Coronavirus Cases may be 10x higher than official count says CDC

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NC coronavirus update June 25: North Carolina's mask mandate goes ...

The real number of U.S. coronavirus cases could be as high as 23 million — 10 times the 2.3 million currently confirmed cases — the Centers for Disease Control and Prevention told reporters yesterday, Axios’ Marisa Fernandez reports.

Between the lines: The new estimate is based on antibody testing, which indicates whether someone has previously been infected by the virus regardless of whether they had symptoms.

  • “This virus causes so much asymptomatic infection. The traditional approach of looking for symptomatic illness and diagnosing it obviously underestimates the total amount of infections,” CDC director Robert Redfield said.

The agency also expanded its warnings of which demographic groups are at risk, which now include younger people who are obese and who have underlying health problems.

  • The shift reflects what states and hospitals have been seeing since the pandemic began, which is that young people can get seriously ill from COVID-19.

The new guidance also categorizes medical conditions that can affect the severity of illness:

  • Conditions that increase risk: Chronic kidney disease; chronic obstructive pulmonary disease; obesity; weakened immune system from solid organ transplant; serious heart conditions, such as heart failure, coronary artery disease or cardiomyopathies; sickle cell disease; Type 2 diabetes.
  • Conditions that may increase risk: Chronic lung diseases, including moderate to severe asthma and cystic fibrosis; high blood pressure; a weakened immune system; neurologic conditions, such as dementia or history of stroke; liver disease; pregnancy.

 

 

 

 

Blocking the deadly cytokine storm is a vital weapon for treating COVID-19

https://theconversation.com/blocking-the-deadly-cytokine-storm-is-a-vital-weapon-for-treating-covid-19-137690?utm_medium=email&utm_campaign=Latest%20from%20The%20Conversation%20for%20May%2022%202020%20-%201630015658&utm_content=Latest%20from%20The%20Conversation%20for%20May%2022%202020%20-%201630015658+Version+A+CID_f23e0e73a678178a59d0287ef452fe33&utm_source=campaign_monitor_us&utm_term=Blocking%20the%20deadly%20cytokine%20storm%20is%20a%20vital%20weapon%20for%20treating%20COVID-19

Blocking the deadly cytokine storm is a vital weapon for treating ...

The killer is not the virus but the immune response.

The current pandemic is unique not just because it is caused by a new virus that puts everyone at risk, but also because the range of innate immune responses is diverse and unpredictable. In some it is strong enough to kill. In others it is relatively mild.

My research relates to innate immunity. Innate immunity is a person’s inborn defense against pathogens that instruct the body’s adaptive immune system to produce antibodies against viruses. Those antibody responses can be later used for developing vaccination approaches. Working in the lab of Nobel laureate Bruce Beutler, I co-authored the paper that explained how the cells that make up the body’s innate immune system recognize pathogens, and how overreacting to them in general could be detrimental to the host. This is especially true in the COVID-19 patients who are overreacting to the virus.

Cell death – a chess game of sacrifice

I study inflammatory response and cell death, which are two principal components of the innate response. White blood cells called macrophages use a set of sensors to recognize the pathogen and produce proteins called cytokines, which trigger inflammation and recruit other cells of the innate immune system for help. In addition, macrophages instruct the adaptive immune system to learn about the pathogen and ultimately produce antibodies.

To survive within the host, successful pathogens silence the inflammatory response. They do this by blocking the ability of macrophages to release cytokines and alert the rest of the immune system. To counteract the virus’s silencing, infected cells commit suicide, or cell death. Although detrimental at the cellular level, cell death is beneficial at the level of the organism because it stops proliferation of the pathogen.

For example, the pathogen that caused the bubonic plague, which killed half of the human population in Europe between 1347 and 1351, was able to disable, or silence, people’s white blood cells and proliferate in them, ultimately causing the death of the individual. However, in rodents the infection played out differently. Just the infected macrophages of rodents died, thus limiting proliferation of the pathogen in the rodents’ bodies which enabled them to survive.

The “silent” response to plague is strikingly different from the violent response to SARS-CoV-2, the virus that causes COVID-19. This suggests that keeping the right balance of innate response is crucial for the survival of COVID-19 patients.

Vintage engraving of a dead cart collecting the bodies of plague victims during the last Great Plague of London, which extended from 1665 to 1666. duncan1890/ Getty Images

Path to a cytokine storm

Here’s how an overreaction from the immune system can endanger a person fighting off an infection.

