Get a Good Night's Sleep Before Your COVID Vaccine

Get a Good Night’s Sleep Before Your COVID Vaccine

  • January 20, 2021

By Robert Preidt


HealthDay Reporter

WEDNESDAY, Jan. 20, 2021 (HealthDay News) — Want to get the most out of your COVID-19 vaccine? Make sure you get some good rest before you get your shot, sleep experts say.

That’s because adequate sleep is an important factor in a strong immune system.

“As COVID-19 vaccines are being distributed, it is of utmost importance that patients continue to prioritize their sleep to maintain optimal health,” American Academy of Sleep Medicine (AASM) president Dr. Kannan Ramar said in an academy news release. “Getting sufficient, high-quality sleep on a regular basis strengthens your body’s immune system and optimizes your response to a vaccine.”

Several studies have found an association between sleep and vaccination response. For example, a 2020 study in the International Journal of Behavioral Medicine found that flu vaccines appear to be more effective in people who get a sufficient amount of sleep during the two nights prior to receiving the shot. Other studies have reported similar findings about patients’ response to vaccines for hepatitis A and hepatitis B.

Dr. Khurshid Khurshid is director of the UMMHC/UMMS Center for Neuromodulation at the University of Massachusetts Medical School, in Westborough, Mass. He said, “The role of sleep in boosting innate and acquired immune response is significant. All people, particularly health workers, should be aware of the immunity-boosting effects of sleep. Studies have shown that normal sleep after vaccination strengthens the immune response against an invading antigen, and this immunity-boosting effect of sleep is clinically significant.”

So, Khurshid added in the news release, “A good night’s sleep before and after vaccination could be very advantageous.”

Most adults should sleep at least seven hours a night, but the COVID-19 pandemic has harmed many Americans’ sleep, a recent AASM survey found.

One-third of respondents said their sleep quality has been affected, 30% have had changes in their ability to fall asleep, and 29% reported an impact on their nightly amount of sleep.

The AASM offered tips for getting a good night’s sleep:

  • Establish a bedtime and morning routine. Use the bedroom only for sleeping, not watching TV or reading. Keep your bedroom quiet, dark and a bit cool.
  • Restrict blue light exposure before bed by turning off your TV and other electronic devices 30 minutes to an hour before bedtime. Silence notifications and charge your devices away from your bed so you’re not tempted to look at social media or news alerts.
  • Limit alcohol, caffeine and large meals before bedtime. If you’re hungry after dinner, limit yourself to small, sugar-free and easily digestible snacks to avoid disrupting sleep.


Continued




More information

The U.S. Centers for Disease Control and Prevention has more on COVID-19 vaccines.


SOURCE: American Academy of Sleep Medicine, news release



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COVID-19 vaccines may become annual shots, UTMB researchers say

COVID-19 vaccines may become annual shots, UTMB researchers say

  • January 19, 2021

GALVESTON — Even after much of the general population gets COVID-19 vaccines, they will likely need to get annual doses to protect against future mutations of the virus, according to researchers at the University of Texas Medical Branch at Galveston.

Scott Weaver, director of the medical branch’s infectious disease research programs, said viruses like COVID-19 will eventually find ways to mutate in order to continue to infect people, even those who have antibodies from vaccines or previous infections.

“We may very well need to do the same thing for influenza vaccines — produce a new one every year or two based on the updated sequences of the rapidly circulating coronavirus strains,” Weaver said during a COVID-19 forum hosted by UTMB Tuesday.

Fortunately, Pfizer and Moderna’s mRNA vaccines, currently authorized for emergency use in the United States, are designed to be adaptable. Weaver said the genetic sequencing of those viruses can “very easily” be swapped with whichever new COVID-19 strain is circulating in a given year.

“In a matter of a couple of months we could generate a new vaccine that’s perfectly designed for the currently circulating strains,” he said.

The UTMB forum was held around the one-year anniversary of the first COVID-19 case on U.S. soil, in Washington state. The medical branch hosted a forum last March, at the beginning of the global pandemic, when information on the virus was still being gathered and much less was known about its long- and short-term effects.

UTMB is one of the institutions on the front lines of COVID-19 research. At the outset of the viral outbreak, medical branch researchers developed a reverse genetic system to manipulate the virus genome. The Galveston National Laboratory at UTMB, a high-security biocontainment lab, was one of three labs in the country to get the coronavirus isolate in February after the Centers for Disease Control worked on the first virus sample in Washington state and cultured it in Atlanta.

That same reverse genetic system continues to yield useful information about the virus. Earlier this month, a study conducted by medical branch researchers found that Pfizer’s COVID-19 vaccine is effective against the mutated strains of the virus known as the United Kingdom and South Africa variants.

The forum also gave UTMB’s experts a chance to answer basic questions about the vaccination process and possible side effects — and even attempt to debunk theories about COVID-19’s origins.

Megan Berman, a professor of internal medicine with the Sealy Institue of Vaccine Sciences at UTMB, said that one of the main reasons young and healthy people should still get vaccinated is because of the uncertainty over whether authorized vaccines protect people against asymptomatic spread of infection.

“This is something that’s going to be researched, but 30 percent of cases are spread by people who do not know they have the infection, so one of the only ways we can stop this infection is by stopping people from getting the virus,” Berman said.

Richard Rupp, assistant director of the Sealy Center for Vaccine Development, said those who have been previously infected by COVID-19 and recovered should still get vaccinated. It is not yet known how long antibodies from the virus are effective against re-infection, he said, and a vaccine would boost the immune system.

