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SNU-BioTalk 2025: Symphony of Cellular Signals in Metabolism and Immune Response – International Conference at Sister Nivedita University, Kolkata, India on 16 & 17 January 2025
Joint Convenor: Dr. Sudipta Saha (Member of LPBI since 2012)
About the Conference:
The International Conference on ‘Symphony of Cellular Signals in Metabolism and Immune Response’ focuses on the complex signalling pathways governing cellular functions in health and disease. It will explore the cellular mechanisms that regulate metabolism, immune responses, and survival, highlighting advances in medical science and biotechnology. Bringing together leading experts and emerging researchers, the conference will feature keynote lectures, panel discussions, research presentations, and interactive sessions, all designed to foster collaboration and innovation. By promoting an exchange of ideas, the event aims to drive transformative insights and solutions that impact human health and sustainable healthcare practices.
The conference will also be livestreamed on YouTube and Facebook
This programme will also host I-STEM: Indian Science, Technology and Engineering facilities Map (I-STEM) is a dynamic and interactive national portal for research cooperation.
Thrust areas:
Intracellular signalling processes of cellular metabolism
Signalling pathways in physiological and pathological processes
Powerful Cancer-Fighting Foods and Their Role in Body Repair
Curator: Dr. Sudipta Saha, Ph.D.
In the search for dietary approaches to prevent and fight cancer, certain foods have been found to possess potent anti-cancer properties. These foods not only help reduce the risk of cancer but also assist in repairing the body. Five such foods are green tea, broccoli like vetables, papaya, purple potatoes, and pomegranate—and the bioactive compounds responsible for their benefits.
1. Green Tea
Green tea, particularly rich in the catechin epigallocatechin gallate (EGCG), has gained considerable attention for its cancer-fighting properties. EGCG functions as a potent antioxidant, neutralizing free radicals and reducing oxidative stress, which is a key factor in the development of cancer. Studies suggest that EGCG can inhibit cancer cell proliferation by disrupting the signaling pathways essential for cell growth and survival, especially in breast, prostate, and colorectal cancers. Additionally, green tea has been shown to enhance the body’s immune function, making it more effective at targeting abnormal cells. EGCG induces apoptosis (programmed cell death) in cancer cells, halts angiogenesis (the formation of new blood vessels that nourish tumors), and inhibits metastasis (the spread of cancer cells to other parts of the body).
2. Broccoli and Cauliflower
Cruciferous vegetables like broccoli and cauliflower are rich in sulforaphane, a compound known for its detoxifying and anti-carcinogenic properties. Sulforaphane activates the body’s natural detoxification enzymes, which help eliminate carcinogens before they can damage cells. Moreover, it has been shown to inhibit the growth of various cancer cells, including those of the colon, breast, and prostate. Sulforaphane enhances the activity of phase II detoxification enzymes and induces apoptosis in cancer cells. It also inhibits histone deacetylase, an enzyme associated with cancer cell growth, thus preventing cancerous cells from replicating.
3. Papaya
Papaya is rich in carotenoids such as beta-carotene, lycopene, and beta-cryptoxanthin, which are powerful antioxidants. These compounds neutralize free radicals, reducing oxidative stress that can lead to cancer. Lycopene, in particular, has been linked to a lower risk of cancers, including those of the prostate, breast, and lung. Papaya also contains other bioactive compounds that help modulate immune responses, supporting the body’s ability to identify and destroy cancer cells. Carotenoids act by scavenging free radicals and reducing oxidative stress. Lycopene has also been shown to regulate cell cycle progression and inhibit growth factor signaling in cancer cells.
4. Purple Potatoes
Purple potatoes are unique due to their high levels of anthocyanins, which not only provide them with their distinctive color but also contribute to cancer prevention. Studies suggest that anthocyanins in purple potatoes help repair damaged tissues by promoting stem cell regeneration. They also have anti-inflammatory and anti-proliferative effects, which are crucial for halting cancer growth. Anthocyanins inhibit the growth of cancer cells by inducing cell cycle arrest and promoting the repair of damaged tissues through stem cell activation.
