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).

Antibody Response to Flu Shaped by Pre-Existing Immunity

Antibody Response to Flu Shaped by Pre-Existing Immunity

  • December 14, 2020

Receiving the seasonal flu vaccine each year, in addition to seasonal infections, exposes people to a lifetime of building up immune responses to influenza antigens. Yet, it remains unclear whether infection and vaccination induce distinct influenza-specific immunological memory. A team led by researchers at the University of Chicago compared antibodies produced by individuals after influenza infection or vaccination. The authors found that a person’s antibody response to influenza viruses is dramatically shaped by their pre-existing immunity, and that the quality of this response differs in individuals who are vaccinated or naturally infected. Their results highlight the importance of receiving the annual flu vaccine to induce the most protective immune response.

The study is published in Science Translational Medicine, in an article titled, “Preexisting immunity shapes distinct antibody landscapes after influenza virus infection and vaccination in humans.

The researchers compared antibodies produced by individuals after influenza infection or vaccination. They found that infection-induced antibodies reacted to non-neutralizing epitopes of influenza virus, whereas vaccination-induced antibodies reacted to neutralizing epitopes.

The team found that most of the initial antibodies stimulated after both influenza infections and influenza vaccinations came from old B cells, indicating the immune system’s memory plays a major role in how the body responds early on to a viral infection. These antibodies displayed higher reactivity toward strains of influenza that circulated during an individual’s childhood compared to more recent strains.

“Most interestingly, we found that people who were actively sick with influenza had old antibodies that predominantly targeted parts of the virus that don’t change—but those antibodies specifically targeted non-neutralizing sites,” said Haley Dugan, co-first author of the study and a PhD candidate in immunology. “When we tested these same antibodies in mice, they weren’t able to protect them from being infected with influenza.”

In contrast, the researchers found that influenza vaccinations boost antibodies that tended to target conserved yet neutralizing regions of the virus, which suggests vaccinations can draw upon pre-existing immunity to prompt more protective responses. Vaccinated individuals also generated many antibodies that targeted new and mutated regions on the virus, suggesting these vaccine-induced antibodies are more adaptable.

Immune system memory ensures a rapid and specific response to previously encountered pathogens. Vaccinations work by exposing the immune system to a small amount of virus, which causes B cells to develop a biological memory to the virus. If the body encounters the same virus later, the immune system is alerted to attack and eliminate the virus.

But in order to be protected, the viral proteins of the infecting strain must typically match those of the strain used in the vaccine. The memory B cells are like keys that fit and bind to the locks—the viral proteins. These memory B cells can survive for decades, providing long-lasting protection from future infections. But if the virus mutates and is significantly different, the memory B cells can no longer recognize the viral proteins, potentially leading to infection.

For this reason, the human body is pitted in an evolutionary arms race with the flu. Because influenza viruses rapidly evolve and mutate each season, our immune system has trouble recognizing the viral surface proteins on new influenza strains. As a result, our bodies often rely on old antibodies to fight new influenza strains; this is possible because some parts of the influenza virus that are critical to its structure or function do not change, remaining familiar to our immune system.

Researchers now understand that specific structural and functional parts of the influenza virus that do not change are better for antibodies to target than others. Antibodies that bind to one of these neutralizing sites are able to prevent infection, while antibodies that target non-neutralizing sites often cannot. Scientists believe a person’s age, history of exposure to the influenza virus, and type of exposure—either through infection or vaccination—all shape whether their immune system antibodies target neutralizing or non-neutralizing sites on a virus.

In the study, scientists sought to address a major knowledge gap: Which conserved viral sites are preferentially targeted following natural infection versus vaccination in people, and how does pre-existing immunity play a role in shaping the landscape of neutralizing and non-neutralizing antibodies?

“For people who have caught the flu, their pre-existing immunity may make them susceptible to infection or increase the severity of their influenza symptoms if their antibodies are targeting ‘bad’ or non-neutralizing viral sites,” said co-first author and immunology postdoctoral fellow Jenna Guthmiller, PhD.

By contrast, vaccination largely induces neutralizing and protective antibodies, old and new, highlighting the importance of receiving the seasonal influenza vaccine.

“This study provides a major framework for understanding how pre-existing immunity shapes protective antibody responses to influenza in humans,” said Patrick Wilson, PhD, a professor of immunology and lead author of the study. “We need more studies to determine whether the targeting of specific neutralizing and non-neutralizing viral sites directly impacts a person’s likelihood of becoming ill.”