Weaver is also optimistic that vaccines being developed by the medical branch might eventually offer stronger protection against infection than the currently authorized mRNA vaccines from Pfizer and Moderna.

UTMB researchers are currently working on live attenuated vaccines for COVID-19, which use a weakened form of the virus that causes infection to immunize people — similar to the measles, mumps, and rubella (MMR) vaccines that children get.

“(Live attenuated vaccines) confer protection for decades, if not longer,” Weaver said. “But those are going to take much longer to develop because showing safety of a live, replicating virus is much tougher than showing that in a messenger RNA vaccine.”

He added that most people should be eligible to receive the vaccine “hopefully by April and May” if the supply of vaccines from the federal government improves.

nick.powell@chron.com

COVID-19 cross-protection? When vaccines provide 'bonus' protection against other diseases

COVID-19 cross-protection? When vaccines provide ‘bonus’ protection against other diseases

  • January 19, 2021

Those of us who avoided COVID-19 over the past year may be somewhat surprised to learn there’s a good chance we’ve already been infected by at least one coronavirus.

They’re thought to be behind up to a third of all common colds. And intriguingly, evidence emerged last year that suggested people who were previously exposed to a common cold coronavirus might have some protection against COVID-19.

So could this cross-protection go the other way? Might the COVID-19 vaccines being rolled out now also cause a dip in seasonal coronaviruses?

While it’s too early to tell, it’s possible. But perhaps not in the way you’d think.

How colds may boost COVID-19 immunity

First, it’s worth looking at how vaccines generate an immune response, and how they compare to real infections.

Vaccines use parts of viruses or bacteria to train what’s called our adaptive immune system.

This part of our immune system protects us against specific microbes. It primarily involves molecules, called antibodies, that neutralise an invading pathogen.

In the case of COVID-19 vaccines, antibodies are made against the virus’s spike protein, which the virus uses to worm its way into our cells.

Your body needs quite a lot of energy to manufacture antibodies, so — ideally — vaccines also establish a few pathogen-specific immune cells called memory T cells and B cells that hang around long after the initial burst of antibodies has waned.

If a pathogen shows up again, T and B cells spring into action, once again churning out antibodies and eliminating infected cells.

When it comes to contracting an actual coronavirus infection, your body produces an immune response to many parts of the virus — not just its spike proteins.

For instance, they might also produce antibodies against other proteins embedded in the coronavirus’s fatty protective layer.

This means that if another coronavirus — perhaps SARS-CoV-2 — shares these proteins, you might have some level of immunity against it as well.

Might COVID vaccines protect against other coronaviruses?

If they do, it’s unlikely that antibodies generated by jabs will play a role, says Kirsty Short, a virologist at the University of Queensland.

A non-COVID coronavirus would need spike proteins to be incredibly similar to those on SARS-CoV-2 for antibodies to recognise and destroy them.

Antibodies latch onto viruses like a lock and key. If the virus protein key is the wrong size or shape for the antibody lock, nothing happens.

But there is a chance that T cell immunity might step up against other coronaviruses. That’s because for them, the shape of a viral protein isn’t quite as important. They recognise smaller bits of viral proteins in the form of short chains of amino acids, or linear peptides.

“Some of those peptides are shared between seasonal coronaviruses and SARS-CoV-2,” Dr Short says.

And while measuring antibody levels from a blood test is relatively straightforward, it’s not as easy to find out what T cells get up to after a COVID-19 jab.

“In terms of T cell responses, they become a little bit more complex,” Dr Short says.

“The type of peptides that my T cells present to the immune system are going to be different to the type of peptides that your T cells will present.

“That just relates to individual genetic differences.”

Shoring up our first line of defence

There is another way vaccines can boost our immune response against other diseases.

The adaptive immune system is just one part of our immune system. We also have our innate immune system.

It’s our first line of immune defence and responds faster than the adaptive immune system, but it doesn’t target specific pathogens. It goes for all of them.

So if you scrape your knee, your innate immune system quickly produces molecules and recruits and activates immune cells to the area to destroy any bacteria or viruses in the wound.

And for a long time, researchers thought immune system memory, involving B and T cells, was solely part of the adaptive immune system.

But in recent years, scientists have found our innate immune system also has an element of memory.

This is called “trained immunity“, and some vaccines trigger this memory response, Dr Short says.

“Mostly, it’s live vaccines that seem to do it, like the MMR vaccine and live polio vaccine.”

It’s a concept being explored by Nigel Curtis, paediatric infectious diseases physician and scientist at the Murdoch Children’s Research Institute.

He and his team are running an international clinical trial to determine if the tuberculosis vaccine — called Bacillus Calmette-Guérin or BCG — can help protect against severe COVID-19 in healthcare workers.

The BCG vaccine contains live but weakened bacteria that stimulate the immune system, but without causing disease.

A hand in a blue glove holding a small brown vial
The BCG vaccine was developed from a bacterium called Mycobacterium bovis, which is similar to the bug that causes tuberculosis, Mycobacterium tuberculosis.(ABC News)

While it helps prevent tuberculosis, it also protects against a wide range of other diseases.

And it’s only in the past decade that immunologists have unpicked some of the mechanisms behind it.

Very simply, the BCG vaccine induces metabolic changes in some of the cells involved in the innate immune system, and this affects how they express certain genes.

Overall, it means your innate immune response better deals with any subsequent infections, Professor Curtis says.

“The idea is that you have BCG, and you induce these changes, then when you get infected with SARS-CoV-2, your response to that virus or any virus — because it’s completely agnostic to pathogen — is stronger than it would be in someone who hadn’t previously had BCG.”

