scholarly journals SARS-CoV-2 seroprevalence and characteristics of post-infection immunity in a general population cohort study in Catalonia, Spain.

Author(s):  
Marianna Karachaliou ◽  
Gemma Moncunill ◽  
Ana Espinosa ◽  
Gemma Castaño-Vinyals ◽  
Alfons Jiménez ◽  
...  

Abstract Sparse data exist on the complex natural immunity to SARS-CoV-2 at the population level. We applied a well-validated multiplex serology test in 5000 participants of a general population study in Catalonia in blood samples collected from end June to mid November 2020. Based on responses to fifteen isotype-antigen combinations, we detected a seroprevalence of 18.1% in adults (n=4740), and modeled extrapolation to the general population of Catalonia indicated a 15.3% seroprevalence. Antibodies persistedup to 9 months after infection. Immune profiling of infected individuals revealed that with increasing severity of infection (asymptomatic, 1-3 symptoms, ≥4 symptoms, admitted to hospital/ICU), seroresponses were more robust and rich with a shift towardsIgG over IgA and anti-spike over anti-nucleocapsid responses. Among seropositive participants, lower antibody levels were observed for those ≥60 years vs <60 years old and smokers vs non-smokers. Overweight/obese participants vs normal weight had higher antibody levels. Adolescents (13-15 years old) (n=260) showed aseroprevalence of 11.5%, were less likely to be tested seropositive compared to their parentsand had dominant anti-spike rather than anti-nucleocapside IgG responses. Our study provides an unbiased estimate of SARS-CoV-2 seroprevalence in Catalonia and new evidence on the durability and heterogeneity of post-infection immunity.

2021 ◽  
Author(s):  
Marianna Karachaliou ◽  
Gemma Moncunill ◽  
Ana Espinosa ◽  
Gemma Vinyals ◽  
Alfons Jiménez ◽  
...  

Abstract Sparse data exist on the complex natural immunity to SARS-CoV-2 at the population level. We applied a well-validated multiplex serology test in 5000 participants of a general population study in Catalonia in blood samples collected from end June to mid November 2020. We detected a seroprevalence of 18.1% in adults (n=4740), and modeled extrapolation to the general population of Catalonia indicated a 15.3% seroprevalence. Antibodies persisted up to 9 months after infection. Immune profiling of infected individuals revealed that with increasing severity of infection (asymptomatic, 1-3 symptoms, ≥4 symptoms, admitted to hospital/ICU), seroresponses were more robust with a shift towards IgG over IgA and anti-spike over anti-nucleocapsid responses. Seropositive smokers showed lower seroresponses than non-smokers. In adolescents (n=260) seroprevalence was 11.5% and IgG anti-spike responses were dominant. Our study provides an unbiased estimate of SARS-CoV-2 seroprevalence in Catalonia and new evidence on the durability and heterogeneity of post-infection immunity.


PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0255649
Author(s):  
Adele Warrilow ◽  
Geoff Der ◽  
Sally-Ann Cooper ◽  
Helen Minnis ◽  
Jill P. Pell

Background Individual neurodevelopmental disorders are associated with premature mortality. Little is known about the association between multiple neurodevelopmental markers and premature mortality at a population level. The ESSENCE (Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations) approach considers multiple neurodevelopmental parameters, assessing several markers in parallel that cluster, rather than considering individual diagnostic categories in isolation. Objectives To determine whether childhood neurodevelopmental markers, including reduced intellectual functioning, are associated with all-cause premature mortality. Methods and procedures In a general population cohort study (n = 12,150) with longitudinal follow up from childhood to middle age, Cox proportional hazard models were used to study the associations between childhood neurodevelopmental markers (Rutter B scale and IQ) and premature all-cause mortality. Outcomes and results The cognitive measures and 21 of the 26 Rutter B items were significantly associated with premature mortality in bivariate analyses with hazard ratios from 1.24 (95% CI 1.05–1.47) to 2.25 (95% CI 1.78–2.90). In the final adjusted model, neurodevelopmental markers suggestive of several domains including hyperactivity, conduct problems and intellectual impairment were positively associated with premature mortality and improved prediction of premature mortality. Conclusions A wide range of neurodevelopmental markers, including childhood IQ, were found to predict premature mortality in a large general population cohort with longitudinal follow up to 60–65 years of age. Implications These findings highlight the importance of a holistic assessment of children with neurodevelopmental markers that addresses a range of neurodevelopmental conditions. Our findings could open the door to a shift in child public mental health focus, where multiple and/or cumulative markers of neurodevelopmental conditions alert clinicians to the need for early intervention. This could lead to a reduction in the risk of broad health outcomes at a population level.


