Millions of people around the world have received two shots of Sinovac, a Chinese-manufactured inactive vaccine that is used in 48 countries to help reduce transmission rates of COVID-19.
However, those vaccinations alone are of no help against the widely circulating Omicron variant, show a new study by researchers at Yale and the Dominican Republic. The results are published in the journal Nature Medicine.
An analysis of blood serum from 101 individuals from the Dominican Republic showed that Omicron infection produced no neutralizing antibodies among those who received the standard two-shot regimen of the Sinovac vaccine. Antibody levels against Omicron rose among those who had also received a booster shot of the mRNA vaccine made by Pfizer-BioNTech.
But when researchers compared these samples with blood serum samples stored at Yale, they found that even those who had received two Sinovac shots and a booster had antibody levels that were only about the same as those who’d received two shots of the mRNA vaccines but no booster shot. In other studies, the two-shot mRNA regimen without a booster has been shown to offer only limited protection against Omicron.
Also, the researchers found that individuals who had been infected by earlier strains of the SARS-Cov-2 virus saw little immune protection against Omicron.
The findings will likely complicate global efforts to combat the Omicron strain, which has supplanted the more dangerous but less transmissible Delta strain as the most dominant circulating virus in much of the world. An additional booster shot — and possibly two — are clearly needed in areas of the globe where the Sinovac shot has been chief source of vaccination, said Akiko Iwasaki, the Waldemar Von Zedtwitz Professor of Immunobiology and senior author of the paper.
“Booster shots are clearly needed in this population because we know that even two doses of mRNA vaccines do not offer sufficient protection against infection with Omicron,” Iwasaki said.
Omicron has proven particularly problematic to combat because it possesses 36 mutations on the spike proteins on its surface, which the virus uses to enter cells, researchers say. Existing mRNA vaccines are designed to trigger antibody response when spike proteins are recognized.
Iwasaki stressed, however, that the human immune system still has other weapons it can use against COVID-19, such as T cells that can attack and kill infected cells and prevent severe disease.
“But we need antibodies to prevent infection and slow transmission of the virus,” she said.
Carolina Lucas and Valter Silva Monteiro, both from the Yale School of Medicine, are co-lead authors of the paper. Eddy Perez-Then, of the Health Ministry of the Dominican Republic, and Marija Miric, of Two Oceans Health in Santo Domingo, are co-lead authors.
Aging leads to a decline in cellular fitness and loss of optimal protein function. Many age-related ailments, including Alzheimer's and Parkinson's diseases, are caused by protein aggregation, a result of errors in protein folding. Yet, the mechanisms underlying how ageing causes proteins to aggregate has largely remained a black box. In new research published Jan. 19 inNature, researchers at Stanford University have traced this problem to age-dependent impairment of the machinery that produces new proteins.
To root out this issue, researchers in the lab of Judith Frydman, the Donald Kennedy Chair in the School of Humanities and Sciences at Stanford, focused on how age affects the functioning of ribosomes -- the cellular machinery responsible for converting messenger RNA into proteins. They used two well-established models of human aging, yeast and roundworms. Through a combination of experiments and computational data analysis, they found that ribosome function degrades with age in both organisms. The increased load of defective proteins with age overwhelms the protective quality control failsafes that would otherwise prevent protein aggregation.
"We've known that protein aggregation with age is a problem linked to many diseases. At the moment, treatments try to address it by trial-and-error testing," said Kevin Stein, lead author of the paper and a former postdoctoral scholar in the Frydman Lab. "Getting down to the basic-biology of these diseases, and understanding what mechanisms cause them, can help us make better decisions about what therapies could be effective before we test them."
A vulnerable time
When folded correctly, proteins carry out their functions and remain soluble in the environment of the cell. Misfolded proteins, by contrast, cannot function properly and tend to stick to each other and other proteins, clogging up cellular processes and generating toxic aggregates. Protein aggregation has been specifically implicated in a wide variety of aging-linked diseases, including Alzheimer's, Parkinson's, frontotemporal dementia, Huntington's disease and ALS (amyotrophic lateral sclerosis).
To guard against the continual production of misfolded proteins, cells have dedicated "quality control" machinery for fixing or degrading misfolded proteins. Previous research has shown that shortcomings in these processes can lead to aggregation. This research is the first to show the folding defect during ageing starts early in the journey of a protein, when it is made by the ribosome. Because ribosomes are constantly producing large amounts of proteins, these defects cause a subsequent snowball of disfunction.