Some of the proteins that trigger inflammation, named chemokines, alert other immune cells – like neutrophils, which are professional microbe eaters – to convene at the site of infections where they can arrive first and digest the pathogen.

Others cytokines – such as interleukin 1b, interleukin 6 and tumor necrosis factor – guide neutrophils from the blood vessels to the infected tissue. These cytokines can increase heartbeat, elevate body temperature, trigger blood clots that trap the pathogen and stimulate the neurons in the brain to modulate body temperature, fever, weight loss and other physiological responses that have evolved to kill the virus.

When the production of these same cytokines is uncontrolled, immunologists describe the situation as a “cytokine storm.” During a cytokine storm, the blood vessels widen further (vasolidation), leading to low blood pressure and widespread blood vessel injury. The storm triggers a flood of white blood cells to enter the lungs, which in turn summon more immune cells that target and kill virus-infected cells. The result of this battle is a stew of fluid and dead cells, and subsequent organ failure.

The cytokine storm is a centerpiece of the COVID-19 pathology with devastating consequences for the host.

When the cells fail to terminate the inflammatory response, production of the cytokines make macrophages hyperactive. The hyperactivated macrophages destroy the stem cells in the bone marrow, which leads to anemia. Heightened interleukin 1b results in fever and organ failure. The excessive tumor necrosis factor causes massive death of the cells lining the blood vessels, which become clotted. At some point, the storm becomes unstoppable and irreversible.

Drugs that break the cytokine storm

One strategy behind the treatments for COVID is, in part, based in part on breaking the vicious cycle of the “cytokine storm.” This can be done by using antibodies to block the primary mediators of the storm, like IL6, or its receptor, which is present on all cells of the body.

Inhibition of tumor necrosis factor can be achieved with FDA-approved antibody drugs like Remicade or Humira or with a soluble receptor such as Enbrel (originally developed by Bruce Beutler) which binds to tumor necrosis factor and prevents it from triggering inflammation. The global market for tumor necrosis factor inhibitors is US$22 billion.

Drugs that block various cytokines are now in clinical trials to test whether they are effective for stopping the deadly spiral in COVID-19.

 

 

 

 

Vaccine experts say Moderna didn’t produce data critical to assessing Covid-19 vaccine

Vaccine experts say Moderna didn’t produce data critical to assessing Covid-19 vaccine

Moderna taps $1.34B stock offering to bankroll its promising COVID ...

Heavy hearts soared Monday with news that Moderna’s Covid-19 vaccine candidate — the frontrunner in the American market — seemed to be generating an immune response in Phase 1 trial subjects. The company’s stock valuation also surged, hitting $29 billion, an astonishing feat for a company that currently sells zero products.

But was there good reason for so much enthusiasm? Several vaccine experts asked by STAT concluded that, based on the information made available by the Cambridge, Mass.-based company, there’s really no way to know how impressive — or not — the vaccine may be.

While Moderna blitzed the media, it revealed very little information — and most of what it did disclose were words, not data. That’s important: If you ask scientists to read a journal article, they will scour data tables, not corporate statements. With science, numbers speak much louder than words.

Even the figures the company did release don’t mean much on their own, because critical information — effectively the key to interpreting them — was withheld.

Experts suggest we ought to take the early readout with a big grain of salt. Here are a few reasons why.

The silence of the NIAID

The National Institute for Allergy and Infectious Diseases has partnered with Moderna on this vaccine. Scientists at NIAID made the vaccine’s construct, or prototype, and the agency is running the Phase 1 trial. This week’s Moderna readout came from the earliest of data from the NIAID-led Phase 1.

NIAID doesn’t hide its light under a bushel. The institute generally trumpets its findings, often offering director Anthony Fauci — who, fair enough, is pretty busy these days — or other senior personnel for interviews.

But NIAID did not put out a press release Monday and declined to provide comment on Moderna’s announcement.

The n = 8 thing

The company’s statement led with the fact that all 45 subjects (in this analysis) who received doses of 25 micrograms (two doses each), 100 micrograms (two doses each), or a 250 micrograms (one dose) developed binding antibodies.

Later, the statement indicated that eight volunteers — four each from the 25-microgram and 100-microgram arms — developed neutralizing antibodies. Of the two types, these are the ones you’d really want to see.