The researchers are now examining how early exposure to the influenza virus in children shapes their immune response later in life as a follow-up to this work.

5 genes linked to severe coronavirus cases, dangerous immune response

5 genes linked to severe coronavirus cases, dangerous immune response

  • December 12, 2020
  • Five genes seem to be associated with life-threatening cases of COVID-19, a new study found.
  • The finding offers a potential explanation for why some patients get severely sick while others don’t.
  • Two of these genes are linked to the innate immune response, while three are tied to inflammation and lung damage.
  • The study offers a direction for more research into certain potential COVID-19 treatments.
  • Visit Business Insider’s homepage for more stories.

A growing body of research is highlighting a select set of genes that may explain why some people develop more severe COVID-19 cases than others. Certain genes, for instance, instruct the body to make more ACE2 receptors, which the coronavirus uses to invade our cells. Studies show that people whose bodies naturally code for more of these receptors could be at higher risk of severe infection.

On Friday, researchers at the University of Edinburgh announced that they’d identified five genes that may be associated with life-threatening cases of COVID-19. The genes are, perhaps unsurprisingly, associated with a weaker innate immune response and more aggressive inflammation.

The new study compared more than 2,200 coronavirus patients in UK intensive-care units to patients of similar ancestry who hadn’t tested positive for COVID-19.

The critically ill COVID-19 patients were found to have a lower expression of IFNAR2, a gene that helps code for proteins called interferons. These act as an emergency flare to warn the immune system of an intruder. The patients also displayed a variation in a cluster of genes called OAS, which normally helps prevent a virus from replicating.

What’s more, the critically ill patients had higher expressions of the genes TYK2 and CCR2, which can drive inflammation and potentially lead to lung injury. And they displayed a variation in the gene DPP9, which scientists have linked to pulmonary fibrosis (damaged or scarred lung tissue).

A weak immune system is at risk of collapse

Typically, when our immune system senses a foreign invader, it dispatches white blood cells to destroy the threat. But in some patients, that innate immune response isn’t strong enough to vanquish the coronavirus right away. This can trigger aggressive inflammation that damages healthy tissue or leads to organ failure.

Dr. Panagis Galiatsatos, a pulmonary physician at Johns Hopkins Bayview Medical Center, compared that process to an earthquake — generally, it’s the falling buildings that kill someone, not the quake itself.

“Your infection is a rattling of your immune system,” he previously told Business Insider. “If your immune system is just not well structured, it’s just going to collapse.”

That means genetic signals that inhibit the body’s natural defenses or encourage inflammation might set off a chain reaction that ultimately leads to critical respiratory failure.

Other factors, including age and underlying health conditions, play a role in severe COVID-19 cases as well.

Implications for COVID-19 treatments

FILE - In this March 2020 photo provided by Gilead Sciences, a vial of the investigational drug remdesivir is visually inspected at a Gilead manufacturing site in the United States. On Wednesday, April 29, 2020, the company says its experimental antiviral drug has proved effective against the new coronavirus in a major U.S. government study that put it to a strict test. (Gilead Sciences via AP)

A vial of remdesivir is inspected at a Gilead manufacturing site in the US.

Gilead Sciences via AP


In unlocking some of the mysteries surrounding severe COVID-19, the Edinburgh researchers also found clues about how to treat patients.

“Our results immediately highlight which drugs should be at the top of the list for clinical testing,” Kenneth Baillie, an academic consultant in critical-care medicine who co-led the research, told Reuters

Drugs that boost the expression of INFAR2, for instance, might help patients fight the virus before it wreaks havoc in the body.

One potential treatment, a multiple sclerosis drug called Rebif, is attempting a similar approach by giving patients a boost of interferon. Merck, the company behind the drug, hopes the therapy might prevent the coronavirus from replicating. 

The Edinburgh study also suggests that drugs targeting inflammation could play a key role in halting the disease’s progression. In particular, the researchers point to a class of anti-inflammatory drugs called Janus kinase (JAK) inhibitors, which are already used to treat rheumatoid arthritis. 

One such arthritis drug, Eli Lilly’s baricitinib, was recently authorized by the FDA for use in combination with remdesivir.

