New Delhi: AYUSH Committee, PHDCCI organized a Webinar on “Proven & Effective Unani System as Immunity Booster during COVID-19”. The webinar was graced with the presence of Padma Bhushan Vd. Devendera Triguna, President of AMAM, All India Ayurvedic Congress and Ayurveda Mahasammelan, Prof. Dr. Asim Ali Khan, Director General – CCRUM, Ministry of AYUSH, Govt. of India, Dr. M.A. Qasmi, Joint Advisor (Unani), Ministry of AYUSH, Govt. of India, Mr. Pradeep Multani, Sr. Vice President, PHDCCI, Mr. Arvind Varchaswi, Chair, AYUSH Committee, PHDCCI & Managing Director, Sri Sri Tattva, Mr. Jitender Sodhi, Co- Chair, AYUSH Committee, PHDCCI & Managing Director, AYUSH Herbs Pvt Ltd and today’s session moderator Mr. Vivek Seigell, Assistant Secretary General, PHDCCI.
The other eminent panellist present were Dr. Mohammad Akram, Associate Professor & Head, Deptt. Of Tahaffuziwa Samaji Tibb, Jamia Hamdard, Prof. Ashhar Qadeer, Dept. Of Kulliyat, Ajmal Khan Tibbia College, AMU Aligarh (U.P), Dr. Khursheed A. Ansari, Associate Professor, Dept. of Anatomy, Jamia Hamdard, New Delhi, Dr. Aleemuddin Qaumri, Reader & Head of Dept. of Moalijat, National Institute of Unani Medicine, Bangalore, Dr. Santosh Joshi, Sr. General Manager, R&D, Hamdard Laboratories India, Mr. Sameer Kant Ahuja, Chief Manager (Regulatory) Multani Pharmaceuticals Ltd.
While welcoming the Government dignitaries Mr. Pradeep Multani, Sr. Vice President, PHDCCI in his welcome remarks deliberated about Unani medicine and its increase in usage in India and abroad. The Unani System of Medicine offers treatment of diseases related to all the systems and organs of the human body. The Unani treatments for chronic ailments are highly effective and acceptable.
Mr. Multani emphasized that Immunity is a defense system within the body to protect the host from invading pathogens. The body can neutralize & eliminate the pathogenic micro-organism & their toxic products, thus protecting the individual. The most common problem of all sort of infections is tackled very successfully by the Unani system of medicine approach in strengthening the immune system which in turn eliminates infectious agents and exert least side effect.
Padma Bhushan Vd. Devendera Triguna, President of AMAM, All India Ayurvedic Congress and Ayurveda Mahasammelan thanked Ministry of AYUSH for their efforts for promoting all AYUSH system and said that Unani medicine has played a critical role in developing overall immunity and fighting against the pandemic.
Mr. Arvind Varchaswi, Chair, AYUSH Committee, PHDCCI & Managing Director, Sri Sri Tattva in his remarks gave an industry perspective and the importance of Unani System as Immunity Booster during COVID-19. He also highlighted that Unani System of Medicine offers treatment of diseases related to all the systems and organs of the human body. The treatments for chronic ailments and diseases of skin, liver, musculo-skeletal and reproductive systems, immunological and lifestyle disorders have been found to be highly effective and acceptable.
Prof. Dr. Asim Ali Khan, Director General – CCRUM, Ministry of AYUSH, Govt. of India talked about Unani system has a global presence in India and various other countries. He said that Unani immunomodulators has played a significant role in building overall immunity of an individual.
Prof. Dr. Khan thanked Ministry of AYUSH, Govt. of India for their continuous support in promoting Unani system of medicine. He said, Central Council for Research in Unani Medicine (CCRUM) has done several clinical trials & research studies during COVID-19. The system has established Unani centers with a specialist for treating patients.He has also mentioned about National Institute of Unani Medicine (NIUM) which has been developed as a model for post graduate, teaching, and research in Unani System of Medicine. He further mentioned that all system of AYUSH is working together for promoting AYUSH system in India.