We don’t know results from the other 37 trial participants. This doesn’t mean that they didn’t develop neutralizing antibodies. Testing for neutralizing antibodies is more time-consuming than other antibody tests and must be done in a biosecurity level 3 laboratory. Moderna disclosed the findings from eight subjects because that’s all it had at that point. Still, it’s a reason for caution.

Separately, while the Phase 1 trial included healthy volunteers ages 18 to 55 years, the exact ages of these eight people are unknown. If, by chance, they mostly clustered around the younger end of the age spectrum, you might expect a better response to the vaccine than if they were mostly from the senior end of it. And given who is at highest risk from the SARS-CoV-2 coronavirus, protecting older adults is what Covid-19 vaccines need to do.

There’s no way to know how durable the response will be

The report of neutralizing antibodies in subjects who were vaccinated comes from blood drawn two weeks after they received their second dose of vaccine.

Two weeks.

“That’s very early. We don’t know if those antibodies are durable,” said Anna Durbin, a vaccine researcher at Johns Hopkins University.

There’s no real way to contextualize the findings

Moderna stated that the antibody levels seen were on a par with — or greater than, in the case of the 100-microgram dose — those seen in people who have recovered from Covid-19 infection.

But studies have shown antibody levels among people who have recovered from the illness vary enormously; the range that may be influenced by the severity of a person’s disease. John “Jack” Rose, a vaccine researcher from Yale University, pointed STAT to a study from China that showed that, among 175 recovered Covid-19 patients studied, 10 had no detectable neutralizing antibodies. Recovered patients at the other end of the spectrum had really high antibody levels.

So though the company said the antibody levels induced by vaccine were as good as those generated by infection, there’s no real way to know what that comparison means.

STAT asked Moderna for information on the antibody levels it used as a comparator. The response: That will be disclosed in an eventual journal article from NIAID, which is part of the National Institutes of Health.

“The convalescent sera levels are not being detailed in our data readout, but would be expected in a downstream full data exposition with NIH and its academic collaborators,” Colleen Hussey, the company’s senior manager for corporate communications, said in an email.

Durbin was struck by the wording of the company’s statement, pointing to this sentence: “The levels of neutralizing antibodies at day 43 were at or above levels generally seen in convalescent sera.”

“I thought: Generally? What does that mean?” Durbin said. Her question, for the time being, can’t be answered.

Rose said the company should disclose the information. “When a company like Moderna with such incredibly vast resources says they have generated SARS-2 neutralizing antibodies in a human trial, I would really like to see numbers from whatever assay they are using,” he said.

Moderna’s approach to disclosure

The company has not yet brought a vaccine to market, but it has a variety of vaccines for infectious diseases in its pipeline. It doesn’t publish on its work in scientific journals. What is known has been disclosed through press releases. That’s not enough to generate confidence within the scientific community.

“My guess is that their numbers are marginal or they would say more,” Rose said about the company’s SARS-2 vaccine, echoing a suspicion that others have about some of the company’s other work.

“I do think it’s a bit of a concern that they haven’t published the results of any of their ongoing trials that they mention in their press release. They have not published any of that,” Durbin noted.

Still, she characterized herself as “cautiously optimistic” based on what the company has said so far.

“I would like to see the data to make my own interpretation of the data. But I think it is at least encouraging that we’ve seen immune responses with this RNA vaccine that we haven’t seen with previous RNA vaccines for other pathogens. Whether it’s going to be enough, we don’t know,” Durbin said.

Moderna has been more forthcoming with data on at least one of its other vaccine candidates. In a statement issued in January about a Phase 1 trial for its cytomegalovirus (CMV) vaccine, it quantified how far over baseline measures antibody levels rose in vaccines.

 

 

 

Reopening the U.S. Economy

https://www.goldmansachs.com/insights/pages/reopening-the-us-economy.html

Click to access report.pdf

Allison Nathan, senior strategist for Goldman Sachs Research, discusses her latest Top of Mind report where she speaks with leading experts across health and policy to understand how well-positioned the U.S. is to achieve a safe reopening of the economy and how quickly it would translate into economic recovery. 