5. Pomegranate
Pomegranates are rich in ellagitannins, compounds that break down into ellagic acid in the body. Ellagic acid has been shown to possess anti-cancer properties by inhibiting tumor growth and promoting apoptosis in cancer cells. Pomegranate juice has demonstrated potential in reducing the progression of cancers such as breast and prostate cancer, due to its ability to suppress inflammation and oxidative stress. Ellagitannins and their metabolites inhibit cell proliferation and induce apoptosis. They also act by reducing inflammation and inhibiting the pathways involved in cancer cell survival and growth.
Conclusion
Incorporating foods like green tea, broccoli, papaya, purple potatoes, and pomegranates into your diet may help fight cancer and promote the repair of damaged tissues. The bioactive compounds found in these foods—EGCG, sulforaphane, carotenoids, anthocyanins, and ellagitannins—work through various mechanisms to inhibit cancer cell growth, induce apoptosis, and support the body’s natural repair processes. Including these nutrient-dense foods in your diet may contribute to overall health and resilience against cancer.
Xenotransplantation: Pioneering a New Era of Organ Availability
Reporter: Dr. Sudipta Saha, Ph.D.
The 2024 World Medical Innovation Forum (WMIF) spotlighted xenotransplantation as a transformative solution to the organ shortage crisis. By leveraging genetically modified pig organs, this emerging field offers a new source of transplants, expanding life-saving care options.
Key breakthroughs in 2024 have brought new hope for patients, but significant hurdles remain, including immunological rejection. Ongoing research focuses on developing immunosuppressive strategies and enhancing organ compatibility.
Collaboration between scientists, clinicians, and regulatory bodies is essential for xenotransplantation’s future. Experts predict wider clinical availability within the next decade, potentially reshaping organ replacement.
This revolutionary step in organ transplantation holds promise for patients and could redefine the future of transplant care globally. Here’s a comprehensive report covering the research contributions of the panelists from the Xenotransplantation: Game Changing Organ Replacement discussion:
1. Jason Gerberry
Specialty Pharma and SMid-Cap Biotech Analyst, BofA Global Research
Gerberry is a prominent financial analyst with deep expertise in specialty pharmaceuticals and small-to-mid-cap biotechnology firms. His research focuses on investment trends, market dynamics, and the financial viability of innovative medical solutions such as xenotransplantation. At WMIF 2024, he provided insights on how breakthroughs in the field could impact the biotech sector, including the potential for significant investments driven by advancements in gene editing and organ transplantation technologies. Gerberry’s analysis offers critical perspectives on the commercial and economic landscape surrounding xenotransplantation.
2. Joren Madsen, MD, PhD
Director, MGH Transplant Center
Paul S. Russell/Warner-Lambert Professor of Surgery, Harvard Medical School Dr. Madsen is a leader in transplant surgery and immunology. His research focuses on allograft rejection and immunosuppressive strategies to enhance transplant tolerance. He has been pivotal in advancing clinical transplant practices at Massachusetts General Hospital (MGH) and has made significant contributions to xenotransplantation research by exploring how genetically engineered pig organs could help mitigate immune rejection in human recipients. Madsen’s work is key to translating laboratory findings into clinical applications.
3. Tatsuo Kawai, MD, PhD
Director of the Legorreta Center for Clinical Transplantation Tolerance
A. Benedict Cosimi Chair in Transplant Surgery, MGH
Dr. Kawai specializes in immune tolerance and organ transplantation. His research emphasizes reducing or eliminating the need for lifelong immunosuppressive drugs in transplant patients. He has led groundbreaking clinical trials on tolerance induction, paving the way for the potential acceptance of xenotransplanted organs without rejection. His research is also closely tied to immune tolerance mechanisms and how xenotransplantation can be made safer for human use.
4. Richard Pierson III, MD
Scientific Director, Center for Transplantation Sciences, MGH
Professor of Surgery, Harvard Medical School
Dr. Pierson is renowned for his work in transplantation immunology, focusing on xenotransplantation. His research addresses the fundamental problem of immune rejection of animal organs in human bodies, particularly tackling hyperacute rejection and graft survival. Dr. Pierson has been instrumental in developing strategies to overcome these barriers by modifying pig genetics and using innovative immunosuppressive therapies, which have brought the field closer to clinical application.