"One of the most vulnerable and key times in the life of a protein -- where it's most prone to misfolding -- is when it's made," said Frydman, who is a professor of biology and of genetics.
To start, the researchers used a technique called ribosome profiling, which allowed them to see exactly how ribosomes are moving on the messenger RNA during the act of translation. Amassing data from all the genes translated in young and aged Caenorhabditis elegans roundworms and yeast, the researchers noticed that in older cells ribosomes periodically moved more slowly and were more likely to stall and bump into each other. As one might expect, the researchers saw that decreases in proper ribosome performance aligned with increases in the aging-dependent aggregation of misfolded proteins. One important insight was that the increase in stalling and misfolding overwhelmed the cell's cleaning-up-and-clearing-out quality control failsafes.
"There is a two-pronged situation where aging leads to increased stalling and increased ribosome collisions, but the cell loses the safety net to deal with it," explained Stein.
In follow-up experiments in worms, the researchers found that even if the overall fraction of newly made proteins with altered translation during aging is low (~10%), this small effect can still be enough to overwhelm the quality control system and trigger significant aggregation that can disrupt many different cellular components or processes.
"Every cell normally makes millions of these newly translated proteins," said Frydman. "So very slight changes in the efficiency of folding with age will escalate in a vicious cycle where defects in translation lead to an overload of the system, which in turn leads to increased protein aggregates with age that are themselves also toxic."
To make matters worse, through further experiments in yeast and C. elegans, the researchers showed that these problems affect the very proteins that cells use to aid in translation and to help correct misfolding issues.
Millions of questions
While this research revealed, for the first time, some intriguing insights about the mechanisms of aging, it inspires many questions for the future. Perhaps the most pressing one: Why does aging affect ribosomes? Also, what can be done about it?
Given the similarities between ageing in yeast, C. elegans and other organisms, the researchers are optimistic that their findings will translate also to humans. One direction for future work will be the application of insights from this study to the development of possible treatments for age-related diseases associated with protein aggregation. Excitingly, the study showed that analysis of mutations that extend lifespan "rejuvenated" ribosomal function in aged yeast.
"This is only the beginning of a very fascinating future," said Fabián Morales-Polanco, a co-author of the research and a postdoctoral scholar in the Frydman lab. "We set a precedent for something new, and there are millions of questions -- and probably hundreds of papers -- that will follow."
This research was funded by the Glenn Foundation for Medical Research, the National Institutes of Health and the Pew Charitable Trusts.
Additional Stanford co-authors of the paper are visiting graduate student Joris van der Lienden and former postdoctoral scholar T. Kelly Rainbolt. Frydman is also a member of Stanford Bio-X, the Stanford Cancer Institute and the Wu Tsai Neurosciences Institute and a faculty fellow of Stanford ChEM-H.
Story Source:
Materials provided by Stanford University. Original written by Taylor Kubota. Note: Content may be edited for style and length.
Journal Reference:
Kevin C. Stein, Fabián Morales-Polanco, Joris van der Lienden, T. Kelly Rainbolt, Judith Frydman. Ageing exacerbates ribosome pausing to disrupt cotranslational proteostasis. Nature, 2022; DOI: 10.1038/s41586-021-04295-4
Immunotherapy given before surgery caused liver cancer tumors to die off in one-third of the patients enrolled in a first-of-its-kind clinical trial, Mount Sinai researchers reported inThe Lancet Gastroenterology & Hepatologyin January.
The phase 2 trial results suggested that the neoadjuvant immunotherapy -- therapy given before surgery -- may kill not only the tumor, but also microscopic cancer cells that surgery would miss and that could later cause the cancer to recur or metastasize, the researchers said. In effect, the therapy teaches the immune system to fight off any recurrences.
"Ultimately, we think it's better for the patient to receive immunotherapy before surgery because people are healthier before metastases, and their immune systems are in better shape to fight off the cancer," said senior author Thomas Marron, MD, PhD, Director of the Early Phase Trials Unit at The Tisch Cancer Institute and Associate Professor of Medicine (Hematology and Medical Oncology) at the Icahn School of Medicine at Mount Sinai. "This study, together with neoadjuvant immunotherapy trials in many other types of tumors, supports the need for continued evaluation of perioperative immunotherapy to decrease recurrence rates."
