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1.
Asia-Pacific Journal of Clinical Oncology ; 18(Supplement 4):42-44, 2022.
Article in English | EMBASE | ID: covidwho-2192240

ABSTRACT

Background: Older patients with cancer remain at high risk for negative outcomes from COVID-19 infection, particularly those who have multimorbidities and on immunosuppressive therapy. These patients have been excluded or underrepresented in pivotal COVID-19 vaccine clinical trials and there are ongoing concerns that they may not acquire the same level of protection from the available vaccines as the immunocompetent adults. Moreover, the level of protection wanes over time making them more susceptible to emerging COVID-19 novel variants of concern. Despite the implementation of global vaccination campaigns which have successfully reduced COVID-related hospitalisations and deaths in many parts of the world, there remains many unresolved issues and challenges to address as the pandemic ensues. With aging, concerns for age-related dysregulation and immune dysfunctions called immunosenescence may lead to potentially lower immunogenicity to vaccines. Despite receiving the primary vaccination, real-world evidence showed that both patients aged > 65 years and those with cancer have a higher risk of developing breakthrough COVID-19 infections and related complications. Subsequent booster doses are found to be effective at improving immune response, particularly against the novel variants, and the vulnerable population should be given the priority in booster campaigns. Method(s): Since the beginning of the pandemic in 2020, The International Society of Geriatric Oncology set up a COVID-19 Working Group comprised of multidisciplinary specialists by developing recommendations, advocacy, and action plans based on expert opinion and evidence related to older adults with cancer. Result(s): The table below summarises the updated recommendations from the SIOG COVID-19 Working Group. Conclusion(s): The SIOG COVID-19 Working Group supports ongoing public health interventions, continued mass immunisations, and booster campaigns targeting the most vulnerable members of the society, including older adults with cancer (Table Presented).

2.
Front Aging Neurosci ; 14: 934346, 2022.
Article in English | MEDLINE | ID: covidwho-2199033

ABSTRACT

Major depressive disorder (MDD) is a multifactorial disease affected by several environmental factors. Although several potential onset hypotheses have been identified, the molecular mechanisms underlying the pathogenesis of this disorder remain unclear. Several recent studies have suggested that among many environmental factors, inflammation and immune abnormalities in the brain or the peripheral tissues are associated with the onset of MDDs. Furthermore, several stress-related hypotheses have been proposed to explain the onset of MDDs. Thus, inflammation or immune abnormalities can be considered stress responses that occur within the brain or other tissues and are regarded as one of the mechanisms underlying the stress hypothesis of MDDs. Therefore, we introduce several current advances in inflammation studies in the brain that might be related to the pathophysiology of MDD due to stress exposure in this review.

3.
Vaccine ; 2022.
Article in English | ScienceDirect | ID: covidwho-2165923

ABSTRACT

With the emergence of the severe acute respiratory syndrome 2 (SARS-CoV-2) B.1.1.529/BA.1 (Omicron) variant in early 2022, Israel began vaccinating individuals 6o years of age or older with a fourth BNT162b2 vaccine. While the decision was based on little experimental data, longer follow-up showed clinical effectiveness of the fourth dose with reduction in the number of severely affected individuals. However, the immune response to fourth vaccine dose in this age group was not yet characterized, and little is known about the immunogenicity of repeated vaccine dosing in this age group. We therefore aimed to evaluate the humoral and cellular immune response pre- and 3-week post- the fourth vaccine dose in patients age 60 years or older. For this purpose, blood samples were collected from donors age 60 years or older, all received their 3rd vaccine dose 5 months prior. Serum samples were evaluated for the presence of anti-Spike protein (anti-S) antibodies (N = 133), and peripheral blood mononuclear cells (PBMCs) were evaluated by flow cytometry for their ability to respond to the SARS-CoV-2 wild type Spike-glycoprotein peptide mix, Membrane-glycoprotein (M) peptide mix and to the mutated Spike-regions of the Omicron variant (N = 34). Three weeks after the fourth vaccine dose, 24 out of 34 donors (70.5%) showed significant increase in the number of cells responding to the wild type S-peptide mix. Of note, out of 34 donors, 11 donors (32.3%) had pre-boost anti-M T-cell response, none of which had history of confirmed COVID-19, suggesting possible asymptomatic exposure. Interestingly, in M non-responding individuals, no statistically significant increase in the cellular response was observed following stimulation with omicron S-mutated regions. While there are limited data regarding the longevity of the observed response, our results are in accordance with the described clinical efficacy, provide mechanistic evidence to support it and argue against vaccine-induced or age-related immunosenescence.