Dr. M.A. Qasmi, Joint Advisor (Unani), Ministry of AYUSH, Govt. of India while lauding the constant efforts of PHD Chamber of Commerce and Industry and assured that we will be working together with the Industry to boost the Unani system.
Dr. Mohammad Akram, Associate Professor & Head, Deptt. Of Tahaffuziwa Samaji Tibb, Jamia Hamdard mentioned that prevention is the only cure in these current times. He further mentioned that COVID-19 will live longer than our expectations and there is no effective treatment in any system of medicines. He also mentioned that people need to focus on immunity-boosting and physical health well-being. Proper ventilation, healthy diet, constant exercise, proper sleep, retention, and elimination of body and less mental illness need to be focus areas for achieving good immunity.
Prof. Ashhar Qadeer, Dept. Of Kulliyat, Ajmal Khan Tibbia College, AMU Aligarh (U.P) talked about the concept of Tabiyat that systematically regulates the body. He mentioned that Covid-19 has its immunity and its power will change according to the immunity of the body. He emphasized that immunity-boosting is the only prevention of COVID-19.
Dr. Khursheed A. Ansari, Associate Professor, Deptt. of Anatomy, JamiaHamdard, New Delhi in his presentation on proven and effective Unani system as immunity booster during covid-19, highlighted that prevention is better than cure. He discussed the self-protection and prevention needed for the spread of the disease like wearing the mask, social distancing, sanitization, and many more. He talked about the general Unani Prophylaxis which included restriction of diet; have nonveg diet; eating citrus foods; have warm sips of water; have afternoon nap; don’t do heavy exercises; no alcohol consumption; steam inhalation; fumigation with sandal, camphor, and pomegranate rind and many more.
Dr. Aleemuddin Qaumri, Reader & Head of Deptt. of Moalijat, National Institute of Unani Medicine, Bangalore in his presentation deliberated about the immune system, types, and process. He further deliberated about the COVID-19 pandemic, its pathogenesis, and factor. He mentioned that immune response determines the host severity of symptoms like severe/moderate/mild. Talking about Unani medicines and immunity he discussed its principles and practices. He mentioned that the regimen has to be taking micro and macronutrients like vitamin C, D and minerals like Cu, Se, Zn, Fe, etc. he also mentioned that vitamin D3 is essential for boosting the immune system.
Dr. Aleemuddin Qaumri emphasized that a novel pandemic condition has no certain treatment. Vaccinations under trial phase and prevention are needed to be prioritized. The role of alternate systems of medicine emerged as an ‘immune booster’ rather than immunomodulators.
Dr. Santosh Joshi, Sr. General Manager, R&D, Hamdard Laboratories India mentioned that people have faith in Unani and, it has grown in a multi-fold manner. He discussed the concept and types of immunity. He also mentioned the programs and products of Hamdard which has helped in boosting immunity in the COVID-19 times.
Mr. Sameer Kant Ahuja, Chief Manager (Regulatory), Multani Pharmaceuticals Ltd while giving a background about Unani medicines, their importance, history, and government regulations towards it discussed the common compound Unani formulations and common immunostimulant single drugs of Unani medicines for boosting immunity. He highlighted that the Unani system is one of the oldest forms of medication. He also urged the Industry to come forward and work together on R&D, so that it reaches more heights of success and meets the global demand.
Mr. Jitender Sodhi, Co-Chair, AYUSH Committee, PHDCCI gave a formal vote of thanked all the eminent dignitaries for joining today’s webinar. Mr. Sodhi also talked about the significance of Unani medicine in boosting overall immunity and use of herbal remedies, dietary practices, and alternative therapies which could help in combating the ongoing pandemic.
The webinar was sponsored by AYUSH Herbs Private Limited and Association of Manufacturers of Ayurvedic Medicine (AMAM) and attended by over 150 participants.
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.
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.
Heliyon. 2021 Jan;7(1):e05957. doi: 10.1016/j.heliyon.2021.e05957. Epub 2021 Jan 14.