5. Leonardo Riella, MD, PhD
Medical Director of Kidney Transplantation, MGH
Harold and Ellen Danser Endowed Chair in Transplantation, Harvard Medical School
Dr. Riella’s research focuses on kidney transplantation and immunosuppressive therapies aimed at improving long-term graft survival. He has been a significant contributor to the field of xenotransplantation, working on improving immune tolerance and understanding how kidneys from genetically modified pigs can function in human bodies without eliciting strong immune responses. His clinical and translational research is critical for the future of xenotransplantation, particularly in renal applications.
Conclusion
These panelists represent leading voices in xenotransplantation, combining their expertise in surgery, immunology, and biotechnology to address the complex challenges of organ transplantation. Their collaborative efforts at MGH and Harvard Medical School are critical in advancing the science of xenotransplantation, bringing it closer to a clinically viable solution for the global organ shortage crisis.
Regulatory T cells (Tregs) are important for sperm tolerance and male fertility
Reporter and Curator: Dr. Sudipta Saha, Ph.D.
Regulatory T cells (Tregs) are specialized immune cells that modulate tissue homeostasis. They are a specialized subset of T lymphocytes that function as suppressive immune cells and inhibit various elements of immune response in vitro and in vivo. While there are constraints on the number or function of Tregs which can be exploited to evoke an effective anti-tumor response, sufficient expansion of Tregs is essential for successful organ transplantation and for promoting tolerance of self and foreign antigens. Current studies have provided evidence that a defect in the number or function of Tregs contributes to the etiology of several reproductive diseases.
In the male reproductive tract, prevention of autoimmune responses against antigenic spermatozoa, while ensuring protection against stressors, is a key determinant of fertility. Using an autoimmunity-induced model, it was uncovered that the role of Tregs in maintaining the tolerogenic state of the testis and epididymis. The loss of tolerance induced an exacerbated immune cell infiltration and the development of anti-sperm antibodies, which caused severe male subfertility. By identifying immunoregulatory mechanisms in the testis and epididymis.
Tregs modulate tissue homeostatic processes and immune responses. Understanding tissue-Treg biology will contribute to developing precision-targeting treatment strategies. Here, it was reported that Tregs maintain the tolerogenic state of the testis and epididymis, where sperm are produced and mature. It was found that Treg depletion induces severe autoimmune orchitis and epididymitis, manifested by an exacerbated immune cell infiltration [CD4 T cells, monocytes, and mononuclear phagocytes (MPs)] and the development of anti-sperm antibodies (ASA).
In Treg-depleted mice, MPs increased projections toward the epididymal lumen as well as invading the lumen. ASA-bound sperm enhance sperm agglutination and might facilitate sperm phagocytosis. Tolerance breakdown impaired epididymal epithelial function and altered extracellular vesicle cargo, both of which play crucial roles in the acquisition of sperm fertilizing ability and subsequent embryo development. The affected mice had reduced sperm number and motility and severe fertility defects.
Deciphering these immunoregulatory mechanisms may lead to the development of therapies for infertility and identifying potential targets for immuno-contraception. Ultimately, such knowledge fills gaps related to reproductive mucosa, which is an understudied facet of human male health.
Eight Subcellular Pathologies driving Chronic Metabolic Diseases – Methods for Mapping Bioelectronic Adjustable Measurements as potential new Therapeutics: Impact on Pharmaceuticals in Use
In this curation we wish to present two breaking through goals:
Goal 1:
Exposition of a new direction of research leading to a more comprehensive understanding of Metabolic Dysfunctional Diseases that are implicated in effecting the emergence of the two leading causes of human mortality in the World in 2023: (a) Cardiovascular Diseases, and (b) Cancer
Goal 2:
Development of Methods for Mapping Bioelectronic Adjustable Measurements as potential new Therapeutics for these eight subcellular causes of chronic metabolic diseases. It is anticipated that it will have a potential impact on the future of Pharmaceuticals to be used, a change from the present time current treatment protocols for Metabolic Dysfunctional Diseases.
According to Dr. Robert Lustig, M.D, an American pediatric endocrinologist. He is Professor emeritus of Pediatrics in the Division of Endocrinology at the University of California, San Francisco, where he specialized in neuroendocrinology and childhood obesity, there are eight subcellular pathologies that drive chronic metabolic diseases.