4.
Ageing Research Reviews ; : 101818, 2022.
Article in English | ScienceDirect | ID: covidwho-2149340

ABSTRACT

The destructive effects of coronavirus disease 2019 (COVID-19) on the elderly and people with cardiovascular disease have been proven. New findings shed light on the role of aging pathways on life span and health age. New therapies that focus on aging-related pathways may positively impact the treatment of this acute respiratory infection. Using new therapies that boost the level of the immune system can support the elderly with co-morbidities against the acute form of COVID-19. This article discusses the effect of the aging immune system against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the pathways affecting this severity of infection.

5.
Aging: From Fundamental Biology to Societal Impact ; : 577-585, 2022.
Article in English | Scopus | ID: covidwho-2149086

ABSTRACT

Immunosenescence and inflammaging are two fundamental age-related changes substantially paving the way to accelerated aging, multidimensional frailty, and poor outcomes of several illnesses including COVID-19. A common misbelief is that immunosenescence and inflammaging, like other age-related changes, are exclusively detrimental. However, they are inserted in a highly complex landscape of physiological changes occurring with increasing age at the biomolecular, organismal, psychosocial, and functional level. The understanding of this complex picture is fundamental to develop strategies aimed at maintaining robustness. Groundbreaking descriptions of frailty paved the way to successful interventions to maintain and restore robustness. To date, frailty is well established as the very core of geriatric medicine, going far beyond multimorbidity and chronological age. © 2023 Elsevier Inc. All rights reserved.

6.
Immun Ageing ; 19(1): 56, 2022 Nov 15.
Article in English | MEDLINE | ID: covidwho-2139337

ABSTRACT

Immunosenescence is an age-dependent decline in immune functions and hallmark of aging in diverse species, ranging from invertebrates to mammals. However, identifying the factors responsible for immunosenescence is challenging because of the complexity of immune systems and aging in mammals. The roundworm Caenorhabditis elegans is suitable for understanding immunosenescence because of its simple immune system and rapid aging process. In this review, we discuss the advances in our understanding of immunosenescence in C. elegans. PMK-1/p38 mitogen-activated protein kinase (MAPK), SKN-1/NRF, and ZIP-10/bZIP transcription factor regulate immunosenescence through p38 MAPK and insulin/IGF-1 signaling pathways. Because these factors and pathways are evolutionarily conserved, the findings discussed in this review may help understand the mechanisms underlying immunosenescence and develop new treatment therapy for immunosenescence in humans.

7.
Psychiatr Clin North Am ; 45(4): 625-637, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-2132125

ABSTRACT

Severe acute respiratory syndrome coronavirus 2, the novel coronavirus responsible for the coronavirus disease (COVID-19), affects the brain. Neurologic and neuropsychiatric symptoms may manifest in the acute and post-acute phases of illness. The vulnerability of the brain with aging further increases the burden of disease in the elderly, who are at the highest risk of complications and death from COVID-19. The mechanisms underlying the effects of COVID-19 on the brain are not fully known. Emerging evidence vis-à-vis pathogenesis and etiologies of COVID-19 brain effects is promising and may pave the way for future research and development of interventions.