BACKGROUND: Viruses are responsible for several diseases, including severe acute respiratory syndrome, a condition caused by today’s pandemic coronavirus disease (COVID-19). A negotiated immune system is a common risk factor for all viral infections, including COVID-19. To date, no specific therapies or vaccines have been approved for coronavirus. In these circumstances, antiviral and immune boosting foods may ensure protection against viral infections, especially SARS-CoV-2 by reducing risk and ensuring fast healing of SARS-CoV-2 illness.
SCOPE AND APPROACH: In this review, we have conducted an online search using several search engines (Google Scholar, PubMed, Web of Science and Science Direct) to find out some traditional foods (plant, animal and fungi species), which have antiviral and immune-boosting properties against numerous viral infections, particularly coronaviruses (CoVs) and others RNA-virus infections. Our review indicated some foods to be considered as potential immune enhancers, which may help individuals to overcome viral infections like COVID-19 by modulating immune systems and reducing respiratory problems. Furthermore, this review will provide information regarding biological properties of conventional foods and their ingredients to uphold general health.
KEY FINDINGS AND CONCLUSIONS: We observed some foods with antiviral and immune-boosting properties, which possess bioactive compounds that showed significant antiviral properties against different viruses, particularly RNA viruses such as CoVs. Interestingly, some antiviral and immune-boosting mechanisms were very much similar to the antiviral drug of COVID-19 homologous SARS (Severe Acute Respiratory Syndrome Coronavirus) and MERS (Middle East Respiratory Syndrome Coronavirus). The transient nature and the devastating spreading capability of COVID-19 lead to ineffectiveness of many curative therapies. Therefore, body shielding and immune-modulating foods, which have previous scientific recognition, have been discussed in this review to discern the efficacy of these foods against viral infections, especially SARS-CoV-2.
More than a year after COVID-19 emerged, many mysteries persist about the disease: why do some people get so much sicker than others? Why does lung damage sometimes continue to worsen well after the body seems to have cleared the SARS-CoV-2 virus? And what is behind the extended, multi-organ illness that lasts for months in people with ‘long COVID’? A growing number of studies suggest that some of these questions might be explained by the immune system mistakenly turning against the body — a phenomenon known as autoimmunity.
“This is a rapidly evolving area, but all the evidence is converging,” says Aaron Ring, an immunologist at the Yale School of Medicine in New Haven, Connecticut.
Early in the pandemic, researchers suggested that some people have an overactive immune response to COVID infection. Immune-system signalling proteins called cytokines can ramp up to dangerous levels, leading to ‘cytokine storms’ and damage to the body’s own cells. Clinical trials have now shown that some drugs that broadly dampen immune activity seem to reduce death rates in critically ill people, if administered at the right time.
But scientists studying COVID are increasingly also highlighting the role of autoantibodies: rogue antibodies that attack either elements of the body’s immune defences or specific proteins in organs such as the heart. In contrast to cytokine storms, which tend to cause systemic, short-duration problems, autoantibodies are thought to result in targeted, longer-term damage, says immunologist Akiko Iwasaki, a colleague of Ring’s at Yale.
Even healthy people make autoantibodies, but not generally in large amounts, and the molecules don’t usually seem to cause damage or attack the immune system.
Yet researchers also have evidence that nefarious autoantibodies do have a role in many infectious diseases.
There are several theories to explain how autoimmunity might emerge from COVID and other infections. Some people might be predisposed to producing autoantibodies that can then wreak havoc during an infection. Alternatively, infections could even trigger the production of autoantibodies. If researchers can establish the link, they might be able to come up with avenues for treatment, both for the repercussions of COVID and for other diseases caused by viruses.
In late September, a group led by Jean-Laurent Casanova at the Rockefeller University in New York City reported that more than 10% of 987 individuals with severe COVID-19 had antibodies that attacked and blocked the action of type 1 interferon molecules, which normally help to bolster the immune response against foreign pathogens1. That was a striking proportion, the researchers say, because people’s antibody repertoires are normally very dissimilar, and noone in a control group for the study had these antibodies. The researchers also saw the antibodies in people before their COVID-19 infection, so Casanova thinks that some people could be genetically predisposed to produce them. And the autoantibodies were more common in men than women — a possible factor in why COVID seems to hit men harder.