These eight subcellular pathologies can’t be measured at present time.
In this curation we will attempt to explore methods of measurement for each of these eight pathologies by harnessing the promise of the emerging field known as Bioelectronics.
Unmeasurable eight subcellular pathologies that drive chronic metabolic diseases
Glycation
Oxidative Stress
Mitochondrial dysfunction [beta-oxidation Ac CoA malonyl fatty acid]
Insulin resistance/sensitive [more important than BMI], known as a driver to cancer development
Membrane instability
Inflammation in the gut [mucin layer and tight junctions]
Epigenetics/Methylation
Autophagy [AMPKbeta1 improvement in health span]
Diseases that are not Diseases: no drugs for them, only diet modification will help
Image source
Robert Lustig, M.D. on the Subcellular Processes That Belie Chronic Disease
These eight Subcellular Pathologies driving Chronic Metabolic Diseases are becoming our focus for exploration of the promise of Bioelectronics for two pursuits:
Will Bioelectronics be deemed helpful in measurement of each of the eight pathological processes that underlie and that drive the chronic metabolic syndrome(s) and disease(s)?
IF we will be able to suggest new measurements to currently unmeasurable health harming processes THEN we will attempt to conceptualize new therapeutic targets and new modalities for therapeutics delivery – WE ARE HOPEFUL
In the Bioelecronics domain we are inspired by the work of the following three research sources:
Michael Levin is an American developmental and synthetic biologist at Tufts University, where he is the Vannevar Bush Distinguished Professor. Levin is a director of the Allen Discovery Center at Tufts University and Tufts Center for Regenerative and Developmental Biology. Wikipedia
THE VOICE of Dr. Justin D. Pearlman, MD, PhD, FACC
PENDING
THE VOICE of Stephen J. Williams, PhD
Ten TakeAway Points of Dr. Lustig’s talk on role of diet on the incidence of Type II Diabetes
25% of US children have fatty liver
Type II diabetes can be manifested from fatty live with 151 million people worldwide affected moving up to 568 million in 7 years
A common myth is diabetes due to overweight condition driving the metabolic disease
There is a trend of ‘lean’ diabetes or diabetes in lean people, therefore body mass index not a reliable biomarker for risk for diabetes
Thirty percent of ‘obese’ people just have high subcutaneous fat. the visceral fat is more problematic
there are people who are ‘fat’ but insulin sensitive while have growth hormone receptor defects. Points to other issues related to metabolic state other than insulin and potentially the insulin like growth factors
At any BMI some patients are insulin sensitive while some resistant
Visceral fat accumulation may be more due to chronic stress condition
Fructose can decrease liver mitochondrial function
A methionine and choline deficient diet can lead to rapid NASH development
The female reproductive lifespan is regulated by the menstrual cycle. Defined as the interval between the menarche and menopause, it is approximately 35 years in length on average. Based on current average human life expectancy figures, and excluding fertility issues, this means that the female body can bear children for almost half of its lifetime. Thus, within this time span many individuals may consider contraception at some point in their reproductive life. A wide variety of contraceptive methods are now available, which are broadly classified into hormonal and non-hormonal approaches. A normal menstrual cycle is controlled by a delicate interplay of hormones, including estrogen, progesterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), among others. These molecules are produced by the various glands in the body that make up the endocrine system.
Hormonal contraceptives – including the contraceptive pill, some intrauterine devices (IUDs) and hormonal implants – utilize exogenous (or synthetic) hormones to block or suppress ovulation, the phase of the menstrual cycle where an egg is released into the uterus. Beyond their use as methods to prevent pregnancy, hormonal contraceptives are also being increasingly used to suppress ovulation as a method for treating premenstrual syndromes. Hormonal contraceptives composed of exogenous estrogen and/or progesterone are commonly administered artificial means of birth control. Despite many benefits, adverse side effects associated with high doses such as thrombosis and myocardial infarction, cause hesitation to usage.