With COVID-19 mitigation measures leading to an apparent leveling off of case
growth globally at the same time that the economic costs of such measures continue
to mount, several countries around the world have begun to plan for—or have
already started to implement—economic reopening. But absent herd immunity or
a vaccine for the virus, such reopenings increase the risk of disease resurgence.
With this in mind, what a safe reopening might look like, how well-positioned the
US is to achieve one and how quickly reopening would really translate into economic
recovery is Top of Mind. We consult three experts on these questions: University of
Pennsylvania’s Dr. Zeke Emanuel, Duke University’s Dr. Mark McClellan and Harvard
University’s Dr. Barry Bloom. And we share our own take on a potential US recovery path, informed by lessons from
China’s reopening experience so far. Finally, with more complete economic normalization only likely with an effective
testing regime, treatments, or a widely available vaccine for COVID-19-we discuss where we are on all of the above.

 

 

 

What you need to know about the COVID-19 vaccine

https://www.gatesnotes.com/Health/What-you-need-to-know-about-the-COVID-19-vaccine?WT.mc_id=20200430164943_COVID-19-vaccine_BG-FB&WT.tsrc=BGFB&linkId=87665504&fbclid=IwAR0SsBGe1GTcy-fOIXz86kImkScsdCGlRVgmDcPOgXMcaU7kdO39SyNpRSs

What you need to know about the COVID-19 vaccine | Bill Gates

Humankind has never had a more urgent task than creating broad immunity for coronavirus.

One of the questions I get asked the most these days is when the world will be able to go back to the way things were in December before the coronavirus pandemic. My answer is always the same: when we have an almost perfect drug to treat COVID-19, or when almost every person on the planet has been vaccinated against coronavirus.

The former is unlikely to happen anytime soon. We’d need a miracle treatment that was at least 95 percent effective to stop the outbreak. Most of the drug candidates right now are nowhere near that powerful. They could save a lot of lives, but they aren’t enough to get us back to normal.

Which leaves us with a vaccine.

Humankind has never had a more urgent task than creating broad immunity for coronavirus. Realistically, if we’re going to return to normal, we need to develop a safe, effective vaccine. We need to make billions of doses, we need to get them out to every part of the world, and we need all of this happen as quickly as possible.

That sounds daunting, because it is. Our foundation is the biggest funder of vaccines in the world, and this effort dwarfs anything we’ve ever worked on before. It’s going to require a global cooperative effort like the world has never seen. But I know it’ll get done. There’s simply no alternative.

Here’s what you need to know about the race to create a COVID-19 vaccine.

The world is creating this vaccine on a historically fast timeline.

Dr. Anthony Fauci has said he thinks it’ll take around eighteen months to develop a coronavirus vaccine. I agree with him, though it could be as little as 9 months or as long as two years.

Although eighteen months might sound like a long time, this would be the fastest scientists have created a new vaccine. Development usually takes around five years. Once you pick a disease to target, you have to create the vaccine and test it on animals. Then you begin testing for safety and efficacy in humans.

Safety and efficacy are the two most important goals for every vaccineSafety is exactly what it sounds like: is the vaccine safe to give to people? Some minor side effects (like a mild fever or injection site pain) can be acceptable, but you don’t want to inoculate people with something that makes them sick.

Efficacy measures how well the vaccine protects you from getting sick. Although you’d ideally want a vaccine to have 100 percent efficacy, many don’t. For example, this year’s flu vaccine is around 45 percent effective.

To test for safety and efficacy, every vaccine goes through three phases of trials:

  • Phase one is the safety trial. A small group of healthy volunteers gets the vaccine candidate. You try out different dosages to create the strongest immune response at the lowest effective dose without serious side effects.
  • Once you’ve settled on a formula, you move onto phase two, which tells you how well the vaccine works in the people who are intended to get it. This time, hundreds of people get the vaccine. This cohort should include people of different ages and health statuses.
  • Then, in phase three, you give it to thousands of people. This is usually the longest phase, because it occurs in what’s called “natural disease conditions.” You introduce it to a large group of people who are likely already at the risk of infection by the target pathogen, and then wait and see if the vaccine reduces how many people get sick.

After the vaccine passes all three trial phases, you start building the factories to manufacture it, and it gets submitted to the WHO and various government agencies for approval.

This process works well for most vaccines, but the normal development timeline isn’t good enough right now. Every day we can cut from this process will make a huge difference to the world in terms of saving lives and reducing trillions of dollars in economic damage.

So, to speed up the process, vaccine developers are compressing the timeline. This graphic shows how:

In the traditional process, the steps are sequential to address key questions and unknowns. This can help mitigate financial risk, since creating a new vaccine is expensive. Many candidates fail, which is why companies wait to invest in the next step until they know the previous step was successful.