The first evidence2 suggesting that autoantibodies against interferon might put people at higher risk of infectious disease was publishedin 1984, and evidence has accumulated since then, Casanova says. But now COVID is drawing more attention to the connection. “Now people understand the problem,” he says, “and all of a sudden they realize that what my lab has been doing for 25 years is actually pretty meaningful.”
Casanova is now screening 40,000 people to see how many have pre-existing autoantibodies and determine whether their distribution by age, ancestry and gender matches that of severe COVID.
Other research groups have supported Casanova’s autoantibody connection. Iwasaki, Ring and others screened 194 patients and hospital workers with varying severities of COVID for a wide range of autoantibodies. Their study, which was posted online in December and has not yet been peer reviewed, found a higher prevalence of autoantibodies against the immune system in infected individuals than in uninfected people3. They found autoantibodies that attacked B cells, as well as some that attacked interferon.
But this study also suggested that SARS-CoV-2 might cause the body to generate autoantibodies that attack its own tissues. Some of the infected individuals had autoantibodies against proteins in their blood vessels, heart and brain. This was particularly intriguing because many of the symptoms seen in the pandemic are linked to these organs. It’s unclear whether COVID-19 infection caused the body to start making these autoantibodies or whether infected people had them already. Iwasaki says they are hoping to study other cases to establish whether there is a causal link; that would require obtaining more blood samples from before people become infected.
Researchers have also found autoantibodies against molecules called phospholipids, adds Michel Goldman, an immunologist at the Free University of Brussels and former director of Europe’s Innovative Medicines Initiative. The largest such study, published in November, found that 52% of 172 people hospitalized with COVID-19 had these autoantibodies4. “That’s a real concern,” he says, because some phospholipids are known to have a role in controlling blood clotting, which goes awry in COVID-19.
This month, another study5, not yet peer reviewed, reported finding autoantibodies that might be spurred by COVID-19. David Lee, an emergency-medicine doctor at New York University (NYU) Langone Health, partnered with NYU microbiologist Ana Rodriguez and others to analyse serum samples from 86 people hospitalized with COVID-19. They looked for autoantibodies against proteins such as annexin A2, which is of particular interest because it helps to keep cell membranes stable and ensures the integrity of small blood vessels in the lungs. The researchers found a significantly higher average level of anti-annexin A2 antibodies in people who had died than in those with non-critical illness. As with other studies, it’s still unclear whether these autoantibodies existed before infection with the coronavirus.
The autoantibody theory might explain some of the delay in the onset of severe symptoms in COVID-19. If evoked by the cellular damage and inflammation stoked by viral infection, as Lee and others think, autoantibodies would take a couple of weeks to build up in the body. This, he says, could be why much of the damage to tissues such as the lungs appears so long after a person develops symptoms such as fever. In this way, autoimmunity might be the real culprit behind the deadly destruction that continues after the coronavirus has cleared. “Clinicians are thinking, ‘Oh, this virus is so deadly, we’ve got to get rid of the virus.’ But then when you talk to the pathologists, they’re like, ‘Yeah, so we’re seeing all this damage, but not seeing much virus,’” Lee says.
An infectious idea
Over the years, scientists have identified numerous instances of infections generating autoimmunity. Some reports suggest that infection with the malaria parasite can cause the body to begin attacking red blood cells, causing anaemia. And Epstein–Barr virus — which causes glandular fever (also known as mononucleosis) — has been implicated in dozens of autoimmune illnesses, including lupus. Finding a rock-solid connection can be tough, because it’s difficult to show whether the infections are the cause of autoimmune disorders or whether they crop up in the body for another reason, says Anish Suri, president of Cue Biopharma, a company in Cambridge, Massachusetts, that is researching therapies to counter autoimmunity.
Strep throat is a well-established example. If left untreated, this illness, which is caused by the bacterium Streptococcus pyogenes, can prompt an autoimmune reaction, known as rheumatic fever, that attacks organs and can lead to permanent heart damage. Other bacteria are also likely to lead to autoimmunity: the stomach bug Helicobacter pylori is thought to cause a disorder called immune thrombocytopenic purpura (ITP), in which the body starts destroying platelets in the blood. In some people with ITP, treatment with antibiotics against H. pylori improves platelet count, suggesting that the drugs help to reverse the autoimmune condition.