Dr. Marron added: "Typically when cancer recurs it is no longer a curable disease. Larger trials in the future will aid in defining the utility, safety, and survival of neoadjuvant immunotherapy, specifically this type of PD-1 blockade."
Liver cancer, the most common type of which is known as hepatocellular carcinoma (HCC), is the third-leading cause of cancer-related deaths globally. While immunotherapies have changed the prognosis of patients with advanced HCC, the majority of patients still die from this disease. Although liver cancer surgery often appears successful, in more than half of patients the cancer comes back, due to either residual micrometastatic disease, or in some cases an entirely new tumor, highlighting the potential benefit of neoadjuvant therapy to improve survival.
This study's findings are important because to date, no therapy given before or shortly after surgery has demonstrated any real improvement in survival for liver cancer patients.
Researchers gave 21 early-stage liver cancer patients two rounds of the immunotherapy agent cemiplimab, an anti-PD-1 antibody, before their surgery in late 2020. Doctors studied tumor death and cancer-fighting immune system activation via magnetic resonance imaging and blood, tumor, and stool samples.
They found that in one-third of the patients, much of their tumors died before surgery. Patients whose immune system was already working against the cancer tended to have more of a response to the immunotherapy, which suggests that the immune system was further activated and would kill any microscopic remnants of cancer. Tumor death in response to neoadjuvant therapy is an indication for improved outcomes in many cancer types, and the researchers are currently following the patients to assess if this rings true for HCC as well.
This study was able to measure the immune system response in a novel way. Dr. Marron and colleagues used a new collaborative approach between researchers and clinicians: The neoAdjuvant Research Group to Evaluate Therapeutics or TARGET, which maximizes the useful information that can be gleaned from smaller neoadjuvant clinical trials. The TARGET platform focuses on coordinating detailed, real-time profiling of the immune system's response in patients receiving cancer immunotherapy as a neoadjuvant treatment.
The TARGET platform showed how the PD1 blockade boosted the number of activated immune cells that invade HCC tumors, induced tumor necrosis, and shrank tumors prior to surgery. The platform helped researchers determine that PD1 blockade is likely beneficial in HCC, but because only some patients had a robust response, the immunotherapy may need to be used in combination with other treatments. The aim of the in-depth analysis of tissue samples is to identify biomarkers -- biological identifiers -- that will help show who will and will not respond well to a therapy. The aim of TARGET is to identify the optimal therapy for each patient, and decrease the likelihood that suboptimal treatments go into large phase 3 trials, wasting resources and the time and efforts of patients.
"You normally don't get to study how drugs work in humans in such a detailed manner," said Dr. Marron. "When you do simple biopsies, you get very little tissue and the analysis often doesn't produce detailed information about the cancer or the immune system's response. With this platform's analysis, you get several biopsies before treatment as well as blood and stool samples. Then when the tumor is removed in surgery, we analyze that as well as more blood and stool samples, so we have a lot of detailed information on what is going on microscopically than ever before. This is an exciting platform to study in that level of detail."
Thomas U Marron, Maria Isabel Fiel, Pauline Hamon, Nathalie Fiaschi, Edward Kim, Stephen C Ward, Zhen Zhao, Joel Kim, Paul Kennedy, Ganesh Gunasekaran, Parissa Tabrizian, Deborah Doroshow, Meredith Legg, Ashley Hammad, Assaf Magen, Alice O Kamphorst, Muhammed Shareef, Namita T Gupta, Raquel Deering, Wei Wang, Fang Wang, Pradeep Thanigaimani, Jayakumar Mani, Leanna Troncoso, Alexandra Tabachnikova, Christie Chang, Guray Akturk, Mark Buckup, Steven Hamel, Giorgio Ioannou, Clotilde Hennequin, Hajra Jamal, Haley Brown, Antoinette Bonaccorso, Daniel Labow, Umut Sarpel, Talia Rosenbloom, Max W Sung, Baijun Kou, Siyu Li, Vladimir Jankovic, Nicola James, Sara C Hamon, Hung Kam Cheung, Jennifer S Sims, Elizabeth Miller, Nina Bhardwaj, Gavin Thurston, Israel Lowy, Sacha Gnjatic, Bachir Taouli, Myron E Schwartz, Miriam Merad. Neoadjuvant cemiplimab for resectable hepatocellular carcinoma: a single-arm, open-label, phase 2 trial. The Lancet Gastroenterology & Hepatology, 2022; DOI: 10.1016/S2468-1253(21)00385-X
Physical activity, nutrition and cognitively stimulating activities are all known to be good ways to prevent Alzheimer's disease and dementia. And older adults at risk can access a variety of lifestyle services to that end, including diet regimes and exercises for their body and mind.