Subject(s)
COVID-19 , Humans , Aged , Brain/pathology , Aging
8.
Immun Ageing ; 19(1): 53, 2022 Nov 11.
Article in English | MEDLINE | ID: covidwho-2119459

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a respiratory infectious disease caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is characterized by having a heterogeneous disease course, ranging from asymptomatic and mild symptoms to more severe and critical cases. In most cases the severity of COVID-19 is related to host factors, especially deregulation of the immune response in patients. Even if COVID-19 indiscriminately affects individuals of different age group, ethnicity and economic status; most severe cases and disproportional mortality occur in elderly individuals. This point out that aging is one risk factor for unfavourable clinical outcomes among COVID-19 patients. The biology of aging is a complex process; Aging can alter the structure and function of cells, tissues, and organs resulting in impaired response to stress. Alongside with other systems, the immune system is also affected with the aging process. Immunosenescence is an age associated change in the immune system that affects the overall response to immunological challenges in the elderly. Similarly, apart from the normal inflammatory process, aging is associated with a low grade, sterile, chronic inflammation which is termed as inflammaging. We hypothesized that inflammaging and immunosenescence could play an important role in SARS-CoV-2 pathogenesis and poor recovery from COVID-19 in elderly individuals. This review summarizes the changes in the immune system with age and how these changes play part in the pathogenesis of SARS-CoV-2 and clinical outcome of COVID-19 which could add to the understanding of age associated targeted immunotherapy in the elderly.

9.
Ann Transl Med ; 10(20): 1142, 2022 Oct.
Article in English | MEDLINE | ID: covidwho-2100656

ABSTRACT

Background and Objective: Aging refers to a progressive decrease in functional performance, leading to increased mortality risk. At present, life expectancy is increasing worldwide and is expected to exceed 80 years by 2040. However, this increase in life expectancy also indicates a rise in the incidence and prevalence of diseases, such as cardiovascular, neurological, musculoskeletal, and oncological diseases, which are associated with aging. The exact underlying mechanisms of aging remain unknown, and whether it is a programmed process or the consequence of an accumulation of stress events remains unclear. Thus, more scientific research is needed to improve the management of complex and frail patients. Methods: Several databases were searched with the following key words: immunosenescence, inflamm-aging, frailty, sarcopenia and skeletal muscle, etc. Key Content and Findings: Skeletal muscle is the core phenotype of frailty and sarcopenia. Immune aging and skeletal muscle decline interplay with each other and form a vicious circle. Maintaining muscle health is beneficial for immune function and delays the onset of frailty. Particularly, in the context of the ongoing corona virus disease (COVID)-19 pandemic, studies have shown that the elderly are more prone to the consequences of the SARS-CoV-2 virus. It has been reported that the rates of hospitalization in the 65-74, 75-84, and ≥85 years old group were 5×, 8×, and 10× greater than the 18-29 years old group, with corresponding COVID-19-related deaths being 60×, 140×, and 330× that of the younger reference group, respectively. Considering the above, this review aims to discuss the relationship between immunosenescence, skeletal muscle, and frailty, and to explore immunosenescence as a potential therapeutic target to prevent frailty and extend healthspan, with some emphasis on the effects of the COVID-19 pandemic on the elderly. Conclusions: Immunosenescence is a promising potential therapeutic target for frailty and is worthy of further investigation.

10.
Brain Behav Immun ; 107: 361-368, 2022 Nov 05.
Article in English | MEDLINE | ID: covidwho-2095083

ABSTRACT

BACKGROUND: The COVID-19 pandemic has highlighted the urgent need to understand variation in immunosenescence at the population-level. Thus far, population patterns of immunosenescence have not well described. METHODS: We characterized measures of immunosenescence from the 2016 Venous Blood Study from the nationally representative U.S Health and Retirement Study (HRS) of individuals ages 50 years and older. RESULTS: Median values of the CD8+:CD4+, EMRA:Naïve CD4+ and EMRA:Naïve CD8+ ratios were higher among older participants and were lower in those with additional educational attainment. Generally, minoritized race and ethnic groups had immune markers suggestive of a more aged immune profile: Hispanics had a CD8+:CD4+ median value of 0.37 (95 % CI: 0.35, 0.39) compared to 0.30 in non-Hispanic Whites (95 % CI: 0.29, 0.31). Non-Hispanic Blacks had the highest median value of the EMRA:Naïve CD4+ ratio (0.08; 95 % CI: 0.07, 0.09) compared to non-Hispanic Whites (0.03; 95 % CI: 0.028, 0.033). In regression analyses, race/ethnicity and education were associated with large differences in the immune ratio measures after adjustment for age and sex. CONCLUSIONS: Lower educational attainment and minoritized racial ethnic status were associated with higher levels of immunosenescence. This population variation may have important implications for both risk of age-related disease and vulnerability to emerging pathogens (e.g., SARS-CoV-2).