Yehuda Shoenfeld, head of the Zabludowicz Center for Autoimmune Diseases in Tel-Hashomer, Israel, suspects that COVID-19 might cause autoimmune disease. Last June, he published an article about COVID-19 and autoimmunity6, and cited an April 2020 case report of a 65-year-old woman with COVID-19 whose platelet count dropped precipitously and who required a platelet transfusion7. Although there is not enough evidence to prove that this was ITP, there have been a few dozen other cases of ITP linked to COVID-19 in the literature8.
Some people might have a genetic predisposition to developing an autoimmune reaction in response to infection. For example, certain individuals have DNA that encodes the immune-system protein HLA-DRB1, which Shoenfeld says is “notorious” for its link to autoimmunity. A related protein, HLA-DQB1, is strongly suspected to have put individuals receiving a now-discontinued vaccine against the H1N1 ‘swine flu’ at risk of developing a form of narcolepsy that is thought to result from an autoimmune attack on neurons in the brain.
Another way pathogens might trigger immunity is if a part of them coincidentally resembles human cell components. For example, S. pyogenes has an ‘M’ protein that mimics certain proteins found in the human heart. This is known as molecular mimicry. In their June 2020 article, Shoenfeld and his collaborators found similarities between numerous short sequences of the SARS-CoV-2 spike protein, which the virus uses to enter the cell, and human proteins. Others caution, however, that this might not have meaningful effects. “This is not to say that mimicry by pathogens is not a real thing,” says Brian Wasik, a virologist at Cornell University in Ithaca, New York. “But most instances of such mimicry have been defined by testing how the pathogens’ proteins actually react to antibodies in the lab.”
Another theory is that inflammation caused by an infection might prime the immune system to mistakenly see the spewed contents of destroyed cells as ‘foreign’ and create autoantibodies against these cellular pieces, says Leona Gilbert, a molecular biologist who is a consultant at a diagnostic company named Te?ted Oy in Finland, which has developed and sells a test for SARS-CoV-2 antibodies. The tissue damage that accompanies inflammation is a recipe for the body to begin attacking itself, Gilbert says: “That just precipitates the whole event in developing autoimmune conditions,” she says.
Lee, the researcher who studied annexin A2, says the evidence that infections can give rise to autoimmunity is not receiving enough attention. “It should make us rethink dozens of diseases, if not hundreds,” he says. “I’m like, ‘How is anybody not seeing this?’”
If an autoimmunity element exists either in predisposing people to COVID-19 or in the fallout from the infection, there might be treatment implications. Casanova says that in cases in which pre-existing autoimmunity against interferon might put people at greater risk of falling ill, then blood tests for autoantibodies, which are becoming more available in research laboratories and university hospitals, could help to identify them.
And if these people become infected with SARS-CoV-2, Casanova suggests, they could receive supplementation as early as is practical with interferon-β, which is not as prone to attack from the immune system as are other interferons. Last November, a preliminary study found that an inhaled form of interferon-β seemed to improve the clinical condition of people with COVID, prompting a larger trial of this therapy9.
Interferon replacements are intended to boost the activity of a weakened immune system. But if autoantibodies attack organs such as the lungs and brain, a blunt strategy for combating them might be to suppress the immune system.
Even before autoantibodies came into focus, the idea that a cytokine storm might be a culprit meant that studies were under way to see whether immunosuppressive steroids such as dexamethasone, or the arthritis drugs tocilizumab and sarilumab, could be used to calm immune systems set awry by COVID. The World Health Organization now “strongly recommends” the use of dexamethasone in severe cases, and the United Kingdom is using the arthritis drugs for people with severe COVID after a clinical trial on 7 January10 suggested that they cut death rates in patients in intensive care.
Physicians emphasize that, whether they are used to quell a cytokine storm or to try to address autoimmunity, administration of the drugs needs to be carefully timed so that they don’t interfere with the body’s battle against SARS-CoV-2. Suri notes that broad-spectrum immunosuppressants make the body more prone to infection. His company is one of a handful conducting preclinical work to develop engineered molecules that go after specific immunity pathways, rather than suppress immunity across the board.