Among other genes, baricitinib targets TYK2: one of the highly expressed genes found in critically ill patients. In September, Eli Lilly announced that together, baricitinib and remdesivir reduced patients’ average recovery time by one day compared to patients who only received remdesivir.

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Clinical trial explores nutritional support to improve immune response to COVID-19

Clinical trial explores nutritional support to improve immune response to COVID-19

  • December 11, 2020

MIAMI – A clinical trial is underway at sites in Miami and around the country to examine whether nutritional support can benefit patients exposed to or infected with COVID-19.

The outpatient study was designed to asses the effects of restoring and maintaining a healthy digestive system.

Researchers are testing an investigational powdered food product to see if it can improve the balance of microbes in the gut.

“By boosting the balance of the digestive system, you can not only get a boost in the balance, but the theory is that you will get a boost as well in the immune system, and the beauty about this is it might not only help COVID-19 patients, which is the primary focus of our study right now, but you can also get that information and try to use it in other infections overall,” said Dr. Jose Pinero, who is the lead investigator.

Patients can participate at home in one of four locations throughout South Florida by clicking here.

In other health news, while there were initial concerns about the mental health impact of COVID-19 on the elderly, recent data shows older Americans are very resilient.

A group of researchers at institutions around the country looked at early data from several global studies on the relationship between older adults and mental health during the pandemic and found they were less negatively affected than younger adults.

One report from the Centers for Disease Control and Prevention found that older adults were less likely to start or increase substance abuse and less likely to think about suicide.

Copyright 2020 by WPLG Local10.com – All rights reserved.

Children's immune response more effective against COVID-19 -- ScienceDaily

Potential cancer therapy may boost immune response — ScienceDaily

  • December 7, 2020

A new approach to cancer therapy shows potential to transform the commonly used chemotherapy drug gemcitabine into a drug that kills cancer cells in a specialized way, activating immune cells to fight the cancer, according to a study led by Cedars-Sinai Cancer investigators. The findings, made in human and mouse cancer cells and laboratory mice, were published today in the peer-reviewed journal Nature Communications.

The investigators discovered that when they added the Food and Drug Administration-approved anti-inflammatory medication celecoxib (Celebrex) to gemcitabine chemotherapy, it converted gemcitabine from a non-immunogenic drug-unable to activate a patient’s own immune response-to an immunogenic drug, which triggered the immune response in the mice. The combination of drugs delivered a “one-two punch” of killing tumor cells and activating immune cells, said Keith Syson Chan, PhD, a Cedars-Sinai Cancer translational scientist and corresponding author of the study. Kazukuni Hayashi, PhD, is the first author.

“I believe that our study has significant clinical potential, as cancer immunotherapy continues to emerge as an important pillar for treating cancer patients,” Chan said. “This discovery, if confirmed in clinical trials, may potentially increase the percentage of patients who respond to cancer immunotherapy.”

Currently, about 70% to 85% of patients taking immunotherapy drugs fail to respond to them, he added.

Since the 1940s, the main treatment for killing cancer cells has involved chemotherapy drugs, which kill the cells directly. But many of the current drugs fail to induce the most efficient form of cell death, known as “immunogenic” cell death, which activates the release of a protein called a “go” or “danger” signal. The “go” signal prompts immune cells-called dendritic cells-to spur T cells to eradicate tumors. Instead, most current chemotherapies for pancreatic, bladder, breast, ovarian and non-small cell lung cancers not only are non-immunogenic-they suppress the immune system.

In recent years, immunotherapy drugs have been added to chemotherapy regimens, or used alone, to help a patient’s own immune cells attack cancer, but the response rate is low.

Certain chemotherapy drugs such as gemcitabine do kill cancer cells and release the “go” signal for an immune response. Scientists, therefore, have believed that those drugs are immunogenic. That is not entirely the case, though, Chan said.

In a surprise discovery, the study investigators-from Cedars-Sinai, Baylor College of Medicine in Houston, and Taipei Medical University in Taiwan-found that while gemcitabine does release the “go” signal, it also prompts the release of an inhibitory signal, or brake, that stops dendritic cells from activating cancer-killing T cells. If the brake is on, “the T cells don’t go anywhere,” Chan explained. It is necessary, therefore, to find a balance between the “go” and “brake” signals to prompt an effective immune response.

The solution to that balance, the investigators discovered, is the anti-inflammatory drug celecoxib, which removed the brake so that only the “go” signal remained. The dendritic and T cells then were better able to perform their immune responses. Gemcitabine was transformed into an immunogenic drug.