For COVID-19, financing development is not an issue. Governments and other organizations (including our foundation and an amazing alliance called the Coalition for Epidemic Preparedness Innovations) have made it clear they will support whatever it takes to find a vaccine. So, scientists are able to save time by doing several of the development steps at once. For example, the private sector, governments, and our foundation are going to start identifying facilities to manufacture different potential vaccines. If some of those facilities end up going unused, that’s okay. It’s a small price to pay for getting ahead on production.

Fortunately, compressing the trial timeline isn’t the only way to take a process that usually takes five years and get it done in 18 months. Another way we’re going to do that is by testing lots of different approaches at the same time.

There are dozens of candidates in the pipeline.

As of April 9, there are 115 different COVID-19 vaccine candidates in the development pipeline. I think that eight to ten of those look particularly promising. (Our foundation is going to keep an eye on all the others to see if we missed any that have some positive characteristics, though.)

The most promising candidates take a variety of approaches to protecting the body against COVID-19. To understand what exactly that means, it’s helpful to remember how the human immune system works.

When a disease pathogen gets into your system, your immune system responds by producing antibodies. These antibodies attach themselves to substances called antigens on the surface of the microbe, which sends a signal to your body to attack. Your immune system keeps a record of every microbe it has ever defeated, so that it can quickly recognize and destroy invaders before they make you ill.

Vaccines circumvent this whole process by teaching your body how to defeat a pathogen without ever getting sick. The two most common types—and the ones you’re probably most familiar with—are inactivated and live vaccines. Inactivated vaccines contain pathogens that have been killed. Live vaccines, on the other hand, are made of living pathogens that have been weakened (or “attenuated”). They’re highly effective but more prone to side effects than their inactivated counterparts.

Inactivated and live vaccines are what we consider “traditional” approaches. There are a number of COVID-19 vaccine candidates of both types, and for good reason: they’re well-established. We know how to test and manufacture them.

The downside is that they’re time-consuming to make. There’s a ton of material in each dose of a vaccine. Most of that material is biological, which means you have to grow it. That takes time, unfortunately.

That’s why I’m particularly excited by two new approaches that some of the candidates are taking: RNA and DNA vaccines. If one of these new approaches pans out, we’ll likely be able to get vaccines out to the whole world much faster. (For the sake of simplicity, I’m only going to explain RNA vaccines. DNA vaccines are similar, just with a different type of genetic material and method of administration.)

Our foundation—both through our own funding and through CEPI—has been supporting the development of an RNA vaccine platform for nearly a decade. We were planning to use it to make vaccines for diseases that affect the poor like malaria, but now it’s looking like one of the most promising options for COVID. The first candidate to start human trials was an RNA vaccine created by a company called Moderna.

Here’s how an RNA vaccine works: rather than injecting a pathogen’s antigen into your body, you instead give the body the genetic code needed to produce that antigen itself. When the antigens appear on the outside of your cells, your immune system attacks them—and learns how to defeat future intruders in the process. You essentially turn your body into its own vaccine manufacturing unit.

Because RNA vaccines let your body do most of the work, they don’t require much material. That makes them much faster to manufacture. There’s a catch, though: we don’t know for sure yet if RNA is a viable platform for vaccines. Since COVID would be the first RNA vaccine out of the gate, we have to prove both that the platform itself works and that it creates immunity. It’s a bit like building your computer system and your first piece of software at the same time.

Even if an RNA vaccine continues to show promise, we still must continue pursuing the other options. We don’t know yet what the COVID-19 vaccine will look like. Until we do, we have to go full steam ahead on as many approaches as possible.

It might not be a perfect vaccine yet—and that’s okay.

The smallpox vaccine is the only vaccine that’s wiped an entire disease off the face of the earth, but it’s also pretty brutal to receive. It left a scar on the arm of anyone who got it. One out of every three people had side effects bad enough to keep them home from school or work. A small—but not insignificant—number developed more serious reactions.

The smallpox vaccine was far from perfect, but it got the job done. The COVID-19 vaccine might be similar.

If we were designing the perfect vaccine, we’d want it to be completely safe and 100 percent effective. It should be a single dose that gives you lifelong protection, and it should be easy to store and transport. I hope the COVID-19 vaccine has all of those qualities, but given the timeline we’re on, it may not.