2016 ◽  
Vol 62 (2) ◽  
pp. 335-342 ◽  
Author(s):  
Jeppe Zacho ◽  
Thomas Benfield ◽  
Anne Tybjærg-Hansen ◽  
Børge G Nordestgaard

AbstractBACKGROUNDThe acute-phase reactant C-reactive protein (CRP) increases rapidly during an infection. We tested the hypothesis that chronic low-level increases in CRP are associated with an increased risk of infectious disease.METHODSWe studied 9660 individuals from a prospective general population cohort, including 3592 in whom infectious disease developed, and another 60 896 individuals from a cross-sectional general population study, of whom 13 332 developed infectious disease; 55% were women, and the mean age was 57 years. Hospital diagnoses of infections in 1977–2010 were based on International Classification of Diseases–coded discharge records from the national Danish Patient Registry. We measured CRP concentrations and conducted genotyping for 4 CRP polymorphisms that increase CRP. Individuals with CRP &gt;10 mg/L were excluded because of possible ongoing infection at the time of testing.RESULTSIndividuals with CRP &gt;3 mg/L had 1.2 and 1.7 times increased risk of infectious disease, in the prospective general population cohort and the cross-sectional general population study, respectively, compared with individuals with CRP &lt;1 mg/L. In the combined populations, individuals in the highest CRP tertile (compared with the lowest) had an increased risk of bacterial diseases (hazard ratio 1.7, 95% CI 1.6–1.8), but not viral, mycosis, and parasitic diseases. The increased risk was mainly carried by pneumonia, sepsis, and particularly gram-negative infections. None of the genotype combinations examined conferred an increased risk of infectious disease.CONCLUSIONSChronic low-level CRP increases were associated with increased risk of bacterial infections, gram-negative infections in particular. Genotypes associated with increases in CRP were not associated with increased risk of infection.


2018 ◽  
Vol 64 (1) ◽  
pp. 219-230 ◽  
Author(s):  
Anette Varbo ◽  
Jacob J Freiberg ◽  
Børge G Nordestgaard