“Rather than focusing on stepping down harder on the gas pedal-releasing proteins that are “go” signals-we removed the impeding brake pedal, allowing the dendritic cells to induce T cells to kill tumors,” Hayashi said.

Chan and Hayashi said they believe that the immune response will perform even better with an immunotherapy drug added to a gemcitabine and celecoxib treatment regimen. A study is underway in Chan’s lab to test that hypothesis. They look forward, they said, to testing the efficacy of the new treatment in randomized, placebo-controlled human trials in collaboration with their Cedars-Sinai clinical colleagues.

“Harnessing the patients’ immune system to attack patients’ tumor cells has become an important tool for physicians treating cancer,” said Dan Theodorescu, MD, PhD, director of the Cedars-Sinai Cancer enterprise. “Unfortunately, our current efforts fail in a significant number of patients. This study unveils at least one potential mechanism explaining these failures, and more importantly, provides a potential solution.”

Research reported in this publication was supported in part by the Department of Defense under award numbers CA181002 and F31 CA247257. The investigators report no conflicts of interest.

New therapy extends breast cancer survival rate, prevents reoccurrence

Potential cancer therapy may boost immune response

  • December 7, 2020

IMAGE

IMAGE: Kazukuni Hayashi, PhD
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Credit: Cedars-Sinai

LOS ANGELES (EMBARGOED UNTIL DEC. 7, 2002 AT 5 A.M. EST) – A new approach to cancer therapy shows potential to transform the commonly used chemotherapy drug gemcitabine into a drug that kills cancer cells in a specialized way, activating immune cells to fight the cancer, according to a study led by Cedars-Sinai Cancer investigators. The findings, made in human and mouse cancer cells and laboratory mice, were published today in the peer-reviewed journal Nature Communications.

The investigators discovered that when they added the Food and Drug Administration-approved anti-inflammatory medication celecoxib (Celebrex) to gemcitabine chemotherapy, it converted gemcitabine from a non-immunogenic drug-unable to activate a patient’s own immune response-to an immunogenic drug, which triggered the immune response in the mice. The combination of drugs delivered a “one-two punch” of killing tumor cells and activating immune cells, said Keith Syson Chan, PhD, a Cedars-Sinai Cancer translational scientist and corresponding author of the study. Kazukuni Hayashi, PhD, is the first author.

“I believe that our study has significant clinical potential, as cancer immunotherapy continues to emerge as an important pillar for treating cancer patients,” Chan said. “This discovery, if confirmed in clinical trials, may potentially increase the percentage of patients who respond to cancer immunotherapy.”

Currently, about 70% to 85% of patients taking immunotherapy drugs fail to respond to them, he added.

Since the 1940s, the main treatment for killing cancer cells has involved chemotherapy drugs, which kill the cells directly. But many of the current drugs fail to induce the most efficient form of cell death, known as “immunogenic” cell death, which activates the release of a protein called a “go” or “danger” signal. The “go” signal prompts immune cells-called dendritic cells-to spur T cells to eradicate tumors. Instead, most current chemotherapies for pancreatic, bladder, breast, ovarian and non-small cell lung cancers not only are non-immunogenic-they suppress the immune system.

In recent years, immunotherapy drugs have been added to chemotherapy regimens, or used alone, to help a patient’s own immune cells attack cancer, but the response rate is low.

Certain chemotherapy drugs such as gemcitabine do kill cancer cells and release the “go” signal for an immune response. Scientists, therefore, have believed that those drugs are immunogenic. That is not entirely the case, though, Chan said.

In a surprise discovery, the study investigators-from Cedars-Sinai, Baylor College of Medicine in Houston, and Taipei Medical University in Taiwan-found that while gemcitabine does release the “go” signal, it also prompts the release of an inhibitory signal, or brake, that stops dendritic cells from activating cancer-killing T cells. If the brake is on, “the T cells don’t go anywhere,” Chan explained. It is necessary, therefore, to find a balance between the “go” and “brake” signals to prompt an effective immune response.

The solution to that balance, the investigators discovered, is the anti-inflammatory drug celecoxib, which removed the brake so that only the “go” signal remained. The dendritic and T cells then were better able to perform their immune responses. Gemcitabine was transformed into an immunogenic drug.