Scientists at the University of the Philippines and Roskilde University are exploring methods to optimize the dosage of exogenous hormones in such contraceptives. Their overall aim is the creation of patient-specific minimizing dosing schemes, to prevent adverse side effects that can be associated with hormonal contraceptive use and empower individuals in their contraceptive journey. Their research data showed evidence that the doses of exogenous hormones in certain contraceptive methods could be reduced, while still ensuring ovulation is suppressed. Reducing the total exogenous hormone dose by 92% in estrogen-only contraceptives, or the total dose by 43% in progesterone-only contraceptives, prevented ovulation according to the model. In contraceptives combining estrogen and progesterone, the doses could be reduced further.
Mimicking vaginal cells and microbiome interactions on chip microfluidic culture
Reporter and Curator: Dr. Sudipta Saha, Ph.D.
Scientists at Harvard University’s Wyss Institute for Biologically Inspired Engineering have developed the world’s first “vagina-on-a-chip,” which uses living cells and bacteria to mimic the microbial environment of the human vagina. It could help to test drugs against bacterial vaginosis, a common microbial imbalance that makes millions of people more susceptible to sexually transmitted diseases and puts them at risk of preterm delivery when pregnant. Vaginal health is difficult to study in a laboratory setting partly because laboratory animals have “totally different microbiomes” than humans. To address this, scientists have created an unique chip, which is an inch-long, rectangular polymer case containing live human vaginal tissue from a donor and a flow of estrogen-carrying material to simulate vaginal mucus.
The organs-on-a-chip mimic real bodily function, making it easier to study diseases and test drugs. Previous examples include models of the lungs and the intestines. In this case, the tissue acts like that of a real vagina in some important ways. It even responds to changes in estrogen by adjusting the expression of certain genes. And it can grow a humanlike microbiome dominated by “good” or “bad” bacteria. The researchers have demonstrated that Lactobacilli growing on the chip’s tissue help to maintain a low pH by producing lactic acid. Conversely, if the researchers introduce Gardnerella, the chip develops a higher pH, cell damage and increased inflammation: classic bacterial vaginosis signs. So, the chip can demonstrate how a healthy / unhealthy microbiome affects the vagina.
The next step is personalization or subject specific culture from individuals. The chip is a real leap forward, it has the prospect of testing how typical antibiotic treatments against bacterial vaginosis affect the different bacterial strains. Critics of organ-on-a-chip technology often raise the point that it models organs in isolation from the rest of the body. There are limitations such as many researchers are interested in vaginal microbiome changes that occur during pregnancy because of the link between bacterial vaginosis and labor complications. Although the chip’s tissue responds to estrogen, but it does not fully mimic pregnancy without feedback loops from other organs. The researchers are already working on connecting the vagina chip to a cervix chip, which could better represent the larger reproductive system.
All these information indicate that the human vagina chip offers a new model to study host-vaginal microbiome interactions in both optimal and non-optimal states, as well as providing a human relevant preclinical model for development and testing of reproductive therapeutics, including live bio-therapeutics products for bacterial vaginosis. This microfluidic human vagina chip that enables flow through an open epithelial lumen also offers a unique advantage for studies on the effect of cervicovaginal mucus on vaginal health as clinical mucus samples or commercially available mucins can be flowed through this channel. The role of resident and circulating immune cells in host-microbiome interactions also can be explored by incorporating these cells into the vagina chip in the future, as this has been successfully done in various other organ chip models.
Sperm damage and fertility problem due to COVID-19
Reporter and Curator: Dr. Sudipta Saha, Ph.D.
Many couples initially deferred attempts at pregnancy or delayed fertility care due to concerns about coronavirus disease 2019 (COVID-19). One significant fear during the COVID-19 pandemic was the possibility of sexual transmission. Many couples have since resumed fertility care while accepting the various uncertainties associated with severe acute respiratory syndrome coronavirus 2 (SARS-Cov2), including the evolving knowledge related to male reproductive health. Significant research has been conducted exploring viral shedding, tropism, sexual transmission, the impact of male reproductive hormones, and possible implications to semen quality. However, to date, limited definitive evidence exists regarding many of these aspects, creating a challenging landscape for both patients and physicians to obtain and provide the best clinical care.