Abstract BACKGROUND We tested whether high remnant cholesterol is associated with high myocardial infarction risk, independent of whether an individual is normal weight, overweight, or obese. METHODS A total of 106216 individuals from the Copenhagen General Population Study were followed for up to 11 years, during which 1565 experienced a myocardial infarction. Individuals were grouped by clinically meaningful remnant cholesterol concentrations of &lt;0.5 mmol/L (19 mg/dL), 0.5 to 0.99 mmol/L (19–38 mg/dL), 1.0 to 1.49 mmol/L (39–58 mg/dL), and ≥1.5 mmol/L (58 mg/dL), and by body mass index (BMI) of &lt;18.5 kg/m2 (underweight), 18.5 to 24.9 kg/m2 (normal weight), 25 to 29.9 kg/m2 (overweight), and ≥30 kg/m2 (obese). RESULTS Median calculated remnant cholesterol was 0.40 mmol/L [interquartile range (IQR), 0.30–0.55 mmol/L] [15 mg/dL (12–21 mg/dL)] for underweight, 0.50 mmol/L (IQR, 0.37–0.71 mmol/L) [19 mg/dL (14–27 mg/dL)] for normal weight, 0.70 mmol/L (IQR, 0.49–1.00 mmol/L) [27 mg/dL (19–39 mg/dL)] for overweight, and 0.85 mmol/L (IQR, 0.61–1.20 mmol/L) [(33 mg/dL (24–46 mg/dL)] for obese individuals. On continuous scales, remnant cholesterol was positively correlated with BMI until reaching a plateau of approximately 1 mmol/L (39 mg/dL) at BMI &gt;35 kg/m2. R2 from an unadjusted linear regression for the correlation between calculated remnant cholesterol and BMI was 12%. Stepwise higher remnant cholesterol was associated with stepwise higher myocardial infarction risk in a similar pattern for normal weight, overweight, and obese individuals. When compared with individuals with remnant cholesterol &lt;0.5 mmol/L (19 mg/dL), individuals with remnant cholesterol ≥1.5 mmol/L (58 mg/dL) had hazard ratios for myocardial infarction of 2.0 (95% CI, 1.3–3.2) for normal weight, 1.9 (95% CI, 1.4–2.6) for overweight, and 2.3 (95% CI, 1.4–3.5) for obese individuals. Directly measured remnant cholesterol increased 0.91 mmol/L (95% CI, 0.89–0.94 mmol/L) [35 mg/dL (34–36 mg/dL)] per 1 mmol/L (39 mg/dL) increase in calculated remnant cholesterol. CONCLUSIONS Remnant cholesterol and BMI were positively correlated; however, high remnant cholesterol was associated with higher myocardial infarction risk across the examined BMI subcategories, indicating that remnant cholesterol is a risk factor for myocardial infarction independent of overweight and obesity.


Thorax ◽  
2021 ◽  
pp. thoraxjnl-2020-216351
Author(s):  
Eskild Morten Landt ◽  
Yunus Çolak ◽  
Børge G Nordestgaard ◽  
Peter Lange ◽  
Morten Dahl

BackgroundObese individuals may be at higher risk of chronic cough. We investigated the risk and impact of chronic cough in obese individuals from the general population.MethodsWe recorded chronic cough, body mass index (BMI) and other related clinical conditions in 44 554 adults from the Copenhagen General Population Study. Individuals with asthma and/or chronic obstructive pulmonary disease were excluded (n=10 977). BMI was divided into: underweight (BMI <18.5 kg/m2), normal weight (18.5–24.9 kg/m2), overweight (25.0–29.9 kg/m2), obese (30.0–34.9 kg/m2) and severely obese (≥35.0 kg/m2).ResultsAmong 33 577 adults from the general population, 27 829 (83%) were non-obese and 5748 (17%) were obese. Compared with individuals with normal weight, multivariable adjusted ORs for chronic cough risk were 1.4 (95% CI 1.2 to 1.6) in overweight, 1.9 (95% CI 1.7 to 2.2) in obese and 2.6 (95% CI 2.1 to 3.2) in severely obese individuals. Mediation analyses showed that chronic cough due to obesity was up to 23% mediated by gastro-oesophageal reflux disease (GERD). Other mediators included low vegetable intake with 10% and occupational exposure with 8%. Among obese individuals, those with versus without chronic cough had worse accompanying respiratory symptoms, more often comorbidities including GERD and diabetes, greater healthcare utilisations, lower lung function and higher blood inflammation (all p<0.05).ConclusionThere is dose–response relationship between BMI and chronic cough, and chronic cough risk is twofold to threefold higher in obese individuals from the general population. This increased risk was partly mediated by GERD, low vegetable intake and occupational exposure, supporting that there may be benefit to gain by ameliorating some of these factors in obese individuals with chronic cough.


Redox Biology ◽  
2021 ◽  
Vol 41 ◽  
pp. 101895
Author(s):  
Anders L. Sørensen ◽  
Hans C. Hasselbalch ◽  
Mads Emil Bjørn ◽  
Claus H. Nielsen ◽  
Sabrina Cordua ◽  
...  