“Rather than focusing on stepping down harder on the gas pedal-releasing proteins that are “go” signals-we removed the impeding brake pedal, allowing the dendritic cells to induce T cells to kill tumors,” Hayashi said.

Chan and Hayashi said they believe that the immune response will perform even better with an immunotherapy drug added to a gemcitabine and celecoxib treatment regimen. A study is underway in Chan’s lab to test that hypothesis. They look forward, they said, to testing the efficacy of the new treatment in randomized, placebo-controlled human trials in collaboration with their Cedars-Sinai clinical colleagues.

“Harnessing the patients’ immune system to attack patients’ tumor cells has become an important tool for physicians treating cancer,” said Dan Theodorescu, MD, PhD, director of the Cedars-Sinai Cancer enterprise. “Unfortunately, our current efforts fail in a significant number of patients. This study unveils at least one potential mechanism explaining these failures, and more importantly, provides a potential solution.”

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Research reported in this publication was supported in part by the Department of Defense under award numbers CA181002 and F31 CA247257. The investigators report no conflicts of interest.

Read more on the Cedars-Sinai Blog: New Approaches to Pancreatic Cancer Care

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

how zinc, selenium and probiotics could boost your immune response

how zinc, selenium and probiotics could boost your immune response

  • December 3, 2020

At the British Nutrition Foundation’s virtual conference last week, leading scientists discussed the critical role of nutrition in the battle against Covid-19. Emerging research on Covid-19 patients, and a wealth of existing studies relating to other viral infections, suggests key nutrients such as selenium, zinc, vitamin D and probiotics may fortify the immune system, limit the severity of coronavirus symptoms and even reduce intensive care admissions and mortality rates. 

Although this nutritional data requires further research, the results so far are intriguing. German research suggests patients who survived Covid-19 had higher levels of selenium – a nutrient found in turkey, sardines, eggs, Brazil nuts, liver and kidney – than those who died of the virus.

A Spanish study found that healthy levels of zinc – a mineral found in meat, poultry, cheese, shellfish and seeds – are linked to higher survival rates. Another paper found that 82.2 per cent of hospitalised coronavirus patients were deficient in vitamin D, which we gain through exposure to the sun. And an Italian study found that probiotics reduced the severity of Covid-19 symptoms and cut mortality rates. 

“Nutrition is very important, not for ‘resistance’ in protecting you from getting Covid-19 but rather for improving your ‘tolerance’ of it,” explains Prof Mike Gleeson, Emeritus Professor of Exercise Biochemistry at Loughborough University and author of Eat, Move, Sleep, Repeat. “Tolerance means a decreased infection burden when you get infected, so you could get less severe symptoms and recover more quickly. That’s the possible role of nutrition. We’re talking about compounds which may optimise immune response or have beneficial anti-inflammatory or antioxidant actions.” 

Nothing you eat is going to stop you contracting Covid-19, warns Prof Gleeson: “This virus is so contagious it is going to get past our immunity barriers.” But a strong immune system will inevitably help you to fight it more effectively. “What we’re relying on is our immune response when we do get infected. And if you’re deficient in micronutrients, it may increase your risk of severe symptoms.” 

The general link between a healthy diet and improved resilience to infections is nothing new, but interest in which nutrients may best support this “tolerogenic” effect is growing. Your body’s immune response to any virus requires a delicate balancing act: if your immune response is too low, your body’s defences will be overwhelmed. But if your immune response is too high, the defensive processes involved can cause excessive tissue damage and drive resources away from other vital functions, weakening your body further. Good nutrition can help to optimise this immune response

“Essentially your immune system gets rid of viruses by seeking out your own cells which have become infected and destroying them,” explains Prof Gleeson. “So there’s a real balance needed in your immune response. You want to be able to tolerate the virus, to some degree, in order to dampen your defence a little bit but still control the infection in order to reduce the risk of acute respiratory distress syndrome (when the lungs cannot provide the vital organs with enough oxygen) which can develop if you get too much inflammation in the lungs.” 

So how might these key nutrients help your body get it right? Research suggests selenium helps to cleverly refine your immune response. “You get less severe inflammation if you have a good selenium status,” says Prof Gleeson. “There’s evidence that you get improved proliferation of your lymphocytes (white blood cells) which help to activate the cell lines that specifically respond to a virus.” 