Because it’s a general enhancement, it’s not technically cross-protection, and the BCG vaccine should not considered a replacement for COVID-19 vaccines, he adds.

Instead, it’s something that may stop you from becoming severely ill, should you be infected.

The goal of the work is to pinpoint the specific compounds that induce trained immunity.

“What we want to do is find out exactly what those key components are and, once we do that, we can make something that’s perhaps better than BCG — something you’d give to everybody to induce a better immune response early or even later on in life,” Professor Curtis says.

Cross-protection and HPV

One vaccine that granted some cross-protection was the human papillomavirus or HPV jab.

Of the more-than-200 HPV strains, around 40 are sexually transmitted. Two of those strains, 16 and 18, cause more than 70 per cent of cervical cancers worldwide.

Australia kicked off its HPV vaccination program in 2007 with the Gardasil vaccine, which vaccinated against types 16 and 18, as well as 6 and 11 — strains that don’t cause cancer, but are responsible for around 90 per cent of genital warts.

Suzanne Garland, a clinical microbiologist, sexual health physician and director of the Women’s Centre for Infectious Diseases in Melbourne, led a team that assessed HPV prevalence in Australian women eight years after the rollout started.

As well as finding Gardasil prevented HPV 16 and 18 infection, they also found vaccinated women were far less likely to be infected by a further three cancer-causing HPV strains when compared to unvaccinated counterparts.

Those additional strains were genetically similar to those targeted by the vaccine. Types 31 and 33 were much like 16, while 45 was close to 18.

Professor Garland calls this cross-protection a “bonus”, but why it happened in some women and not others isn’t clear.

The latest generation HPV vaccine, Gardasil 9, covers nine high-risk strains — including 16, 18, 31, 33 and 45 — which are responsible for 93 per cent of cervical cancers.

It was only introduced to the National Immunisation Program in 2018, “so it’s important that women who were vaccinated as schoolgirls have regular cervical screenings, because … you’re still at risk of infection and disease for the types not covered by the vaccine”, Professor Garland says.

Get COVID-19 Vaccine As Soon As You’re Allowed, Experts Urge

Get COVID-19 Vaccine As Soon As You’re Allowed, Experts Urge

  • January 16, 2021

COVID-19’s record surges along with the discovery of more contagious variants of the coronavirus make getting as many people vaccinated as soon as possible critical for ending the pandemic.

“Every time the virus multiplies in a body, there is a chance for mutation,” said Stuart Cohen, chief of the Division of Infectious Diseases and director of hospital epidemiology and infection control at UC Davis Health. “If it doesn’t have people to go into, there will be no mutations.”

Cohen spoke Thursday (Jan. 14) on a UC Davis LIVE program about COVID-19 vaccines. His hope is that enough people will get vaccinated and that we will reach a level of herd immunity relatively soon — possibly within the coming months or by the end of the year — so the coronavirus won’t be able to keep mutating.

“If enough people get vaccinated, the virus stops circulating,” Cohen said. “It’s cutoff and doesn’t have people to go into, so no mutations develop.”

If it does continue to mutate, Cohen worries the virus might eventually create a variant that can evade the vaccine.

“If we slowly, slowly roll out the vaccine, that’s the perfect way to generate mutants,” he said, because vaccine-resistant variants will have a survival advantage and could multiply. “If we get people vaccinated quickly, then we have a fighting chance to stop it.”

Vaccines effective and safe

Cohen and Stephen McSorley, a professor in the School of Veterinary Medicine and director of the Center for Immunology and Infectious Diseases at UC Davis, both said that everything they know about the Pfizer-BioNTech and Moderna vaccines shows both are effective and safe.

Clinical trials showed both vaccines are about 95 percent effective, and though some people have a day or two of reactions, the vaccines are safe. But both men said they worry about some people’s hesitancy to get vaccinated, or worse, about anti-vaccination activists spreading misinformation.

“I’m old enough, I had classmates with polio,” Cohen said. “The herd immunity we have now from polio or measles or other diseases is from vaccinations, and it’s what allows people who don’t believe in vaccines to get away with it.”

McSorley said the COVID-19 vaccines have a slightly different design, but work the way all vaccines work.

“They try to fool your immune system into thinking you’ve had this infection before,” he said. “Your body has the capacity to respond to any infection. If an alien race came from outer space with a pathogen, you actually have the ability to respond to that.”

But often our immune systems need to be taught how to do that. That’s what the COVID-19 vaccines do. They teach our bodies to make more of the cells that recognize the infection, and teach them how to find it and how to combat it, McSorley said.

The COVID-19 vaccines use a system that started to be developed during the 2003 SARS outbreak. It injects us with messenger RNA, or mRNA, which is natural in our bodies. The mRNA teaches our cells to build the spike protein on the coronavirus. “Your immune system responds to that, and now it’s ready to respond to the coronavirus,” McSorley said.

