomolecular lubricant, the test runs autonomously in minutes, and can be read with a detector roughly the size of a tablet.
'The detector is battery powered and the test doesn't require any power at all, so you can throw the whole thing into a backpack and truly test at the point-of-care with minimal resources,' said Jason Liu, a PhD student working in the Chilkoti lab who designed and built the detector.
The researchers tested the assay's ability to detect and quantify antibodies produced against three parts of the virus -- a subunit of the spike protein, a binding domain within the protein that grabs on to cells, and the nucleocapsid protein that packages the virus's RNA.
The spike protein helps the virus to enter and infect the human cells.
The test was able to spot the antibodies in all of the 31 patients tested with severe cases of COVID-19 after two weeks, the researchers said.
It also reported zero false-positives in 41 samples taken from healthy people before the pandemic started as well as 18 samples taken from individuals infected with four other widely circulating coronaviruses, they said.
The researchers said that the platform's proven accuracy and flexibility make it a prime candidate for developing into other types of tests or for use in future outbreaks.
For example, the platform could potentially be able to test whether or not people have immunity to the various strains of SARS-CoV-2 that continue to emerge, they said.
'There are a lot of questions from people about whether or not they're protected from new variants of COVID-19, and our test could answer some of those,' said Jake Heggestad, a PhD student working in the Chilkoti lab who developed the chip for the test.
'We believe that our platform should be able to distinguish between whether people have antibodies that can neutralise emerging variants of concern or if those antibodies aren't going to be protective against new variants,' Heggestad added. PTI SAR SAR
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26 June, 2021 - 11:31am
If you’re not part of the solution, you’re part of the problem. So the rest of us may have to live with this virus and hope that booster vaccines will be able to control future emerging variants of concern.
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Honest. Really. I have been trying hard not to write anything about COVID as I, and undoubtedly most of you readers, have been happy beyond belief about seeing COVID getting smaller and smaller in the rearview mirror as we tentatively try to get back to our prior lives before this pandemic disrupted all of our lives in ways we are only now beginning to fathom.
Yet a couple of observations have become evident to those paying attention that deserve highlighting lest we start moving backwards.
The first are the reports coming in from large medical centers around the country that the vast majority of those COVID patients sick enough to be admitted are unvaccinated. The COVID related hospitalized patients now are 95-99% are not fully vaccinated individuals.
The second observation of great concern is that the Delta variant, first identified in India during its catastrophic experience with this pandemic, in now increasingly becoming the dominant form in countries where it has made its appearance. Although it appears to be about 60% more infective, it does not appear to be significantly more lethal. And the current approved in the U.S. COVID vaccines offer good protection against it. So far.
So what are the take away points from these observations? Let’s start with basic principles about biology. The first principle is that reproduction is the basic task of all life. What drives evolution are the adaptations that randomly arise in any given environment that give some mutation a survival advantage. This is a basic Darwinian observation. I leave it for those who believe that there is another factor in play here to explain why mutations arise to test them to live with that logic.
What ties these two observations together is that continued infections provide the substrate for mutations to occur. In biologic times, the life cycle duration of an organism dictates the frequency of which mutations may randomly occur. Mutations that occur in tortoises that have very long life spans are only noticeable over thousands of years and if there is little outside influence. Thus, the Galapagos tortoise hasn’t noticeably changed in millennia.
Viruses, on the other hand, replicate very quickly and each generation of viruses has a small, but random, incidence of genetic coding errors, or mutations. The vast majority of these have no survival (i.e., reproduction) benefit, so they literally die off. Those that enhance transmissibility, and hence infectivity, provide a survival benefit so those mutations, or “variations,” will eventually overtake the others strains. This is why the original SARS-CoV-2 virus was superseded by the UK variant, then the South African, Brazilian, a few others that transiently flourished, but now the Delta variant.
In the uncontrolled viral breeding environment that was the overwhelmed Indian healthcare system, variant strains undoubtedly occurred with the Delta variant emerging as the current dominant strain, based on its infectivity. As long as the virus can run amok in a population, mutations will occur until a “badder” mutation takes over because it’s better at reproducing, because it’s more infectious. We will be in trouble if it also is more lethal (not by intent, but as an incidental feature). The worse scenario will be if the mutations also allow it to have “vaccine escape,” that is, our extant vaccines can no longer attenuate the infectivity and severity of the virus.
The other serious coronaviruses that have crossed over to humans, the original SARS-CoV-1 in 2002 and MERS in 2012, were more lethal than SARS-CoV-2 (that causes COVID-19), but much less transmissible. So they never became pandemics, though virologists and epidemiologists were very watchful of that possibility. Our disbanding of our monitoring stations and pulling our epidemiologists out of prior coronavirus endemic areas in 2018 allowed SARS-CoV-2 to sneak up on us. That we had little emphasis on our testing capability allowed it to spread unabated until it was widely disseminated.
So this gets us back to the first point. The approved vaccines we have in the U.S. work. They reduce the risk of getting infected with COVID, and even if one gets infected, the severity of the illness is not usually severe enough to require hospitalization and certainly hugely reduces the risk of death. Thus, the observation that patients now being hospitalized with COVID are overwhelmingly those who have not been fully vaccinated.
As long as there are those who choose not to get vaccinated, the breeding environment for mutations will exist. We will not likely reach herd immunity given the numbers of our fellow citizens who choose not to get vaccinated. As the apocryphal saying goes, if you’re not part of the solution, you’re part of the problem. So the rest of us may have to live with this virus and hope that booster vaccines will be able to control future emerging variants of concern.
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