Now an international team of researchers led by Université de Montréal psychology professor Sylvie Belleville has determined how many of those intervention sessions are needed prevent cognitive decline in people at risk: only about a dozen.
Published in Alzheimer's & Dementia : The Journal of the Alzheimer's Association, the study by Dr. Belleville and colleagues at the universities of Toulouse and Helsinki show that 12 to 14 sessions are all that's were needed to observe an improvement in cognition. Until now, the number of sessions or "doses" needed for optimal effect has been unknown.
"In pharmacological studies, every effort is made to define an optimal treatment dose needed to observe the expected effects, " said Belleville, a neuropsychologist and researcher at the research centere of the UdeM-affiliated Institut universitaire de gériatrie de Montréal. "This is rarely done in non-pharmacological studies, especially those on the prevention of cognitive decline, where little information is available to identify this dose.
"Defining an optimal number of treatment sessions is therefore crucial.," she continued. "Indeed, proposing too few sessions will produce no noticeable improvement effects, but too many sessions is also undesirable as these interventions are costly. They are costly both for the individual who follows the treatments, in terms of time and involvement, and for the organization offering these treatments."
The study is based on a secondary analysis of data from the three-year Multidomain Alzheimer Preventive Trial (MAPT) and looked at 749 participants who received a range of interventions aimed at preventing cognitive decline. These included dietary advice, physical activity and cognitive stimulation to improve or maintain physical and cognitive abilities.
People's individuality important
In their research, Belleville's team noted that people's individuality should be considered when determining the optimal treatment dose.
In their study, the researchers evaluated the effects of the sessions in terms of each participant's age, gender, education level, and cognitive and physical condition. The relationship between the "dose" each received and their cognitive improvement was then analyzed.
The main results show an increase with dose followed by a plateau effect after 12 to 14 sessions. In other words, you need enough dose to see an effect but offering more than 12 to 14 sessions of treatment does not mean better results. That said, participants with lower levels of education or more risk factors for frailty did benefit from more sessions.
The conclusion? It's important to identify and target an optimal dose and to customize the treatment for each individual, the researchers say. Not only is "dosage" an important component of behavioural interventions, it can also provide valuable information when time and money are limited, helping public-health agencies develop effective prevention programs and offer guidance to older adults and clinicians.
Sylvie Belleville, Simon Cloutier, Samira Mellah, Sherry L Willis, Bruno Vellas, Nicola Coley, Sandrine Andrieu, Tiia Ngandu. When is more better? Modeling the effect of dose on the efficacy of the MAPT multidomain intervention as a function of individual characteristics. Alzheimer's & Dementia, 2021; 17 (S10) DOI: 10.1002/alz.054948
Iowa State University scientists may have uncovered an important clue that sheds light on why pigs don't get sick when exposed to the coronavirus.
Studies since the start of the pandemic have noted that pigs can be infected by the virus if exposed to high doses, but the infection is self-limited and pigs don't show clinical signs of disease nor do they transmit the virus to other animals. So Rahul Nelli, a research assistant professor of veterinary diagnostic and production animal medicine, and Luis Gimenez-Lirola, an associate professor of veterinary diagnostic and production animal medicine, set out to find out why in a newly published study in the academic journal Cell Death Discovery. What they found could lead to new ways to treat humans who contract COVID-19, the disease that results from infection by the virus SARS-CoV-2, said Nelli and Gimenez-Lirola.
Nelli and Gimenez-Lirola have studied how coronaviruses affect pigs for years. They've developed models that allow them to study in detail how viruses infect pigs and pig cells and how the cells respond to fight the infection. For the latest experiments, they introduced the virus to cultured porcine and human respiratory epithelial cells, which line most of the respiratory tract. They found the pig cells underwent apoptosis, or controlled cell death, in response to infection at a higher rate than human epithelial cells.
"When we looked under the microscope there was an interesting phenomenon going on inside the cells," Nelli said. "The nuclei of the infected pig cells were starting to shred into fragments but not uninfected pig cells."