Q&A highlights

  • The vaccines require two doses, and both scientists urged people to get both shots on the prescribed schedule that came out of the clinical trials — which is 21 days apart for the Pfizer vaccines and 28 days for Moderna’s. “The second dose will always boost the immune response,” McSorley said.
  • Are the 21-day and 28-day intervals totally fixed? Can you wait longer? “I don’t know the answer,” Cohen said. “But I do know the best way to take it is the way it’s been studied. Freelancing is not a good idea.”
  • Some immunity starts 10 to 14 days after the first dose, but full immunity appears seven to 14 days after the second, according to the studies. “If you get just one shot,” Cohen said, “we don’t know how long the immune response will last or if one dose will even do anybody any good.”
  • Pfizer’s vaccine was shown effective in lab studies against the newest variants. Although Moderna’s vaccine has not been studied, it is likely equally effective. “The vaccines are very similar,” Cohen said. “There is no reason to think Moderna’s would be any different with the variant.”
  • It’s unclear if the vaccines actually prevent us from getting infected with COVID-19 or if a vaccinated person can spread the virus. That’s why masking and social distancing are still crucial. “Many of us believe the vaccine prevents infection. That’s how other vaccines work. We just don’t have data for that yet,” Cohen said. “We do know it keeps people from getting sick.” McSorley added: “The studies were designed to keep people out of the hospital. They weren’t studying whether you can spread infection. That’s coming.”

Other advice

Among other advice from McSorley and Cohen: It’s OK to get vaccinated if you have a cold (though if you’re feeling lousy, you might want to wait). People who’ve had COVID-19 still should get vaccinated, but it’s best to wait until 90 after all symptoms are gone. Don’t worry about which vaccine you get. They are too much alike. 

“People ask whether I would choose to take the Pfizer or the Moderna vaccine,” Cohen said. “I say, ‘I’ll take the one they have. Whichever comes first.’ The only thing to know is, get vaccinated.”

Follow Dateline UC Davis on Twitter.

Covid vaccines and immunity: does past infection help? | Coronavirus

  • January 14, 2021

The first phase of the NHS vaccination programme aims to protect millions of the UK’s most vulnerable people against coronavirus. Meanwhile, research from Public Health England suggests that a previous Covid infection might protect as much as a vaccine, at least for five months. So what difference does it make to have such immunity?

Can I still catch the virus if I have had the vaccine or been previously infected?

You can still catch the virus if you’ve had the vaccine or a previous coronavirus infection. Clinical trials for the Covid vaccines approved so far show that they can substantially reduce the risk of becoming ill with the virus, but some people may still get infected and even be able to spread the disease. The same is true for a previous infection.

A Public Health England study of healthcare workers found that Covid infection led to about 83% protection against reinfection for at least five months. That still means almost two out of every 10 people could become reinfected within five months of their first skirmish with the disease. Some who became reinfected had high enough viral loads to pass the disease on. More encouragingly, less than a third of those who were reinfected had symptoms the second time around, compared with 78% the first time.

Deborah Dunn-Walters, professor of immunology at the University of Surrey and chair of the taskforce on immunology and Covid-19, run by the British Society for Immunology, said: “Your immune system could work at 100% and protect you from disease and the virus, or it could work less well and protect you from the disease, but not stop you getting and transmitting the virus on. Or it could work even less well, where you still get ill, but not as bad as you would have done.”

Should I still have the vaccine if I’ve had Covid?

Yes. The immune system’s response to coronavirus infection varies from person to person. Age, genetic makeup and the amount of virus you were exposed to all play a role. The variability makes it hard to predict how well a particular person will be protected after infection. A benefit of the vaccines is that they have gone through trials to assess how well standard doses prevent disease, so there is far more certainty over the protection that they confer and the impact they will have on public health.

Another point is that many people who believe they caught Covid last year have no proof of it. Is it safe to be vaccinated after having Covid? “There is no harm in giving the vaccine to a person who has had the disease – it will act as a booster,” said Dunn-Walters.

Should people who have had Covid be last to get the vaccine?

No. This would complicate an already highly complex vaccination programme. Healthcare workers are at high risk of infection and many have already caught the disease. The vaccines will boost their natural immunity, making them less likely to become reinfected. Others at the front of the queue are older people. Their immune systems tend to be weaker, so even if they have recovered from Covid-19 they remain vulnerable and the vaccines will bolster their resistance to reinfection.

The uncertainties about who is well protected or not after an infection makes it hard to justify sending any group to the back of the queue, regardless of age and health. “For the time being, everyone should be offered the vaccine, whether or not they have previously had the disease,” said Eleanor Riley, professor of immunology at Edinburgh University.

Can I see my grandchildren after having the vaccine?

As vaccines are administered, public health authorities will get a clearer picture of how well they protect older people. Riley recommends waiting for about a month after the second dose to ensure that the immune response is as strong and long-lasting as possible.

There is still some uncertainty about how well the vaccines will protect against some of the new variants of coronavirus, but scientists hope to have a better idea by the time the lockdown is lifted. “We very much hope, and expect, that it will be safe for people to see, and to hug and kiss, their grandchildren in the very near future. But we need to proceed cautiously,” Riley said. Dunn-Walters warned that grandparents could potentially still spread the virus after being vaccinated.

When do we get back to a more normal life?

Riley says she believes the route back to normality is to ensure, first, that everyone at risk of developing severe Covid-19 is vaccinated, and then that those at risk of developing symptomatic disease and long Covid are vaccinated.

“It is very likely that we can achieve this for the UK population by the summer for the first group – those over 50 years of age, and those under 50 with underlying health conditions – and by the end of the year for the second group, all other adults over the age of 18.”

The first sign that the strategy is working will be a fall in hospital admissions and deaths, and if the vaccines prevent transmission as well as illness, then a fall in new infections as the vaccines are given to less vulnerable adults.

“This should allow life in the UK to return to something close to normal. However, if new virus variants emerge that are able to escape the vaccine, this could delay things. This will be evident if we start to see people becoming sick with variant viruses despite having been vaccinated,” Riley said.