Lee, meanwhile, says that if autoantibodies against annexin A2 and other proteins prove to be a consequence of COVID-19, then it might make sense to study what happens when patients’ plasma is run through a process that clears these antibodies out before returning the plasma.
Scientists are very interested in understanding whether autoimmunity is linked to long COVID, too. “First of all, we don’t know if these autoantibodies contribute to long COVID, but if they do, what is the longevity? How long will they last? How long is the body going to keep producing those antibodies?” Ring says. But answering these questions is a complicated endeavour, because people naturally produce many different kinds of antibody, including autoantibodies.
Ring hopes that research into viruses and autoimmunity will eventually get much-needed answers for individuals with post-viral autoimmunity, which might include those with COVID-19. “These patients are just so frustrated,” he says. “Their physicians don’t believe them and so they get psych referrals. Just to be able to tell these people they have a real disease and here’s what’s causing it — that would be really meaningful.”
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.
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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.
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.
It’s a question that has no doubt crossed our minds especially in recent weeks, with the start of COVID-19 vaccination rollout: Do I need to get vaccinated if I’ve already had the virus?
And the answer is: Yes.
Regardless of previous infection, the U.S. Centers for Disease Control and Prevention says people who have had the COVID-19 virus should plan on getting vaccinated when it’s their turn.
“It’s a pretty straightforward question,” said Johns Hopkins infectious disease specialist Dr. Amesh Adalja. “Yes, you need to get vaccinated.”
After someone recovers, their immune system should keep them from getting sick again right away.
“Your immune system is able to identify the virus, and protect itself,” said Dr. Saskia Popescu, an infectious disease expert at George Mason University.
Scientists still don’t know exactly how long this immunity lasts or how strong it is, though recent research suggests the protection could last for several months.
It’s impossible to know how long a person might be immune, said Dr. Prathit Kulkarni, an infectious disease expert at Baylor College of Medicine. “There’s no way to calculate that.”
Vaccines, by contrast, are designed to bring about a more consistent and optimal immune response. And they should boost whatever preexisting immunity a person might have from an infection, experts say.
“Since we’re in this pandemic, and don’t have a handle on it, the safer approach is to vaccinate,” Kulkarni said. “You don’t lose anything and you stand to benefit.”
If you’ve been infected in the last three months, the CDC says it’s OK to delay vaccination if you want to let others go first while supplies are limited.
“All things being equal you would want the person with no protection to go first,” Adalja said.
The coronavirus disease 2019 (COVID-19) pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), continues to spread worldwide. Since the virus first emerged in late-2019, over 95.55 million cases and more than 2 million deaths have been reported.
Many countries have commenced targeted vaccination efforts to control the spread of the virus and immunize vulnerable groups. However, vaccine rollout may still lag behind ongoing infections, as fast-spreading new variants threaten many countries. Finding an effective therapy to help patients fight the infection remains crucial.
Passive immunotherapy treatment, wherein SARS-CoV-2-neutralizing antibodies (nAbs) from the plasma of recovered patients are administered to acutely sick patients, is a promising method for COVID-19 treatment in severe cases.
A team of researchers at the University of Washington, Fred Hutchinson Cancer Research Center, and the National Institute of Health, USA, recently studied the neutralizing antibodies from patients recovering from COVID-19 to investigate which clinical factors predict good passive immunotherapy donors.
In the study, published in the Journal of Clinical Investigation, the research team measured SARS-CoV-2-nAb titers in the plasma of 250 people with SARS-CoV-2 infection.
In the USA, convalescent plasma therapy for COVID-19 patients was approved under emergency use authorization by the Food and Drug Administration (FDA) on August 23, 2020. This mode of therapy uses antibody-containing blood from recovered individuals to help promote passive immunity in severely ill patients still battling the infection.
Blood donated by people who have recovered from COVID-19 is processed to remove blood cells, leaving behind the plasma and neutralizing antibodies against SARS-CoV-2.