That shredding of the nucleus is a telltale sign of apoptosis, which may be a key in helping pigs avoid symptoms after exposure to SARS-CoV-2. Triggering apoptosis early in the infection essentially causes minimal tissue damage and confines viral replication, thus limiting severe illness. Human cells can undergo apoptosis in response to coronavirus infection as well, but the study found human cells do so much less frequently than porcine cells. Pig cells are roughly 100 times more likely to undergo apoptosis than human cells, according to the study.
Human cells are more likely to go through necrosis, another form of cell death that's less controlled than apoptosis. During necrosis, the contents of a cell release into the surrounding space, provoking a strong hyperimmune response that isn't triggered during apoptosis.
The researchers surmise that a wide-scale apoptosis response is helpful for avoiding disease because it disposes of infected cells quickly without the immune system overreacting, while wide-scale necrosis and the resulting hyperimmune response is less favorable to host cells.
"We don't want to over-conclude, but this response is probably something intrinsic to the pig immune system that is innate and not acquired," Giminez-Lirola said. "The idea is to kill the virus subtly but fast enough so there's not an excessive immune response triggered."
The researchers said further study could lead to therapies designed to trigger apoptosis in human cells, allowing people infected with the coronavirus to avoid severe symptoms.
The next step for the ISU research team is to identify all the genes activated during the infectious process and compare them with other animal species in which those genes are present. That could give them further clues about how and why other animals, such as deer, can carry the virus without suffering symptoms of disease.
In addition to Nelli and Gimenez-Lirola, the research team included Kruttika Phadke, Gino Castillo, Lu Yen and Bryan Bellaire at Iowa State. Amy Saunders, Rolf Rauh and William Nelson of Maryland-based Tetracore, Inc., are also listed as co-authors of the study.
Rahul K. Nelli, Kruttika-S Phadke, Gino Castillo, Lu Yen, Amy Saunders, Rolf Rauh, William Nelson, Bryan H. Bellaire, Luis G. Giménez-Lirola. Enhanced apoptosis as a possible mechanism to self-limit SARS-CoV-2 replication in porcine primary respiratory epithelial cells in contrast to human cells. Cell Death Discovery, 2021; 7 (1) DOI: 10.1038/s41420-021-00781-w
Results of a large study led by UCLA Jonsson Comprehensive Cancer Center researchers could help guide treatment planning for patients with high-risk prostate cancer.
An international effort consisting of a consortium of 16 research centers in collaboration with two international cooperative trial groups found that patients receiving high-dose external beam radiation therapy alone may benefit from androgen deprivation therapy (ADT) lasting longer than 18 months, while those with external beam radiation therapy and a brachytherapy boost -- the implantation of radioactive seeds to deliver a higher total dose to the prostate -- may be optimally managed with 18 months of ADT or possibly less. Results are published in the Jan. 20 issue of JAMA Oncology.
"Adding androgen deprivation therapy to radiation therapy has been consistently shown to improve survival when treating men with high-risk prostate cancer. However, lowering testosterone levels is associated with a number of side effects, including not only a decrement in quality of life, but possibly more serious adverse events when longer durations are used. While it has long been hypothesized that by delivering extremely high doses of radiation, one might be able to shorten the required duration of ADT, this has never been proven," said lead author Amar Kishan, MD, associate professor and vice chair of clinical and translational research in the Department of Radiation Oncology at UCLA and a researcher at the UCLA Jonsson Comprehensive Cancer Center.
The researchers analyzed individual patient data from three cohorts of patients: a retrospective cohort of patients from 16 cancer treatment referral centers between 2000 and 2014 who received either high-dose external beam radiotherapy or external beam radiotherapy with a brachytherapy boost; a cohort of patients enrolled in a randomized phase 3 trial that included patients from 23 treatment centers in Australia and New Zealand; and a cohort of patients enrolled in a randomized phase 3 trial conducted across 10 treatment centers in Spain. This is the only analysis to include both retrospective and prospective data in evaluating optimal ADT duration in high-risk prostate patients receiving these two forms of radiation therapy.
"Because of androgen deprivation therapy's unpleasant side effects, it is often underutilized, with men receiving considerably shorter durations of ADT than might be recommended. To discern the ADT duration thresholds that provide the greatest metastasis-free survival benefit for these patients, we analyzed a multi-institutional database of patients, developed hypotheses, and then evaluated our findings by analyzing individual patient data from randomized trials," said Kishan.