According to a new study, which looked at sperm quality in patients who suffered symptomatic coronavirus (COVID-19) infections, showed that it could impact fertility for weeks after recovery from the virus. The data showed 60% COVID-19 infected men had reduction in sperm motility and 37% had drop in sperm count, but, 2 months after recovery from COVID-19 the value came down to 28% and 6% respectively. The researchers also of the view that COVID-19 could not be sexually transmitted through semen after a person had recovered from illness. Patients with mild and severe cases of COVID-19 showed similar rate of drop in sperm quality. But further work is required to establish whether or not COVID-19 could have a longer-term impact on fertility. The estimated recovery time is three months, but further follow-up studies are still required to confirm this and to determine if permanent damage occurred in a minority of men.
Some viruses like influenza are already known to damage sperm mainly by increasing body temperature. But in the case of COVID-19, the researchers found no link between the presence or severity of fever and sperm quality. Tests showed that higher concentrations of specific COVID-19 antibodies in patients’ blood serum were strongly correlated with reduced sperm function. So, it was believed the sperm quality reduction cause could be linked to the body’s immune response to the virus. While the study showed that there was no COVID-19 RNA present in the semen of patients who had got over the virus, the fact that antibodies were attacking sperm suggests the virus may cross the blood-testis barrier during the peak of an infection.
It was found in a previous report that SARS-CoV-2 can be present in the semen of patients with COVID-19, and SARS-CoV-2 may still be detected in the semen of recovering patients. Due to imperfect blood-testes/deferens/epididymis barriers, SARS-CoV-2 might be seeded to the male reproductive tract, especially in the presence of systemic local inflammation. Even if the virus cannot replicate in the male reproductive system, it may persist, possibly resulting from the privileged immunity of testes.
If it could be proved that SARS-CoV-2 can be transmitted sexually in future studies, sexual transmission might be a critical part of the prevention of transmission, especially considering the fact that SARS-CoV-2 was detected in the semen of recovering patients. Abstinence or condom use might be considered as preventive means for these patients. In addition, it is worth noting that there is a need for studies monitoring fetal development. Therefore, to avoid contact with the patient’s saliva and blood may not be enough, since the survival of SARS-CoV-2 in a recovering patient’s semen maintains the likelihood to infect others. But further studies are required with respect to the detailed information about virus shedding, survival time, and concentration in semen.
The Framingham Study: Across 6 Decades, Cardiovascular Disease Among Middle-Aged Adults – mean life expectancy increased and the RLR of ASCVD decreased. Effective primary prevention efforts and better screening increased.
Reporter: Aviva Lev-Ari, PhD, RN
UPDATED on 8/27/2023
Cardiovascular disease & why we should change the way we assess risk | The Peter Attia Drive Podcast
Background: The remaining lifetime risk (RLR) is the probability of developing an outcome over the remainder of one’s lifespan at any given age. The RLR for atherosclerotic cardiovascular disease (ASCVD) in three 20-year periods were assessed using data from a single community-based cohort study of predominantly White participants
Methods: Longitudinal data from the Framingham study in 3 epochs (epoch 1, 1960-1979; epoch 2, 1980-1999; epoch 3, 2000-2018) were evaluated. The RLR of a first ASCVD event (myocardial infarction, coronary heart disease death, or stroke) from 45 years of age (adjusting for competing risk of death) in the 3 epochs were compared overall, and according to the following strata: sex, body mass index, blood pressure and cholesterol categories, diabetes, smoking, and Framingham risk score groups.
Results: There were 317 849 person-years of observations during the 3 epochs (56% women; 94% White) and 4855 deaths occurred. Life expectancy rose by 10.1 years (men) to 11.9 years (women) across the 3 epochs. There were 1085 ASCVD events over the course of 91 330 person-years in epoch 1, 1330 ASCVD events over the course of 107 450 person years in epoch 2, and 775 ASCVD events over the course of 119 069 person-years in epoch 3. The mean age at onset of first ASCVD event was greater in the third epoch by 8.1 years (men) to 10.3 years (women) compared with the first epoch. The RLR of ASCVD from 45 years of age declined from 43.7% in epoch 1 to 28.1% in epoch 3 (P<0.0001), a finding that was consistent in both sexes (RLR [epoch 1 versus epoch 3], 36.3% versus 26.5% [women]; 52.5% versus 30.1% [men]; P<0.001 for both). The lower RLR of ASCVD in the last 2 epochs was observed consistently across body mass index, blood pressure, cholesterol, diabetes, smoking, and Framingham risk score strata (P<0.001 for all). The RLR of coronary heart disease events and stroke declined in both sexes (P<0.001).