The plasma given to severely ill patients will help boost the body’s immune system. In a recent phase II clinical trial in Argentina, scientists found that convalescent plasma with high levels of neutralizing antibodies, particularly when given early in the infection, had a marked beneficial health impact.
Yet, not all SARS-CoV-2-infected people produce a strong neutralizing antibody response. Hence, convalescent plasma from donors should be screened for SARS-CoV-2-neutralizing antibody activity to make sure the recovered patients are suitable donors.
In the current study, the researchers tested the serum of 250 potential convalescent plasma donors with confirmed SARS-CoV-2 infection for the presence of SARS-CoV-2 spike protein S1 domain, nucleoprotein (NP), and for neutralizing antibodies.
The team found that among the participants, 97 percent were seropositive on one or more assays. About 60 percent of the donors had nAb titers. The correlates of higher nAb titer included old age, male, and severity of the illness. Also, patients with more severe COVID-19 symptoms, like the difficulty of breathing and fever, had higher levels of neutralizing antibodies against SARS-CoV-2.
Moreover, a longer period between the infection and antibody screening had decreased nAb titers. The study results showed that severe COVID-19 illness produces higher levels of antibodies than less severe illness. This also means that the neutralizing antibodies in the blood of recovered patients wane over time.
COVID-19 seems to be one of a group of infections where the sicker one is, and presumably the more virus and therefore the more antigen that is around, the higher the levels of antibody,” Dr. David Koelle of the Koelle Laboratory, University of Washington, said in a statement.
He explained that the potential cause of this discrepancy is that the immune system in people who had a severe illness, was not effective in stopping it. There is a probable temporal race between the proliferation of the virus and host adaptive immunity.
The researchers concluded that nAb titers correlated with disease severity, sex, and age. Also, they suggested that commercially available SARS-CoV-2 immunoglobulin G (IgG) results can become an alternative for nAb testing.
Functional nAb levels were found to decline and a small proportion of persons recovered from COVID-19 lack adaptive immune responses,” they added.
Once you test positive for COVID-19, what should you do next? Doctors say staying on top of any changes in your symptoms and taking the proper precautions is a good start, but doctors who have been treating patients’ recovery at home say there are other things you can do to boost your immune system.
Shortly before Christmas, 43-year-old Juliana Shain tested positive for COVID-19. Five days later, the same would happen to her fiancé.
“I felt like I had been beaten up. I felt really hungover,” she said. “We had aches and pains then a cough and then sneezing. Really at the end of it, we had difficulty breathing.”
Fear of being hospitalized soon set in. Internal medicine specialist Dr. Aamir Iqbal with Agoura Family Practice in California says he’s been getting several calls a day from frantic patients.
“When you’ve tested positive, it’s a big moment. A lot of people get very scared and nervous about what’s going to happen,” he said. “‘What do I do?’ Or ‘My husband tested positive or my spouse tested positive or my kid tested positive, and now I live with them.”
Iqbal’s first suggestion is to buy an over-the-counter pulse oximeter.
“It’s a little device that attaches to your finger and right on top of the screen it has a percentage,” he said. “When you get below 94%, that starts throwing up some flags. And any number under 90% is a big red flag.”
He suggests hydrating with beverages such as Pedialyte or Gatorade. Shain’s doctor told her to take a cocktail of supplements.
“The doctor gave us a bunch of vitamins,” she said. Shain started taking Vitamin C, B12, D3 and zinc.
“Some of these home remedies can actually help. We know they can’t hurt you,” Iqbal said.
He also suggested over-the-counter medicines such as acetaminophen, mucus thinners and a baby aspirin to prevent blood clots.
“While the baby aspirin doesn’t equivalent to a full blood thinner medication, it can give you some protection,” Iqbal said.
Studies show sleeping on your stomach helps get more oxygen to your lungs. Iqbal said if its comfortable, try it, but he tells his patients it’s not a requirement.
Some advice online includes waking up every two hours to get your blood circulating. To that Iqbal said quality sleep is much more important As for eating more bananas, avocados or asparagus, he said good nutrition is important, but food alone can’t stop worsening symptoms.
A month after her infection, Shain is back at work
“I feel exhausted, and I still have some brain fog,” she said.