11.
Lancet Healthy Longevity ; 3(7):E461-E469, 2022.
Article in English | Web of Science | ID: covidwho-2068426

ABSTRACT

Background Older age and frailty are risk factors for poor clinical outcomes following SARS-CoV-2 infection. As such, COVID-19 vaccination has been prioritised for individuals with these factors, but there is concern that immune responses might be impaired due to age-related immune dysregulation and comorbidity. We aimed to study humoral and cellular responses to COVID-19 vaccines in residents of long-term care facilities (LTCFs). Methods In this observational cohort study, we assessed antibody and cellular immune responses following COVID-19 vaccination in members of staff and residents at 74 LTCFs across the UK. Staff and residents were eligible for inclusion if it was possible to link them to a pseudo-identifier in the COVID-19 datastore, if they had received two vaccine doses, and if they had given a blood sample 6 days after vaccination at the earliest. There were no comorbidity exclusion criteria. Participants were stratified by age (<65 years or >= 65 years) and infection status (previous SARS-CoV-2 infection [infection-primed group] or SARS-CoV-2 naive [infection-naive group]). Anticoagulated edetic acid (EDTA) blood samples were assessed and humoral and cellular responses were quantified. Findings Between Dec 11, 2020, and June 27, 2021, blood samples were taken from 220 people younger than 65 years (median age 51 years [IQR 39-61];103 [47%] had previously had a SARS-CoV-2 infection) and 268 people aged 65 years or older of LTCFs (median age 87 years [80-92];144 [43%] had a previous SARS-CoV-2 infection). Samples were taken a median of 82 days (IQR 72-100) after the second vaccination. Antibody responses following dual vaccination were strong and equivalent between participants younger then 65 years and those aged 65 years and older in the infection-primed group (median 125 285 Au/mL [1128 BAU/mL] for <65 year olds vs 157 979 Au/mL [1423 BAU/mL] for >= 65 year olds;p=0.47). The antibody response was reduced by 2.4-times (467 BAU/mL;p <= 0.0001) in infection-naive people younger than 65 years and 8.1-times (174 BAU/mL;p <= 0.0001) in infection-naive residents compared with their infection-primed counterparts. Antibody response was 2.6-times lower in infection-naive residents than in infection-naive people younger than 65 years (p=0.0006). Impaired neutralisation of delta (1.617.2) variant spike binding was also apparent in infection-naive people younger than 65 years and in those aged 65 years and older. Spike-specific T-cell responses were also significantly enhanced in the infection-primed group. Infection-naive people aged 65 years and older (203 SFU per million [IQR 89-374]) had a 52% lower T-cell response compared with infection-naive people younger than 65 years (85 SFU per million [30-206];p <= 0.0001). Post-vaccine spike-specific CD4 T-cell responses displayed single or dual production of IFN-gamma and IL-2 were similar across infection status groups, whereas the infection-primed group had an extended functional profile with TNF alpha and CXCL10 production. Interpretation These data reveal suboptimal post-vaccine immune responses within infection-naive residents of LTCFs, and they suggest the need for optimisation of immune protection through the use of booster vaccination. Copyright (C) 2022 The Author(s). Published by Elsevier Ltd.