The two priorities, as I mentioned earlier, are safety and efficacy. Since we might not have time to do multi-year studies, we will have to conduct robust phase 1 safety trials and make sure we have good real-world evidence that the vaccine is completely safe to use.

We have a bit more wiggle room with efficacy. I suspect a vaccine that is at least 70 percent effective will be enough to stop the outbreak. A 60 percent effective vaccine is useable, but we might still see some localized outbreaks. Anything under 60 percent is unlikely to create enough herd immunity to stop the virus.

The big challenge will be making sure the vaccine works well in older people. The older you are, the less effective vaccines are. Your immune system—like the rest of your body—ages and is slower to recognize and attack invaders. That’s a big issue for a COVID-19 vaccine, since older people are the most vulnerable. We need to make sure they’re protected.

The shingles vaccine—which is also targeted to older people—combats this by amping up the strength of the vaccine. It’s possible we do something similar for COVID, although it might come with more side effects. Health authorities could also ask people over a certain age to get an additional dose.

Beyond safety and efficacy, there are a couple other factors to consider:

  • How many doses will it be? A vaccine you only get once is easier and quicker to deliver. But we may need a multi-dose vaccine to get enough efficacy.
  • How long does it last? Ideally, the vaccine will give you long-lasting protection. But we might end up with one that only stops you from getting sick for a couple months (like the seasonal flu vaccine, which protects you for about six months). If that happens, the short-term vaccine might be used while we work on a more durable one.
  • How do you store it? Many common vaccines are kept at 4 degrees C. That’s around the temperature of your average refrigerator, so storage and transportation is easy. But RNA vaccines need to be stored at much colder temperature—as low as -80 degrees C—which will make reaching certain parts of the world more difficult.

My hope is that the vaccine we have 18 months from now is as close to “perfect” as possible. Even if it isn’t, we will continue working to improve it. After that happens, I suspect the COVID-19 vaccine will become part of the routine newborn immunization schedule.

Once we have a vaccine, though, we still have huge problems to solve. That’s because…

We need to manufacture and distribute at least 7 billion doses of the vaccine.

In order to stop the pandemic, we need to make the vaccine available to almost every person on the planet. We’ve never delivered something to every corner of the world before. And, as I mentioned earlier, vaccines are particularly difficult to make and store.

There’s a lot we can’t figure out about manufacturing and distributing the vaccine until we know what exactly we’re working with. For example, will we be able to use existing vaccine factories to make the COVID-19 vaccine?

What we can do now is build different kinds of vaccine factories to prepare. Each vaccine type requires a different kind of factory. We need to be ready with facilities that can make each type, so that we can start manufacturing the final vaccine (or vaccines) as soon as we can. This will cost billions of dollars. Governments need to quickly find a mechanism for making the funding for this available. Our foundation is currently working with CEPI, the WHO, and governments to figure out the financing.

Part of those discussions center on who will get the vaccine when. The reality is that not everyone will be able to get the vaccine at the same time. It’ll take months—or even years—to create 7 billion doses (or possibly 14 billion, if it’s a multi-dose vaccine), and we should start distributing them as soon as the first batch is ready to go.

Most people agree that health workers should get the vaccine first. But who gets it next? Older people? Teachers? Workers in essential jobs?

I think that low-income countries should be some of the first to receive it, because people will be at a much higher risk of dying in those places. COVID-19 will spread much quicker in poor countries because measures like physical distancing are harder to enact. More people have poor underlying health that makes them more vulnerable to complications, and weak health systems will make it harder for them to receive the care they need. Getting the vaccine out in low-income countries could save millions of lives. The good news is we already have an organization with expertise about how to do this in Gavi, the Vaccine Alliance.

With most vaccines, manufacturers sign a deal with the country where their factories are located, so that country gets first crack at the vaccines. It’s unclear if that’s what will happen here. I hope we find a way to get it out on an equitable basis to the whole world. The WHO and national health authorities will need to develop a distribution plan once we have a better understanding of what we’re working with.

Eventually, though, we’re going to scale this thing up so that the vaccine is available to everyone. And then, we’ll be able to get back to normal—and to hopefully make decisions that prevent us from being in this situation ever again.

It might be a bit hard to see right now, but there is a light at the end of the tunnel. We’re doing the right things to get a vaccine as quickly as possible. In the meantime, I urge you to continue following the guidelines set by your local authorities. Our ability to get through this outbreak will depend on everyone doing their part to keep each other safe.