Healthy sleep and immune response to COVID-19 vaccination

Healthy sleep and immune response to COVID-19 vaccination

  • January 13, 2021

Healthy sleep is integral to a strong immune system, and as COVID-19 vaccines are distributed, it’s important that people continue to get sufficient sleep for optimal immune response.

Sleep loss is associated with changes in several immune processes. Poor sleep may weaken your defenses against a virus, and it may affect how your body responds to a vaccine, increasing your risk for illness. For this reason, sleep deprivation in the age of a global pandemic is especially risky.

“As COVID-19 vaccines are being distributed, it is of utmost importance that patients continue to prioritize their sleep to maintain optimal health,” said American Academy of Sleep Medicine President Dr. Kannan Ramar. “Getting sufficient, high-quality sleep on a regular basis strengthens your body’s immune system and optimizes your response to a vaccine.”

There is extensive evidence of the link between sleep and immunity, and several studies have found an association between sleep duration and vaccination response. A 2020 study in the International Journal of Behavioral Medicine found that the flu vaccine appears to be more effective in people who get a sufficient duration of sleep for the two nights prior to receiving the shot. Other studies have made similar findings evaluating patients’ response to vaccines for hepatitis A and hepatitis B, concluding that shorter sleep duration before and after vaccination is associated with lower antibody response and a decreased likelihood of disease protection.

The role of sleep in boosting innate and acquired immune response is significant. All people, particularly health workers, should be aware of the immunity-boosting effects of sleep. Studies have shown that normal sleep after vaccination strengthens the immune response against an invading antigen and this immunity boosting effect of sleep is clinically significant,” said Dr. Khurshid A. Khurshid, director of the UMMHC/UMMS Center for Neuromodulation at the University of Massachusetts Medical School. “A good night’s sleep before and after vaccination could be very advantageous.”

When we sleep, our body recovers from the day, working to repair muscles, organs and cells. Hormones are regulated that support our metabolism, immune response and other key physical functions. Our brain sorts and stores new information and prepares us mentally for the next day by regulating our mood.

For many though, the pandemic has negatively impacted sleep. One third (33%) of respondents to an AASM survey have experienced an impact to sleep quality, 30% have seen change in their ability to fall asleep, and 29% noted an impact to nightly amount of sleep. While it’s easy for stress and scheduling conflicts to interrupt nightly sleep, the AASM recommends that most adults should be sleeping at least 7 hours each night.

Follow these tips to get a better night’s sleep:

  • Establish a bedtime and morning routine – Consider developing a nightly routine that evokes calm and relaxation, which may include reading, journaling or meditating. Even for those working remotely, allow ample time to wake, reflect and prepare for the day ahead.
  • Ensure the bedroom is a space for sleep – Limit noise and distractions by making your bedroom quiet, dark and a little bit cool – and only use the bed for sleeping, not watching TV or reading.
  • Set boundaries for blue light exposure – Consider setting a technology curfew by turning off your TV and other electronic devices 30 minutes to an hour before bedtime. Silence your notifications and charge your devices away from your bed so you are not tempted to look at social media or news alerts.
  • Limit alcohol, caffeine and large meals before bedtime – Avoid consuming caffeine after lunch and avoid alcohol near bedtime, as both can disrupt sleep. If hungry after dinner, keep snacks small, sugar-free and easily digestible to avoid disrupting sleep.
  • Sleep on it: try to get good sleep on the night after vaccination.

For PDFs of the AASM’s 2019 and 2020 Sleep Prioritization Survey results, please visit https://aasm.org/about/newsroom/.

For more information on the importance of healthy sleep, visit SleepEducation.org.

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About the 2020 Survey

The July 2020 Sleep Prioritization Survey involved 2,007 adult participants. The sample consisted of 1,005 parents with children between the ages of five and 18 years old. The margin of error is +/- 2 percentage points with a confidence interval of 95 percent. Atomik Research, an independent market research agency, conducted the survey.

About the American Academy of Sleep Medicine

Established in 1975, the American Academy of Sleep Medicine (AASM) is advancing sleep care and enhancing sleep health to improve lives. The AASM has a combined membership of 11,000 accredited member sleep centers and individual members, including physicians, scientists and other health care professionals (aasm.org).

How the immune system can be a vaccine’s enemy

How the immune system can be a vaccine’s enemy

  • January 6, 2021
Barbie Furtado is a 32-year-old Brazilian college teacher who has not stepped out of her house since March 18. A Washington Post report says, “The only thing that will bring her out of her isolation is a vaccine.”

Furtado might sound like an extreme case of Covid anxiety but about 1% of Brazilians had not left home for over eight months before the country’s second wave started in November, the report says.

Anyone who has religiously sheltered at home since the first lockdown would be tired and very impatient for a vaccine by now. But while December brought lots of good news about vaccine approvals, January has forced a reality check.

The US is way behind its vaccination schedule. Russia is nowhere close to its vaccine production target. Deliveries of the Pfizer vaccine have been delayed in Europe. The reasons range from a shortage of vials and manufacturing equipment to the difficulty of maintaining the right storage temperature.



In some cases, however, the body’s unexpected response to the virus components used in a vaccine has derailed plans.

HIV Shock

Amid all the success stories, one vaccine sank unsung early last month. Called UQ-CSL-v451, it had been developed by the University of Queensland in Australia and a private biotech company called CSL. It looked like a solid performer and the Australian government had placed an order for 51 million shots – enough to immunise the country’s entire 25-million population.