Conclusions: Over the past 6 decades, mean life expectancy increased and the RLR of ASCVD decreased in the community based, predominantly White Framingham study. The residual burden of ASCVD underscores the importance of continued and effective primary prevention efforts with better screening for risk factors and their effective treatment.
Comparative Study: Four SARS-CoV-2 vaccines induce quantitatively different antibody responses against SARS-CoV-2 variants
Reporter: Aviva Lev- Ari, PhD, RN
Marit J. van Gils, A. H. Ayesha Lavell, Karlijn van der Straten, Brent Appelman, Ilja Bontjer, Meliawati Poniman, Judith A. Burger, Melissa Oomen, Joey H. Bouhuijs, Lonneke A. van Vught, Marleen A. Slim, Michiel Schinkel, Elke Wynberg, Hugo D.G. van Willigen, Marloes Grobben, Khadija Tejjani, Jonne Snitselaar, Tom G. Caniels, Amsterdam UMC COVID-19 S3/HCW study group, Alexander P. J. Vlaar, Maria Prins, Menno D. de Jong, Godelieve J. de Bree, Jonne J. Sikkens, Marije K. Bomers, Rogier W. Sanders doi:https://doi.org/10.1101/2021.09.27.21264163
Abstract
Emerging and future SARS-CoV-2 variants may jeopardize the effectiveness of vaccination campaigns. We performed a head-to-head comparison of the ability of sera from individuals vaccinated with either one of four vaccines (BNT162b2, mRNA-1273, AZD1222 or Ad26.COV2.S) to recognize and neutralize the four SARS-CoV-2 variants of concern (VOCs; Alpha, Beta, Gamma and Delta). Four weeks after completing the vaccination series, SARS-CoV-2 wild-type neutralizing antibody titers were highest in recipients of BNT162b2 and mRNA-1273 (median titers of 1891 and 3061, respectively), and substantially lower in those vaccinated with the adenovirus vector-based vaccines AZD1222 and Ad26.COV2.S (median titers of 241 and 119, respectively). VOCs neutralization was reduced in all vaccine groups, with the largest (5.8-fold) reduction in neutralization being observed against the Beta variant. Overall, the mRNA vaccines appear superior to adenovirus vector-based vaccines in inducing neutralizing antibodies against VOCs four weeks after the final vaccination.
Figure 2:Binding and neutralization titers post-vaccination against VOCs.
(A) Median with interquartile range of binding titers to wild-type and VOCs S proteins represented as mean fluorescence intensity (MFI) of 1:100,000 diluted sera collected four-five weeks after full vaccination for the four vaccination groups. The lower cutoff for binding was set at an MFI of 10 (grey shading). Vaccine groups are indicated by colors with BNT162b2 in green, mRNA-1273 in purple, AZD1222 in orange and Ad26.COV2.S in blue. (B) Median with interquartile range of half-maximal neutralization (ID50) titers of D614G and VOCs pseudoviruses for sera collected after full vaccination for the four vaccination groups. The lower cutoff for neutralization was set at an ID50 of 100 (grey shading). Vaccine groups are indicated by colors with BNT162b2 in green, mRNA-1273 in purple, AZD1222 in orange and Ad26.COV2.S in blue. (C) Median ID50 neutralization of D614G and VOCs plotted against the reported vaccine efficacy against symptomatic infection2–5,12–17. Vaccine groups are indicated by colors with BNT162b2 in green, mRNA-1273 in purple, AZD1222 in orange and Ad26.COV2.S in blue. Circles represent WT data, squares for Alpha, diamond for Beta, nabla triangle for Gamma and delta triangle for Delta. Spearman’s rank correlation coefficient with p value are indicated. The result of the AZD1222 phase 3 trial conducted in South Africa, demonstrating poor (10%) efficacy against Beta variant, is not shown.
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