 

 

 

We Work on the Front Lines of COVID-19. Here’s What Hospitals Should Do

https://www.medpagetoday.com/infectiousdisease/covid19/86185?xid=fb_o&trw=no&fbclid=IwAR3iM5LMZj3BxWisk3puZ2T3bOCeBaDS_xCRoTrnVaZYfj4-DZPmUfr01cw

We Work on the Front Lines of COVID-19. Here's What Hospitals ...

A game plan from ground zero.

It’s only a matter of time before all of us are directly affected by COVID-19. Proper preparation is the only way to ensure high-quality patient care and staff well-being in this challenging time. Having collectively spent time caring for patients at two different tertiary care facilities in New York on the medical floors and intensive care units, common themes are emerging that represent opportunities for hospitals in other parts of the country to start taking action before COVID-19 patients start filling up beds en masse.

Staffing

It takes a LOT of people to care for a COVID-19 onslaught; mapping out different staffing scenarios in the event you have 40 or 400 COVID patients is imperative. Staffing needs for COVID patients are higher than normal because of the patients’ complex medical needs — many require ICU level nursing and respiratory therapists — and because both clinical and non-clinical staff will inevitably become sick and need to be taken out of work. Staff should be screened for symptoms and high-risk contacts; those who are symptomatic should be proactively encouraged to stay home instead of showing up to work not feeling well and putting other care team members and patients at risk. This requires back-up staffing plans to fill in when your people become sick. Shutting down non-urgent and elective departments provides staffing redundancy to pull from when needed. All employees should be given advance notice about staffing plans so that potential role changes are clear.

Testing

Robust testing processes for both patients and your healthcare workforce are critical for success. Hospitals should be taking this time to obtain in-house rapid testing kits to avoid unnecessary patient isolation and conserve personal protective equipment (PPE) while waiting for test results.

Healthcare workers are understandably scared about contracting COVID-19 themselves and giving it to their family members. We recommend all staff members be tested for active infection so that those who are infected can be proactively quarantined.

Forward-thinking institutions should be prioritizing antibody testing for healthcare workers. While this testing is still in its infancy, it is quite likely that those with strong antibodies to COVID-19 possess some degree of immunity. Therefore, if you can identify which doctors, nurses, respiratory therapists, physical therapists, and janitorial staff have already developed an immune response to COVID-19, these staff members can take priority staffing infected units with the goal of reducing the number of new infections in healthcare workers and limiting exposure to those who have yet to contract the virus.

Communication

Each institution’s COVID-19 protocols and policies change rapidly as we learn more about the virus. How you communicate these ever-changing procedures with staff is critical. Most hospitals rely on daily email updates that are text-heavy; however, overwhelmed inboxes and less time with devices while wearing PPE limits the success of email as a sole communication channel.

Communication through graphics takes on new importance — signage noting changes in hospital geography, large pictures of donning and doffing instructions, phone numbers to call with equipment shortages, and clear instructions to staff about testing protocols, isolation, and removing patients from isolation need to be conveniently placed where staff can access information in real time without consulting their electronic devices. High-yield locations for just-in-time visual communication include outside patient rooms, nursing stations, break rooms, and elevators, so that the target information reaches its busy, hard-working audience successfully and repeatedly, minimizing confusion and augmenting clarity.

Limiting the Need to Enter the Room

Given ongoing PPE shortages, particularly around single-use gowns and N95 masks, minimizing the number of instances that staff, particularly nurses, need to enter the room is critical. This requires an adjustment from normal patient care. We recommend extension tubing to bring IV poles and medications outside the room. Tablets such as iPads can permit video calls with patients to check on non-urgent items. Centralized monitoring of oxygen saturations for all admitted patients can minimize the frequency of supplemental oxygen adjustment.

Similarly, given the increased risk of COVID-19 in diabetic patients, continuous blood glucose monitoring can minimize the need for frequent manual fingerstick measurements for patients receiving supplemental insulin.

Discharge Planning

Discharging patients to home or rehabilitation facilities presents novel challenges. A home discharge requires education, equipment, and follow-up. Education on home monitoring of vitals signs like oxygen saturation and blood pressure with instructions on critical values that should prompt patients to return to the hospital can expedite discharge and open hospital beds for other sick patients. Both patients and family members must also be educated on quarantine procedures to limit household transmission.