Zinc, meanwhile, helps to prevent viruses from proliferating. “Viruses have a protective coat which surrounds their genetic material and the first thing they do when they get into your cells is un-coat themselves, release their genetic material and take over your own machinery for enzymes to help generate other viruses within that cell,” explains Gleeson. “But zinc helps to inhibit that viral un-coating, as well as the enzyme which allows that genetic material to be reproduced in the cell, to help prevent a virus from proliferating.” 

Probiotics may also play an important role because your gut is a key part of your immune system. “About 70 per cent of your immune cells are located in and around the gut,” explains Prof Gleeson. But your gut is also a harbouring site for Covid-19.

“The gut is a nice nutrient soup which bacteria and viruses love to feed on. Research suggests probiotics can modify that gut population of bacteria to give it a healthier profile. Probiotics can also modify immune cells in the gut which can then migrate to other areas, including the lungs – and this may be where you get some protection.”

The link between vitamin D and Covid-19 is not yet confirmed but the vitamin plays a key role in general immunity. “We know from studies on the common cold that with low vitamin D you’re more likely to pick up viral infections,” says Gleeson. “Although 10ug is the recommended dose, if you’ve not had sun for months that’s not enough to get you up to the levels you want for optimal immune function, so we suggest at least 1000IU, or 25ug.”  

So Vitamin D supplements may be necessary over winter but Prof Gleeson insists we can get most of the other immunity-optimising nutrients from our everyday diet. As well as the foods listed above, nuts, cod and wholegrains also contain selenium (RDA 75μg for men, 60ug for women); beef, dairy and spinach also provide zinc (RDA 9.5mg for men, 7mg for women); and a healthy mix of fruit and veg will contribute to your healthy gut bacteria, which can be topped up with probiotics. 

But if this nutritional evidence is not compelling enough, it seems that improving your diet may even help you ahead of the imminent roll-out of Covid-19 vaccines. “We know that with vaccines like the one for the influenza virus, selenium and vitamin D are linked to stronger antibody responses to the vaccination,” explains Prof Gleeson. “So it makes sense to boost up, ready for when we all get the chance to have this vaccine.”

 

Cancer vaccine cocktail boosts immune response after surgery, study says

Cancer vaccine cocktail boosts immune response after surgery, study says

  • November 20, 2020

Immunotherapies have transformed cancer care by enlisting the body’s own immune system to fight tumors that have evaded or hijacked normal defenses. But while checkpoint inhibitor drugs and bespoke CAR-T treatments have gained significant ground in recent years, another type of immunotherapy — cancer vaccines — have seen far less success.

New research published this week in Nature Cancer, however, suggests combining a cancer vaccine with adjuvant molecules might boost effectiveness in preventing melanoma recurrence, potentially opening the door to future combinations with other immunotherapies to vanquish cancers. 

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The AstraZeneca Oxford COVID-19 Vaccine Safe and Provokes Immune Response

The AstraZeneca Oxford COVID-19 Vaccine Safe and Provokes Immune Response

  • November 19, 2020

In a phase 2 study with nearly half of the participants being over the age of 70, the AstraZeneca/Oxford COVID-19 vaccine, ChAdOx1 nCoV-19, was found to be safe and invoke an immune response.

The trial conducted has 560 healthy adults and 240 of the participants over 70, provoked a T cell response within 14 days of the first dose of the vaccination, and an antibody response within 28 days of the booster dose of vaccination.

“The robust antibody and T-cell responses seen in older people in our study are encouraging,” co-author Maheshi Ramasamy, MD, University of Oxford, UK, said.

The vaccine induced antibodies 28 days after a single low or standard dose across all age groups. Following the booster dose of the vaccine, antibody levels increased at day 56 of the trial, irrespective of dose or participant age. The same was seen with levels of neutralizing antibodies at day 42, 2 weeks after the booster vaccine dose. By 14 days after the boost dose, 208 of 209 (more than 99%) participants (selected from participants of all ages and doses) had neutralizing antibody responses.

Adverse reactions to the vaccine were mild, with the most common effects being injection-site pain and tenderness, fatigue, headache, feverishness and muscle pain.

The vaccine had similar immunogenicity across all age groups after a boost dose.

“The phase 2 trial finds that the vaccine causes few side effects, and induces immune responses in both parts of the immune system in all age groups and at low and standard dose – provoking a T cell response within 14 days of the first dose of vaccination (ie, a cellular immune response, it could find and attack cells infected with the virus), and an antibody response within 28 days of the booster dose of vaccination (ie, humoral immune response, it could find and attack the virus when it was circulating in the blood or lymphatic system),” the investigators reported.