"The consistency of our results across multiple different patient cohorts greatly strengthens our findings," said Tahmineh Romero, senior statistician in the UCLA Department of Medicine Statistics Core and the senior author of the article.
In the retrospective cohort -- looking at ADT durations of less than six months, six to 18 months, and greater than 18 months -- a significant interaction was seen between treatment type and ADT duration. A duration of 18 months or more was associated with improved outcomes, relative to shorter durations, for patients receiving high-dose external beam radiation therapy without a brachytherapy boost. In contrast, among patients receiving radiation therapy and brachytherapy, an ADT duration of at least six months but less than 18 months was associated with improved metastasis-free survival and overall survival, compared to receipt of less than six months of ADT. But there appeared to be no improvement in metastasis-free survival for those receiving both forms of radiation therapy and more than 18 months of ADT.
With further analysis, the researchers determined that for patients receiving radiation therapy without brachytherapy, the optimal ADT duration was 26.3 months; for those treated with radiation therapy and a brachytherapy boost, the minimum threshold was 12 months. Their hypotheses drawn from the retrospective study appeared to be supported by effects observed in the randomized clinical trials.
"Contrary to findings in a previous study, our results suggest that optimal duration of ADT for patients receiving high-dose radiation therapy may be more than 18 months. This is implied by findings from all the cohorts we analyzed. A secondary conclusion, based on the retrospective dataset, is that ADT duration shorter than 18 months may be sufficient for patients undergoing both radiation therapy and brachytherapy. Although current and future studies will continue to offer clarification, individual patient meta-analyses incorporating data from various trials may provide the best current guidance for doctors and patients. We have additional studies underway to explore this concept further," said Kishan.
Amar U. Kishan, Alison Steigler, James W. Denham, Almudena Zapatero, Araceli Guerrero, David Joseph, Xavier Maldonado, Jessica K. Wong, Bradley J. Stish, Robert T. Dess, Avinash Pilar, Chandana Reddy, Trude B. Wedde, Wolfgang A. Lilleby, Ryan Fiano, Gregory S. Merrick, Richard G. Stock, D. Jeffrey Demanes, Brian J. Moran, Phuoc T. Tran, Santiago Martin, Rafael Martinez-Monge, Daniel J. Krauss, Eyad I. Abu-Isa, Thomas M. Pisansky, C. Richard Choo, Daniel Y. Song, Stephen Greco, Curtiland Deville, Todd McNutt, Theodore L. DeWeese, Ashley E. Ross, Jay P. Ciezki, Derya Tilki, R. Jeffrey Karnes, Jeffrey J. Tosoian, Nicholas G. Nickols, Prashant Bhat, David Shabsovich, Jesus E. Juarez, Tommy Jiang, T. Martin Ma, Michael Xiang, Rebecca Philipson, Albert Chang, Patrick A. Kupelian, Matthew B. Rettig, Felix Y. Feng, Alejandro Berlin, Jonathan D. Tward, Brian J. Davis, Robert E. Reiter, Michael L. Steinberg, David Elashoff, Paul C. Boutros, Eric M. Horwitz, Rahul D. Tendulkar, Daniel E. Spratt, Tahmineh Romero. Interplay Between Duration of Androgen Deprivation Therapy and External Beam Radiotherapy With or Without a Brachytherapy Boost for Optimal Treatment of High-risk Prostate Cancer. JAMA Oncology, 2022; DOI: 10.1001/jamaoncol.2021.6871
If you are vaccinated againstCOVID-19, there is still a possibility of infection, but a lower risk of severe sickness, or of developing long-lasting symptoms from the disease, according to experts and research.
“Vaccination with at least two doses of COVID-19 vaccine was associated with a substantial decrease in reporting the most common post-acute COVID-19 symptoms,” the study authors said.
The study included more than 3,000 individuals who filled out an online questionnaire. Among the 637 vaccinated people who got COVID-19, they were less likely to report symptoms of fatigue, headache, weakness and persistent muscle pain compared to those who were unvaccinated and infected, the study said.
More than two years into the pandemic, experts are still trying to determine the impact of long COVID — when symptoms last at least a month after a person is diagnosed with COVID-19 — and learn how to help people suffering from it. Those people are often referred to as COVID long haulers.