Many patients will have temporary oxygen requirements and we have seen home oxygen shortages in our areas. Coordinating a strategy with your outpatient clinicians, home oxygen suppliers, and insurance companies can facilitate getting patients home sooner on home oxygen and freeing up beds for sicker patients. Further, many patients are eager to go home earlier since hospital visitation limitations mean they’re sitting in bed alone away from family and the more a hospital can do to safely discharge patients home with appropriate supplies and follow-up will be beneficial to both patients and the hospital.

Hospitals must also be prepared to integrate these patients into their existing telehealth infrastructure, which has become the mainstay of ambulatory medicine in lieu of traditional office visits. For many patients, this will be a new way of accessing care. Prior to discharge, hospital staff should ensure patients have downloaded the necessary apps with login information and feel comfortable they will be able to follow up with their physician using technology following discharge.

There is a huge opportunity for hospitals that have not been caring for large numbers of COVID-19 patients to prepare ahead of time in a manner that optimizes patient care and minimizes risks to staff. Those of us on the early front lines have learned many of these lessons the hard way. An ounce of prevention is worth a pound of cure — we encourage all healthcare systems to take action before the storm comes.

 

 

 

 

“Immunity passports” in the context of COVID-19

https://www.who.int/news-room/commentaries/detail/immunity-passports-in-the-context-of-covid-19

Charu Kaushic (@CKaushic) | Twitter

Scientific Brief

WHO has published guidance on adjusting public health and social measures for the next phase of the COVID-19 response.1 Some governments have suggested that the detection of antibodies to the SARS-CoV-2, the virus that causes COVID-19, could serve as the basis for an “immunity passport” or “risk-free certificate” that would enable individuals to travel or to return to work assuming that they are protected against re-infection. There is currently no evidence that people who have recovered from COVID-19 and have antibodies are protected from a second infection.

 

The measurement of antibodies specific to COVID-19

The development of immunity to a pathogen through natural infection is a multi-step process that typically takes place over 1-2 weeks. The body responds to a viral infection immediately with a non-specific innate response in which macrophages, neutrophils, and dendritic cells slow the progress of virus and may even prevent it from causing symptoms. This non-specific response is followed by an adaptive response where the body makes antibodies that specifically bind to the virus. These antibodies are proteins called immunoglobulins. The body also makes T-cells that recognize and eliminate other cells infected with the virus. This is called cellular immunity. This combined adaptive response may clear the virus from the body, and if the response is strong enough, may prevent progression to severe illness or re-infection by the same virus. This process is often measured by the presence of antibodies in blood.

WHO continues to review the evidence on antibody responses to SARS-CoV-2 infection.2-17 Most of these studies show that people who have recovered from infection have antibodies to the virus. However, some of these people have very low levels of neutralizing antibodies in their blood,4 suggesting that cellular immunity may also be critical for recovery. As of 24 April 2020, no study has evaluated whether the presence of antibodies to SARS-CoV-2 confers immunity to subsequent infection by this virus in humans.

Laboratory tests that detect antibodies to SARS-CoV-2 in people, including rapid immunodiagnostic tests, need further validation to determine their accuracy and reliability. Inaccurate immunodiagnostic tests may falsely categorize people in two ways. The first is that they may falsely label people who have been infected as negative, and the second is that people who have not been infected are falsely labelled as positive. Both errors have serious consequences and will affect control efforts. These tests also need to accurately distinguish between past infections from SARS-CoV-2 and those caused by the known set of six human coronaviruses. Four of these viruses cause the common cold and circulate widely. The remaining two are the viruses that cause Middle East Respiratory Syndrome and Severe Acute Respiratory Syndrome. People infected by any one of these viruses may produce antibodies that cross-react with antibodies produced in response to infection with SARS-CoV-2.

Many countries are now testing for SARS-CoV-2 antibodies at the population level or in specific groups, such as health workers, close contacts of known cases, or within households.21 WHO supports these studies, as they are critical for understanding the extent of – and risk factors associated with – infection.  These studies will provide data on the percentage of people with detectable COVID-19 antibodies, but most are not designed to determine whether those people are immune to secondary infections.

 

Other considerations

At this point in the pandemic, there is not enough evidence about the effectiveness of antibody-mediated immunity to guarantee the accuracy of an “immunity passport” or “risk-free certificate.” People who assume that they are immune to a second infection because they have received a positive test result may ignore public health advice. The use of such certificates may therefore increase the risks of continued transmission. As new evidence becomes available, WHO will update this scientific brief.