But a hitch arose. Some of the volunteers who took the vaccine tested HIV-positive. They did not have an HIV infection but had made HIV antibodies, thanks to an HIV protein used in the vaccine.

The “gp41” protein from the HIV virus was used only to stabilise the vaccine. It served as a clamp to hold the coronavirus’s spike protein in a folded shape that would help the immune system recognise it easily. Instead, the immune system picked on the HIV protein, started making antibodies against it, and aborted Australia’s indigenous vaccine plan.

Familiarity Breeds Contempt

Earlier, vaccines contained the whole virus that caused a disease. But for Covid, many vaccines have been made using unrelated viruses that contain only a part of the coronavirus. The Oxford vaccine that has been approved in the UK and India, and Russia’s Sputnik V vaccine, are of this type.

Such vaccines, called “viral vector” vaccines, have their own peculiar problem. If the immune system is familiar with the unrelated virus used as a courier, it will attack it. This is called “anti-vector immunity” and it can make a vaccine less effective.

https://timesofindia.indiatimes.com/#
To avoid this problem, scientists at Oxford made a chimpanzee virus the base of their vaccine. Which works fine for the first ‘priming’ dose, but when it’s time for the second or ‘booster’ dose, the immune system knows the courier virus and might attack it.


This can “reduce the efficacy of booster shots,” says The Guardian. A Reuters report says it could “neutralise the second booster shot.” This might explain why the Oxford vaccine is only 70% effective.

Strange Bedfellows

Russia’s Sputnik vaccine got around anti-vector immunity by using two different virus bases for its two doses. It claims over 90% efficacy, and now AstraZeneca, which makes the Oxford vaccine, and the Gamaleya institute, which makes Sputnik, are running an experiment that combines one dose of the Oxford vaccine with one dose of Sputnik for better results.

Gamaleya director Alexander Gintsburg says the combination will provide immunity from Covid for two years because “memory cells will form much better as a result of using such a hybrid two-component vaccine.”

Oxford + Pfizer?

Some scientists have expressed alarm over the UK’s plan to allow a combination of Oxford and Pfizer vaccines, but others say this can boost immunity as the Pfizer vaccine is better at producing antibodies and the Oxford vaccine makes more T cells.

Hetero Pair

Scientists have a term for mixing and matching vaccines: ‘heterologous prime-boost’. But even this has its limitations. The Sputnik vaccine uses two types of human common cold viruses called Ad26 and Ad5. In Africa, 80% of the population has been exposed to the Ad5 virus, so the second or booster dose might be less effective. Replacing it with the Oxford vaccine could help.

https://timesofindia.indiatimes.com/#

But for now, Sputnik’s biggest challenge is to make enough of the Ad5 virus for its booster dose. This virus grows slower than Ad26, so its sluggish yield has upset the Sputnik vaccination programme, The Wall Street Journal says. Russia had planned to make 30 million doses last year but finished with around 2 million.

Even then, Russia had a surplus of Ad26 shots, Reuters says, so it shipped 300,000 first doses to Argentina to kickstart their vaccination programme. Without the booster dose, though, immunity from Sputnik is said to last only 3-4 months.

Graphics: www.sputnikvaccine.com


Source: Media reports

How COVID-19 vaccines work

How COVID-19 vaccines work

  • December 23, 2020
Dec 23, 2020 (Nanowerk News) With two, FDA-approved vaccines now rolling out across the US—and at least one other promising candidate potentially available as soon as early 2021—the beginning of the end of the COVID-19 pandemic may one day soon be in sight. Developing safe and effective vaccines for a novel disease in less than a year was an unprecedented scientific achievement, made possible by use of a novel vaccine technology: mRNA. We asked two Columbia Engineering experts to break down the science behind it. Prof. Sam Sia is a biomedical engineer who specializes in tools for rapid diagnosis. Current commercial COVID-19 testing is either very fast or highly accurate; Sia’s group is devising a new, NIH-funded COVID-19 test that is both, by combining state-of-the art molecular diagnostics with a streamlined platform that returns results in under ten minutes. Prof. Jingyue Ju is a chemical engineer who recently identified a whole library of molecules with COVID-19 therapeutic potential. The coronavirus that causes COVID-19 uses a type of protein called “polymerase” to replicate its genome inside human cells; Ju’s molecules terminate the polymerase reaction, stopping the coronavirus’ growth so our immune systems can eradicate it. The two COVID-19 vaccines currently with FDA approval—developed by drug companies Pfizer and Moderna—use something called “messenger RNA” to provoke an immune response. How do these vaccines work? Sam Sia: Messenger RNA, or mRNA, vaccines are a more recent method for creating vaccines. They work by delivering instructions to a patient’s cells for making a viral protein. These instructions include only a very limited set of protein-coding instructions compared to the whole viral genome; in this way, they simulate a viral infection without risk of a real infection. They can potentially provoke a robust immune response because by activating two different arms of the immune system, one dealing with antibodies and another dealing with immune cells. These immune cells include “memory” T-cells, which may lead to longer immunity. Traditional antiviral vaccines focus on provoking mostly an antibody response. Why do you need to take two doses? SS: The two-dose schedule is what has been tested in the clinical trials to be effective. It is based on previous vaccines where the first injection primes the immune system for an initial response, while a second boost dose could result in a fast and strong response due to immune memory. However, it is still possible that other dosing schedules also provide an effective response—but they have not yet been rigorously tested.

Why must these types of vaccines be kept so cold?