She hasn’t mustered enough energy to take down her Christmas decorations and Shain had to postpone her wedding day. But, she’s grateful to be on the mend.
“Just be kind to yourself. Take it one day at a time and you’ll get through it,” she said.
We’ve lived COVID-19 for nearly a year and health experts are now saying getting the virus shouldn’t be your only concern. Randy Grabill, a dietician with UPMC Altoona, says he’s seen an increase of patients with diabetes and cardiovascular disease.
Grabill says people haven’t moved around as much as they did before the pandemic started with stay at home orders and gyms being closed on and off. You may have also ordered a little more take out or enjoyed your favorite comfort foods more than usual, Grabill says all of that might have caught up to you.
“We’re always familiar with the term freshman 15 for people that go to college, well this has been 2020 has been known as the year of the quarantine 15,” said Grabill.
It’s not too late to turn things around, Grabill says to get started set realistic health goals and take steps to eat more unprocessed foods and stay active. Small changes Grabill says can lead to big results, and a healthier lifestyle Grabill says can boost your immune system which is very important during the pandemic.
It’s also important to stay up to date with doctor visits and procedures. Throughout the pandemic Grabill says people have stayed away from the hospital for fear of catching COVID, but he reassures people it’s very safe to see your doctor. If you don’t check in with your doctor as needed Grabill says it can have even more of a negative impact on your health.
“Maybe all of sudden we have blockages in the arteries that led to heart attacks or strokes. Or maybe we were more sedentary we gained weight we have a family history of diabetes and now we have diabetes and that can lead to a whole cascade of health issues,” said Grabill
Gritstone Oncology, the biotech working on cancer vaccines based on traditional infectious disease immunology, is bringing that approach back to its roots. It’s working on a vaccine against SARS-CoV-2, the virus that causes COVID-19, that could also work against other viruses in this family in the case of a future pandemic.
The company is developing the vaccine alongside the Bill & Melinda Gates Foundation, which provided a grant to bankroll preclinical work, and the National Institute of Allergy and Infectious Diseases, which will carry out a phase 1 study through the Infectious Diseases Clinical Research Consortium.
The vaccine is based on Gritstone’s EDGE technology—which uses machine learning to predict antigens presented by tumor cells or cells infected by a virus that the immune system can see—and work out of the La Jolla Institute of Immunology, which has studied hundreds of patients recovering from COVID-19. Under a license agreement with La Jolla, Gritstone has access to epitopes of the SARS-CoV-2 virus—a part of the virus to which antibodies bind—identified in its studies.
Like the first generation of COVID-19 vaccines, Gritstone’s candidate targets the spike protein of the new coronavirus, but it also contains other targets that could help boost T-cell immunity.
“Gritstone’s vaccine may provide more comprehensive viral protection by inducing a better combination of T cell responses and neutralizing antibodies as compared to the currently available vaccines,” said Daniel Hoft, M.D., Ph.D., director of Saint Louis University’s Center for Vaccine Development and Division of Infectious Diseases, Allergy and Immunology, National Vaccine Advisory Committee member, and protocol chair and lead principal investigator of Gritstone’s COVID-19 study, in a statement.
“It is important that we move forward with developing these next generation vaccines because we do not yet know whether the existing vaccines that have been granted emergency use authorization will provide long-term immunity or prevent transmission. Improved vaccines that can accomplish these additional benefits may be needed to continue mitigating the ongoing pandemic,” Hoft added.
Besides potentially provoking a stronger immune response than the first generation of COVID-19 vaccines does, a new vaccine aimed at targets beyond the spike protein could come in handy in the face of new variants of the SARS-CoV-2 virus.
What’s more, Gritstone hopes this approach could make the vaccine useful against other coronaviruses as well as the one that causes COVID-19.
“As well as a potential role in protection against SARS-CoV-2, the notion of using evolutionarily conserved viral antigens (in addition to Spike) as the basis for a vaccine that induces antibody and T-cell responses to provide protection against future coronavirus pandemics is an exciting concept that springs from our current work. We plan to pursue this in 2021,” said Karin Jooss, Ph.D., chief scientific officer of Gritstone.