12.
Trials ; 23(1): 865, 2022 Oct 08.
Article in English | MEDLINE | ID: covidwho-2064838

ABSTRACT

BACKGROUND: In the ongoing COVID-19 pandemic, advanced age is a risk factor for a severe clinical course of SARS-CoV-2 infection. Thus, older people may benefit in particular from booster doses with potent vaccines and research should focus on optimal vaccination schedules. In addition to each individual's medical history, immunosenescence warrants further research in this population. This study investigates vaccine-induced immune response over 1 year. METHODS/DESIGN: EU-COVAT-1-AGED is a randomised controlled, adaptive, multicentre phase II protocol evaluating different booster strategies in individuals aged ≥75 years (n=600) already vaccinated against SARS-CoV-2. The initial protocol foresaw a 3rd vaccination (1st booster) as study intervention. The present modified Part B of this trial foresees testing of mRNA-1273 (Spikevax®) vs. BNT162b2 (Comirnaty®) as 4th vaccination dose (2nd booster) for comparative assessment of their immunogenicity and safety against SARS-CoV-2 wild-type and variants. The primary endpoint of the trial is to assess the rate of 2-fold antibody titre increase 14 days after vaccination measured by quantitative enzyme-linked immunosorbent assay (Anti-RBD-ELISA) against wild-type virus. Secondary endpoints include the changes in neutralising antibody titres (Virus Neutralisation Assay) against wild-type as well as against Variants of Concern (VOC) at 14 days and up to 12 months. T cell response measured by qPCR will be performed in subgroups at 14 days as exploratory endpoint. Biobanking samples are being collected for neutralising antibody titres against potential future VOC. Furthermore, potential correlates between humoral immune response, T cell response and neutralising capacity will be assessed. The primary endpoint analysis will be triggered as soon as for all patients the primary endpoint (14 days after the 4th vaccination dose) has been observed. DISCUSSION: The EU-COVAT-1-AGED trial Part B compares immunogenicity and safety of mRNA-1273 (Spikevax®) and BNT162b2 (Comirnaty®) as 4th SARS-CoV-2 vaccine dose in adults ≥75 years of age. The findings of this trial have the potential to optimise the COVID-19 vaccination strategy for this at-risk population. TRIAL REGISTRATION: ClinicalTrials.gov NCT05160766 . Registered on 16 December 2021. PROTOCOL VERSION: V06_0: 27 July 2022.


Subject(s)
COVID-19 , Vaccines , Adult , Aged , Antibodies, Neutralizing , Antibodies, Viral , BNT162 Vaccine , Biological Specimen Banks , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Clinical Trials, Phase II as Topic , Humans , Pandemics/prevention & control , Randomized Controlled Trials as Topic , SARS-CoV-2
13.
Quality of Life in Asia ; 16:83-104, 2022.
Article in English | Scopus | ID: covidwho-2048182

ABSTRACT

The elderly population is particularly susceptible to infectious diseases because of the declining immune response with age. The risk is even higher for elders with co-morbidities such as chronic lung diseases, diabetes mellitus, stroke and cancer. Furthermore, an increase in life expectancy in the elderly population results in an increase in adults residing in long stay care homes where cross infection and infectious disease outbreaks occur more frequently. Vaccination is the most effective strategy to prevent infections. Therefore, the elderly is an important target group for vaccination. Vaccination strategies vary among different countries. Nonetheless, most authorities recommend vaccination for the elderly against COVID-19, pneumococcus infection, seasonal influenza and herpes zoster. Some countries also recommend vaccination against diphtheria, tetanus and pertussis. In this chapter, we will review the justifications, efficacy, side effects and contraindications of these vaccines. Many people after retirement like to travel abroad. Vaccines against hepatitis A, encephalitis and meningococcus infection might be necessary and vaccination schedule should be individually modified for elders with cancer and other chronic diseases. Current vaccines are less immunogenic and effective for the elderly when compared with the younger adult population. We will discuss the challenges faced in improving the immune response and enhancing the coverage rate. © 2022, The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd.

14.
Aims Allergy and Immunology ; 6(3):170-187, 2022.
Article in English | Web of Science | ID: covidwho-2044069

ABSTRACT

The components of the immune system develop in utero and like a computer, some components are immediately functional (the innate components) but other components must learn the programs and details necessary to function (antigen adaptive components). Like other systems, including military and municipal, the innate and antigen specific components develop into an immune system that helps maintain and surveil the other body processes and systems for aberrations, provide surveillance and protection of the mucoepithelial borders and protection from microbial invasion. Inability, excesses, or errors in these processes cause disease. Aging of the immune system brings immunosenescence, inflammaging, more errors, and decreased surveillance which increases risk for new infections (e.g. COVID-19, influenza), recurrence of latent infections, cancer and autoimmune and inflammatory diseases. With greater understanding of the surveillance, effector and regulatory deficits upon aging, better therapies can be developed.