SS: There are two reasons, having to do with the two main components to the vaccine. First, RNA molecules are not very stable, and refrigeration prevents them from quickly degrading. This RNA component is similar for the Pfizer and Moderna vaccines. The difference between the two vaccines is the lipid nanoparticle that contains the RNA. This lipid component is different for the two vaccines, thus the two vaccines require different temperatures for storage. There is also currently one, single-dose vaccine in Stage 3 clinical trials that are expected to wrap up by the end of January. That vaccine takes a different approach, using an Adenovirus. How do Adenovirus vaccines work? Jingyue Ju: Adenovirus vaccines for COVID-19 are DNA-based. This type of vaccine uses non-replicating Adenovirus—strains of common viruses engineered to be harmless to humans—to serve as a vector to transport DNA codes for the coronavirus’ spike protein to the host cell nucleus. Again, the key is, what these vaccines deliver is just that sliver of the viral DNA, so that the vaccine itself doesn’t make you sick. Inside the nucleus, our cells produce mRNA based on the DNA codes. The mRNA is then used as a template to produce the coronavirus protein, which in turn will activate the immune system in order to protect the host from infection by the real virus.

From the recipients’ perspective, is there any difference between the two approaches?

JJ: The final viral proteins generated from mRNA and Adenovirus-based DNA vaccines are essentially the same. Once doses are optimized, there’s virtually no difference from the recipients’ perspective. One special consideration with Adenovirus-based vaccines is to select the right strain to start with. Developers have to ensure that these vaccines are also effective in individuals who have already developed immunity for Adenoviruses that frequently infect human populations, which is why vectors derived from a rarer Adenovirus subtype or chimpanzee Adenoviruses are sometimes used to produce DNA vaccines.

Logistically, do the two different types of vaccines need to be handled differently?

JJ: If they’re proven to work, DNA vaccines using Adenovirus as a vector are more stable than mRNA vaccines and are easier to produce.
How do the new COVID-19 vaccines work?

How do the new COVID-19 vaccines work?

  • December 22, 2020

What seemed impossible an eyeblink ago is now a reality.

Amazingly, not one but two COVID-19 vaccines — from Pfizer and Moderna, respectively — are spilling out of the chute within days of each other. The new vaccines work the same way, but they differ somewhat from the conventional ones that have long protected us from measles, yellow fever, smallpox, polio and many other infectious diseases.

They are the first vaccines ever approved for clinical use that use an information-coding molecule called RNA to generate an immune response to a microbial pathogen. This is revolutionary because what the immune system responds to is not the RNA, but something the RNA teaches our cells to make.

To understand the new vaccines’ magic, consider how older vaccines detect, defang and destroy invading bacterial and viral pathogens.

How conventional vaccines work

At the heart of every vaccine is a component called an antigen — typically a chunk of a protein that’s identical to one borne by the targeted pathogen — that can excite the immune system to recognize it, then rally and retaliate against it.

When a vaccine dose is shot into your arm, it draws the attention of front-line immune sentinels called dendritic cells, Stanford Medicine vaccine expert Bali Pulendran, PhD, told me. Widely distributed throughout the body’s tissues (notably under the skin and in or near muscle tissue), dendritic cells sit around waiting for trouble.

As soon as these dendritic cells sense an antigen, suggesting an invading pathogen is present, they slurp it up, chew it into little pieces, display these tidbits on their surfaces like battle trophies and head for the lymph nodes, the barracks of the immune system.

There, they alert an assemblage of diverse immune-cell types, which launch a coordinated attack on anything possessing features identical to those antigenic battle trophies.

How the new RNA-based COVID-19 vaccines are different

So, how are the new vaccines different? Instead of antigen payloads, they carry copies of the recipe for making the antigen, in the form of RNA, a molecule that stores information.

Figuring out what microenvironment best preserves a protein-based vaccine’s antigenicity, then producing it in ultra-pure form for clinical trials, is a slow process. But generating purified RNA molecules that mimic a pathogen’s gene is a snap. It took less than a year for an effective vaccine for SARS-CoV-2, the coronavirus that causes COVID-19, to be developed and gain Food and Drug Administration emergency use approval.

Like its close chemical cousin DNA, RNA is a string of chemicals representing, similarly to letters of the alphabet, the genetic code that all living cells use as instructions for producing their component proteins.

The newly licensed COVID-19 vaccines contain myriad RNA strands all coding for a critical section of the coronavirus’s spike protein. This protein is easy for the immune system to attack because it sits on the virus’s outer surface. It’s also indispensable to the virus, as it’s absolutely required for entry into our cells; So the virus doesn’t have the option of altering its spike protein, via mutation, to escape immune detection.

The vaccine’s RNA strands are hidden inside of nanoscale fat globules, which keeps our immune systems from flipping out and going all medieval on our tissues. (Your immune system isn’t used to seeing RNA floating around outside of cells. When it does, its first hunch is that the out-of-place genetic material belongs to a viral or bacterial pathogen, and it may react aggressively and indiscriminately.)

The primary target for an RNA vaccine, as for traditional vaccines, is dendritic cells, which, Pulendran told me, “love to gobble up nanoscale droplets.” They shuttle the RNA-laden fat globules through their outer membranes into the cytoplasm, a cell’s factory floor. Once inside, the RNA strands make their way to protein-producing power tools called ribosomes and perch on them.

“The ribosomes decipher the strands’ coded instructions and churn out new SARS-CoV-2 spike-protein bits of incomparable purity by the bucketful — it’s like a cellular protein factory,” Pulendran said.