COVID-19 ‘long-haulers’ describe shakes, trouble breathing weeks after testing positive
While the research — including this latest study — looking at the effectiveness of vaccinations on long-term symptoms is encouraging, experts say it remains inconclusive.
“I think there is a suggestion that those who are fully vaccinated are less likely to develop long COVID,” said Dr. Janna Williams, an infectious diseases specialist at Northwestern Medicine in Chicago.
This is because if you are fully immunized, the chances of contracting COVID-19 are reduced and since vaccines are highly effective at preventing severe disease, there is a smaller likelihood of developing debilitating symptoms that are associated with long COVID, she explained.
What does the science say?
Neuroplasticity expert Ashok Gupta has been researching long-haul COVID at the Gupta program, a global clinic helping people with chronic illnesses. He said this latest preprint from Israel is consistent with other studies.
“I think it’s still preliminary data, but it seems to be encouraging,” he said.
Gupta said if the body has already had a pre-warning of a coronavirus infection through vaccination and is able to recognize the virus, the body can then fend it off more effectively. And when the infection is not as severe, it may not lead to long COVID symptoms, he added.
Dr. Allison McGeer, an infectious disease physician at the Sinai Health System in Toronto, said there is some evidence that long COVID was less common in vaccinated people who got breakthrough infections with previous variants like Delta.
But the “jury is still out” on what role a person’s vaccination status can play in protecting them from long COVID, she said.
“We are seeing more of these papers and not all of the papers have this finding that there’s a substantial reduction, but I think more of them do than not,” she told Global News.
Italian “super taster” helping COVID-19 survivors regain sense of smell
A peer-reviewed U.K. study published in the Lancet medical journal in September 2021 found that the full two-dose series of a COVID-19 vaccine reduced the risk of persistent symptoms — lasting at least 28 days post-infection among those who got COVID-19.
According to data collected by the U.K. Office for National Statistics in October 2021, a first dose of a COVID-19 vaccine was associated with a 13 per cent decrease in the likelihood of self-reported long COVID, defined by researchers as symptoms persisting for at least 12 weeks after getting COVID-19. A second shot was associated with a nine per cent decline relative to the first.
However,another preprint paperfrom the U.S. that analyzed more than 10,000 breakthrough cases in November 2021 suggested that at least one dose of a COVID-19 vaccine did not offer protection against long-COVID features.
Complex condition
There are limitations to the findings with selection bias and subjective reporting occurring, according to Dr. Christopher Carlsten, a professor of medicine at the University of British Columbia and the director for Legacy for Airway Health.
McGeer said none of the studies so far are conclusive and more time and research are needed.
“Long COVID is a complex condition that people are just starting to work on understanding,” she said.
“So a piece of it is, it takes time to assess it, to really understand how we make the diagnosis.”
What makes it challenging to study this condition is the fact that there is no standardized definition of long COVID, experts say.
According to the World Health Organization (WHO), “post COVID-19 condition” occurs in individuals with a history of probable or confirmed SARS-CoV-2 infection, usually three months from the onset of COVID-19, with symptoms that last for at least two months and cannot be explained by an alternative diagnosis.
Long-haulers: Some kids struggle with lingering effects of COVID-19
Long-haulers: Some kids struggle with lingering effects of COVID-19 – Feb 19, 2021
Common symptoms associated with long COVID are fatigue, shortness of breath, chest discomfort, headaches, brain fog — a state of forgetfulness, poor concentration or feeling confused — memory loss, and muscle and joint pain, said Williams.
Some people may continue to test positive for COVID-19 as they suffer through long COVID, while others may not, she added.
Over the last year, experts said there have been a number of anecdotal stories about “long haulers” getting better after receiving the vaccine, but they have also heard the opposite too.
“There’s a small number of patients that feel like the vaccine has cured them of their illness, although that’s not persistent in all cases, either,” Dr. Jesse Greiner, medical director of the Post-COVID-19 Recovery Clinic at St. Paul’s Hospital in Vancouver, told Global News in December.
“It’s difficult to say because there’s still so much that we don’t understand about how long COVID works,” he said.
Despite the unanswered questions, Williams said everyone should get vaccinated, adding there is no detriment to the shots for those suffering from long COVID.
“Preventing the acquisition of COVID upfront is your best protection of preventing long COVID,” she said.