Author(s):  
Amedeo Minichino ◽  
Matthew A. Jackson ◽  
Marta Francesconi ◽  
Claire J. Steves ◽  
Cristina Menni ◽  
...  

AbstractAnhedonia and amotivation are debilitating symptoms and represent unmet therapeutic needs in a range of clinical conditions. The gut-microbiome-endocannabinoid axis might represent a potential modifiable target for interventions. Based on results obtained from animal models, we tested the hypothesis that the endocannabinoid system mediates the association between gut-microbiome diversity and anhedonia/amotivation in a general population cohort. We used longitudinal data collected from 786 volunteer twins recruited as part the TwinsUK register. Our hypothesis was tested with a multilevel mediation model using family structure as random intercept. The model was set using alpha diversity (within-individual gut-microbial diversity) as predictor, serum and faecal levels of the endocannabinoid palmitoylethanolamide (PEA) as mediator, and anhedonia/amotivation as outcome. PEA is considered the endogenous equivalent of cannabidiol, with increased serum levels believed to have anti-depressive effects, while increased stool PEA levels, reflecting increased excretion, are believed to have opposite, detrimental, effects on mental health. We therefore expected that either reduced serum PEA or increased stool PEA would mediate the association between microbial diversity and anhedonia amotivation. Analyses were adjusted for obesity, diet, antidepressant use, sociodemographic and technical covariates. Data were imputed using multiple imputation by chained equations. Mean age was 65.2 ± 7.6; 93% of the sample were females. We found a direct, significant, association between alpha diversity and anhedonia/amotivation (β = −0.37; 95%CI: −0.71 to −0.03; P = 0.03). Faecal, but not serum, levels of the endocannabinoid palmitoylethanolamide (PEA) mediated this association: the indirect effect was significant (β = −0.13; 95%CI: −0.24 to −0.01; P = 0.03), as was the total effect (β = −0.38; 95%CI: −0.72 to −0.04; P = 0.03), whereas the direct effect of alpha diversity on anhedonia/amotivation was attenuated fully (β = −0.25; 95%CI: −0.60 to 0.09; P = 0.16). Our results suggest that gut-microbial diversity might contribute to anhedonia/amotivation via the endocannabinoid system. These findings shed light on the biological underpinnings of anhedonia/amotivation and suggest the gut microbiota-endocannabinoid axis as a promising therapeutic target in an area of unmet clinical need.


2007 ◽  
Vol 156 (6) ◽  
pp. 631-636 ◽  
Author(s):  
Gerasimos E Krassas ◽  
Konstantinos Tziomalos ◽  
Nikolaos Pontikides ◽  
Hadas Lewy ◽  
Zvi Laron

Objective: We aimed to test the viral hypothesis in the pathogenesis of autoimmune thyroid disease (AITD). Design: We determined the pattern of month of birth (MOB) distribution in patients with AITD and in the general population and searched for differences between them. Methods: A total of 1023 patients were included in this study; 359 patients had Graves’ hyperthyroidism (GrH) and 664 had Hashimoto’s hypothyroidism (HH). We divided the patients with HH into three subgroups according to their thyroid peroxidase (TPO) antibody titers at diagnosis: low levels (<500 IU/ml), high levels (500–1000 IU/ml), and extremely high levels (>1000 IU/ml). We used cosinor analysis to analyze the data. Results: Overall, patients with GrH and HH had a different pattern of MOB distribution when compared with the general population and between groups. Furthermore, among both patients with GrH and HH, both genders had a different pattern of MOB distribution when compared with the general population and this pattern was also different between genders. Finally, only women with extremely high titers of TPO antibodies at diagnosis and men with low or extremely high TPO antibody levels showed rhythmicity in MOB, with a pattern of MOB distribution different from that in controls. Conclusions: The different MOB seasonality in both GrH and HH points towards a similar maybe even common etiology with type 1 diabetes mellitus and multiple sclerosis, namely a seasonal viral infection as the initial trigger in the perinatal period, the clinical disease resulting from further specific damage over time.


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