Dendritic cells in the vicinity of the shot take up the antigen-coding RNA and can, as a result, produce tons of antigen on their own. This triggers an effect similar to traditional vaccines, in which dendritic cells displaying their antigenic trophies on their surfaces race to the lymph nodes to tip off the immune cells hanging out there.

Dendritic cells’ newfound ability to brew up the SARS-CoV-2 antigen they’ve produced by themselves may result in bits of chewed-up antigen being displayed all the more abundantly on these cells surfaces. This, Pulendran suggested, could boost the immune response — and could help explain the effectiveness of both RNA-based COVID-19 vaccines.

Some unknowns

Non-immune cells such as those in muscle or nearby fat tissue — which wouldn’t have ingested the antigens contained in traditional vaccines —  can, in principle, take up RNA; but they do so far less efficiently than dendritic cells.

If any non-immune cells in the vicinity were to take up RNA from the COVID-19 vaccine, they, too, would produce the spike protein. And they, too, would chew up a fraction of these newly produced protein pieces into little tidbits and display them on their surfaces for inspection by roving immune cells that survey our tissues for signs of intruders.

This, Pulendran said, could amplify the antigen’s exposure to those patrolling inspectors on the lookout for invaded cells — for instance, in the lung and upper respiratory tract, where SARS-CoV-2 most likes to get a toehold. This would further strengthen the immune response.

Importantly, the genes of cells that ingest vaccine RNA aren’t altered. The RNA delivered by a vaccine needs only to get to the cytoplasm, not to penetrate the cell nucleus — where the genes reside — to produce antigenic material. Even if the vaccine RNA did get into the nucleus, our cells are unable to convert RNA into the DNA our genes are made of.

Nor can the vaccine RNA molecules taken up by our cells replicate themselves — our cells contain no capacity to perform that operation.

While the COVID-19 vaccines have been proven effective in preventing severe disease, their ability to block disease transmission remains unknown. But, Pulendran pointed out, that caveat applies to most vaccines we’ve been routinely using for years.

Another unknown, the durability of immunity the vaccines confer, can only be assessed as the months and years roll by.

The 19th-century poet and philosopher Ralph Waldo Emerson once called the opening volley of the American Revolutionary War “the shot that was heard around the world.”

The revolutionary new RNA vaccines may someday be recalled as the shots that cured around the world.

Image by Markus Mainka

Covid-19 Variant Could Make Herd Immunity More Difficult, Says BioNTech

Covid-19 Variant Could Make Herd Immunity More Difficult, Says BioNTech

  • December 22, 2020

BERLIN—The new coronavirus variant that is spreading across the U.K. could make it more difficult to reach so-called herd immunity, according to the chief executive of

BioNTech SE,

the German company that developed the Covid-19 vaccine with

Pfizer Inc.

British authorities have said the new variant of the coronavirus is more contagious than the existing one—prompting a raft of countries to cut off travel to and from the U.K.

A more contagious version of the virus means a greater number of people than originally expected would need to be vaccinated to halt its spread, said

Ugur Sahin,

CEO of BioNTech. The Pfizer-BioNTech vaccine is now being deployed in the U.S. and U.K. and is expected to roll out in the European Union from next week.

The Covid-19 variant discovered in the U.K. has nine mutations, chief executive and co-founder of BioNTech, Ugur Sahin, said Tuesday.



Photo:

ralph orlowski/Reuters

Herd immunity occurs when a sufficient proportion of a population has been immunized by vaccination or after having been infected, effectively ending the disease’s spread. The threshold at which herd immunity is achieved varies between diseases.

That threshold is related to the speed of the viral spread, known as R. Most experts agree the herd immunity threshold for coronavirus is between 60% and 70% of a population.

Should the new variant—which is believed to have originated in the U.K. but has now spread in small numbers to a handful of other countries—boost the R number of the virus, the threshold for collective immunity will go up and governments will need more vaccines to stop contagion, Dr. Sahin said Tuesday.

“If the virus becomes more efficient in infecting people, we might need even a higher vaccination rate to ensure that normal life can continue without interruption,” he said.

If the new strain becomes prevalent and boosts the R number, countries may face further outbreaks even after 70% of their population has been immunized, Dr. Sahin said. But, in that case, the severity of the spread would be greatly reduced, allowing for a gradual return to normal life, he said.

More on the New Covid-19 Variant

The Pfizer-BioNTech vaccine, which has now been administered to over one million people world-wide, is highly likely to be effective against the new coronavirus variant, Dr. Sahin said. It will take about two weeks to confirm that through testing, he said, adding that the company will publish the resulting data.

“We have scientific confidence that the vaccine might protect, but we will know it only when the experiment is done,” he said.

Pfizer and BioNTech’s vaccine works by injecting genetic material known as messenger RNA, or mRNA, into the body, which then alerts the immune system to a protein used by the virus to cause infection. The variant that was discovered in the U.K. has nine mutations, Dr. Sahin said, but only 1% of the protein targeted by the vaccine has changed—making it unlikely likely the vaccine could become less efficient.

The vaccine has already proven effective against 20 other known mutations that appeared in recent months, he added.

Should a new mutation render the vaccine ineffective, BioNTech can develop another tailored to the new coronavirus variant in six weeks, according to Dr. Sahin. It is, however, unclear whether regulators such as the U.S. Food and Drug Administration would require a new vaccine to undergo fresh trials and a new authorization process.

In Europe, the BioNTech-Pfizer vaccine will as of this week be marketed under the brand name Comirnaty. Dr. Sahin said the name was derived from the words Covid, mRNA, community and immunity.

Write to Bojan Pancevski at bojan.pancevski@wsj.com

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