The investigational vaccine is undergoing phase 3 trials, which is conducting it looking at a broader range of people, including older adults with underlying health conditions.

“The populations at greatest risk of serious COVID-19 disease include people with existing health conditions and older adults. We hope that this means our vaccine will help to protect some of the most vulnerable people in society, but further research will be needed before we can be sure,” Ramasamy concluded.

Oxford Covid Vaccine Trials Indicate It Is Safe, Produces Robust Immune Response Among Older Adults – NBC10 Philadelphia

Oxford Covid Vaccine Trials Indicate It Is Safe, Produces Robust Immune Response Among Older Adults – NBC10 Philadelphia

  • November 19, 2020
  • The study of 560 healthy adults, including 240 over the age of 70-years-old, found the vaccine to be safe and produced a similar immune response among people aged over 56-years-old and those aged between 18 and 55.
  • British pharmaceutical giant AstraZeneca, which is working in collaboration with the University of Oxford, has previously said interim data showed their experimental vaccine had produced an immune response in older and younger adults.
  • The authors of the Oxford study said their results could be encouraging if the immune responses are found to be associated with protection against Covid-19 infection.
  • The phase two trial did not assess vaccine efficacy, however, and phase three trials are ongoing to confirm this.

LONDON — The coronavirus vaccine being developed by the University of Oxford and AstraZeneca is safe and triggers a similar immune response among all adults, according to the preliminary findings of a peer-reviewed phase two trial.

The promising early-stage results were published in The Lancet, one of the world’s top medical journals, on Thursday.

The study of 560 healthy adults, including 240 over the age of 70-years-old, found the vaccine to be safe and produced a similar immune response among people aged over 56-years-old and those aged between 18 and 55.

Vaccines do not tend to work as well among people in older age groups as immune systems gradually deteriorate over time. These trial results indicate this may not be a problem, however.

British pharmaceutical giant AstraZeneca, which is working in collaboration with the University of Oxford, has previously said interim data showed their experimental vaccine had produced an immune response in older and younger adults.

A safe and effective vaccine is seen by many as a game-changer in the battle against the coronavirus pandemic, which has claimed the lives of over 1.3 million people worldwide.

Huge challenges remain before a vaccine can be rolled out. The global battle to secure prospective supplies has raised alarm about equitable access, while questions remain over logistics, distribution, and cost.

The Oxford vaccine candidate was found to cause few side effects and triggered immune responses in both parts of the immune system in all age groups and at low and standard doses.

The preliminary results showed that the vaccine — ChAdOx1 nCoV-19 — prompted what’s known as a “T-cell response” within 14 days of the first dose, and an antibody response within 28 days of the booster dose. Scientists expect T-cell responses to play a role in long-term immunity against the virus.

Dr. Maheshi Ramasamy, a co-author of the study at the University of Oxford, said the antibody and T-cell responses among older adults were “robust” and “encouraging.”

“The populations at greatest risk of serious COVID-19 disease include people with existing health conditions and older adults,” Ramasamy said.

“We hope that this means our vaccine will help to protect some of the most vulnerable people in society, but further research will be needed before we can be sure.”

Study limitations

The authors of the Oxford study said their results could be encouraging if the immune responses are found to be associated with protection against Covid-19 infection. The phase two trial did not assess vaccine efficacy, however, and phase three trials are ongoing to confirm this.

Results are expected later this year depending on the rate of infection within clinical trial communities.

The authors noted some limitations to their study, including that participants in the oldest age group had an average age of 73 to 74 and few underlying health conditions, and almost all participants were White and non-smokers.

People from a range of backgrounds, countries, and ethnicities were said to be included in the phase three trial.

The study comes days after two other vaccine makers announced encouraging results from phase three trials. They said their experimental vaccines were found to be highly effective in protecting against the coronavirus, boosting optimism at a time when health systems in Europe and the U.S. are once again being pushed to breaking point.

Pfizer and BioNTech said on Wednesday a final analysis found their vaccine candidate was 95% effective in preventing Covid-19 and appeared to fend off severe disease. Earlier this week, Moderna had said preliminary phase three trial data showed its vaccine was 94.5% effective.

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