15.
Aging ; : 577-585, 2023.
Article in English | ScienceDirect | ID: covidwho-2041390

ABSTRACT

Immunosenescence and inflammaging are two fundamental age-related changes substantially paving the way to accelerated aging, multidimensional frailty, and poor outcomes of several illnesses including COVID-19. A common misbelief is that immunosenescence and inflammaging, like other age-related changes, are exclusively detrimental. However, they are inserted in a highly complex landscape of physiological changes occurring with increasing age at the biomolecular, organismal, psychosocial, and functional level. The understanding of this complex picture is fundamental to develop strategies aimed at maintaining robustness. Groundbreaking descriptions of frailty paved the way to successful interventions to maintain and restore robustness. To date, frailty is well established as the very core of geriatric medicine, going far beyond multimorbidity and chronological age.

16.
Front Immunol ; 13: 945016, 2022.
Article in English | MEDLINE | ID: covidwho-2022724

ABSTRACT

Immune system is a versatile and dynamic body organ which offers survival and endurance of human beings in their hostile living environment. However, similar to other cells, immune cells are hijacked by senescence. The ageing immune cells lose their beneficial functions but continue to produce inflammatory mediators which draw other immune and non-immune cells to the senescence loop. Immunosenescence has been shown to be associated with different pathological conditions and diseases, among which atherosclerosis has recently come to light. There are common drivers of both immunosenescence and atherosclerosis; e.g. inflammation, reactive oxygen species (ROS), chronic viral infections, genomic damage, oxidized-LDL, hypertension, cigarette smoke, hyperglycaemia, and mitochondrial failure. Chronic viral infections induce inflammaging, sustained cytokine signaling, ROS generation and DNA damage which are associated with atherogenesis. Accumulating evidence shows that several DNA and RNA viruses are stimulators of immunosenescence and atherosclerosis in an interrelated network. DNA viruses such as CMV, EBV and HBV upregulate p16, p21 and p53 senescence-associated molecules; induce inflammaging, metabolic reprogramming of infected cells, replicative senescence and telomere shortening. RNA viruses such as HCV and HIV induce ROS generation, DNA damage, induction of senescence-associated secretory phenotype (SASP), metabolic reprogramming of infected cells, G1 cell cycle arrest, telomere shortening, as well as epigenetic modifications of DNA and histones. The newly emerged SARS-CoV-2 virus is also a potent inducer of cytokine storm and SASP. The spike protein of SARS-CoV-2 promotes senescence phenotype in endothelial cells by augmenting p16, p21, senescence-associated ß-galactosidase (SA-ß-Gal) and adhesion molecules expression. The impact of SARS-CoV-2 mega-inflammation on atherogenesis, however, remains to be investigated. In this review we focus on the common processes in immunosenescence and atherogenesis caused by chronic viral infections and discuss the current knowledge on this topic.


Subject(s)
Atherosclerosis , COVID-19 , Immunosenescence , Atherosclerosis/metabolism , Endothelial Cells/metabolism , Humans , Inflammation/metabolism , Reactive Oxygen Species/metabolism , SARS-CoV-2
17.
Clin Infect Dis ; 2021 Dec 03.
Article in English | MEDLINE | ID: covidwho-2017792

ABSTRACT

BACKGROUND: Residents of nursing homes (NH) are at high risk of COVID-19 related morbidity and death and may respond poorly to vaccination because of old age and frequent comorbidities. METHODS: Seventy-eight residents and 106 staff members, naïve or previously infected with SARS-CoV-2, were recruited in NH in Belgium before immunization with two doses of 30µg BNT162b2 mRNA vaccine at day 0 and day 21. Binding antibodies (Ab) to SARS-CoV-2 receptor binding domain (RBD), spike domains S1 and S2, RBD Ab avidity, and neutralizing Ab against SARS-CoV-2 wild type and B.1.351 were assessed at days 0, 21, 28, and 49. RESULTS: SARS-CoV-2 naïve residents had lower Ab responses to BNT162b2 mRNA vaccination than naïve staff. These poor responses involved lower levels of IgG to all spike domains, lower avidity of RBD IgG, and lower levels of Ab neutralizing the vaccine strain. No naïve resident had detectable neutralizing Ab to the B.1.351 variant. In contrast, SARS-CoV-2 infected residents had high responses to mRNA vaccination, with Ab levels comparable to infected staff. Cluster analysis revealed that poor vaccine responders not only included naïve residents but also naïve staff, emphasizing the heterogeneity of responses to mRNA vaccination in the general population. CONCLUSIONS: The poor Ab responses to mRNA vaccination observed in infection naïve residents and in some naïve staff members of NH suggest suboptimal protection against breakthrough infection, especially with variants of concern. These data support the administration of a third dose of mRNA vaccine to further improve protection of NH residents against COVID-19.

18.
Mech Ageing Dev ; 204: 111672, 2022 06.
Article in English | MEDLINE | ID: covidwho-2015814

ABSTRACT

Ageing is associated with modified function of both innate and adaptive immunity. It is believed that changes occurring in ageing immune system are responsible for increased severity and deadliness of COVID-19 in the elderly. Although supported by statistics and epidemiology, these finding do not compute at the mechanistic level as depending solely on chronological and biological ageing. The phenomena describing changes in the aging immune system are immunosenescence and inflammageing, which develop in time depending on challenges to the individual immune system (immunobiography). Thus, "richer" immunobiography (in addition to other factors, including genetic, epigenetics or metabolic) may adversely affect the reactivity to the SARS-CoV-2 not only at later decades of life, but also earlier, in young and middle-aged individuals. On the other hand, infection with SARS-CoV-2 is affecting the function of both innate and adaptive branches of the immune system, adding to the individual immunobiography. Summarizing, immunosenescence and inflammaging may aggravate, but also may be aggravated by SARS-CoV-2 infection.


Subject(s)
COVID-19 , Immunosenescence , Adaptive Immunity , Aged , Aging , Humans , Middle Aged , SARS-CoV-2
19.
Frontiers in Immunology ; 13, 2022.
Article in English | EMBASE | ID: covidwho-2005865

ABSTRACT

Sparked by the development of genome sequencing technology, the quantity and quality of data handled in immunological research have been changing dramatically. Various data and database platforms are now driving the rapid progress of machine learning for immunological data analysis. Of various topics in immunology, T cell receptor repertoire analysis is one of the most important targets of machine learning for assessing the state and abnormalities of immune systems. In this paper, we review recent repertoire analysis methods based on machine learning and deep learning and discuss their prospects.

20.
Frontiers in Cardiovascular Medicine ; 9, 2022.
Article in English | EMBASE | ID: covidwho-2005852

ABSTRACT

Prolonged critical care stays commonly follow trauma, severe burn injury, sepsis, ARDS, and complications of major surgery. Although patients leave critical care following homeostatic recovery, significant additional diseases affect these patients during and beyond the convalescent phase. New cardiovascular and renal disease is commonly seen and roughly one third of all deaths in the year following discharge from critical care may come from this cluster of diseases. During prolonged critical care stays, the immunometabolic, inflammatory and neurohumoral response to severe illness in conjunction with resuscitative treatments primes the immune system and parenchymal tissues to develop a long-lived pro-inflammatory and immunosenescent state. This state is perpetuated by persistent Toll-like receptor signaling, free radical mediated isolevuglandin protein adduct formation and presentation by antigen presenting cells, abnormal circulating HDL and LDL isoforms, redox and metabolite mediated epigenetic reprogramming of the innate immune arm (trained immunity), and the development of immunosenescence through T-cell exhaustion/anergy through epigenetic modification of the T-cell genome. Under this state, tissue remodeling in the vascular, cardiac, and renal parenchymal beds occurs through the activation of pro-fibrotic cellular signaling pathways, causing vascular dysfunction and atherosclerosis, adverse cardiac remodeling and dysfunction, and proteinuria and accelerated chronic kidney disease.

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