Background: SARS-CoV-2 reinfections increased substantially after the emergence of Omicron variants. Methods: We conducted a cross-sectional study of 2095 individuals with prior Omicron BA.2 infection in Shanghai, China, during the early post-zero-COVID period. Data on demographics, infection history, and lifestyle factors were collected via questionnaire, and blood samples were obtained for ancestral RBD-blocking antibody measurement. Results: Meeting WHO physical activity recommendations (≥600 MET-min/week) was associated with lower reinfection odds (OR = 0.59, 95% CI: 0.46–0.74, p < 0.001). The overall median ancestral RBD-blocking antibody level was 263.93 U/mL (IQR: 36.41–331.87). Older age was associated with lower ancestral RBD-blocking antibody levels (β = –0.0038 per year, 95% bootstrap CI: –0.0057 to –0.0019, p < 0.001). All vaccinated groups had significantly higher ancestral RBD-blocking antibody levels than unvaccinated individuals: partially vaccinated (β = 0.4440, 95% CI: 0.1569 to 0.6830, p < 0.001), fully vaccinated (β = 0.8516, 95% CI: 0.7464 to 0.9595, p < 0.001), homologous booster (β = 1.0297, 95% CI: 0.9408 to 1.1223, p < 0.001), and heterologous booster (β = 1.0838, 95% CI: 0.9387 to 1.2226, p < 0.001). Time since last immune event was inversely associated with ancestral RBD-blocking antibody levels (β = –0.0232 per month, 95% CI: –0.0385 to –0.0077, p = 0.0031). Conclusions: In this cross-sectional study, meeting WHO physical activity recommendations was associated with 41% lower odds of SARS-CoV-2 reinfection, although reverse causality cannot be ruled out. All vaccinated groups had higher ancestral RBD-blocking antibody levels than unvaccinated individuals. Older age and longer time since last immune event were associated with lower ancestral RBD-blocking antibody levels. These associations need confirmation in prospective, well-powered studies.

A major barrier in mucosal vaccine development is achieving localized immunity without systemic toxicity. Here we engineered NanoCF501, a nanoparticulate STING agonist formulated with a 2-ethyl-2-oxazoline polymer. As an adjuvant, NanoCF501 facilitates efficient mucus penetration and localized respiratory retention, minimizing systemic exposure as confirmed by pharmacokinetics in rats. In mice, intranasal co-administration of NanoCF501 (1/20th the systemic dose) with an antigen comprising multivalent fragments derived from different coronaviruses induced robust mucosal and systemic immunity, conferring protection against homologous/heterologous pan-β-coronaviruses. Single-cell transcriptomics reveals STING-dependent reprogramming of lung antigen-presenting cells, enhancing adaptive responses. Our results were further validated in non-human primates and were extended to licensed influenza vaccines, showing that NanoCF501 can be used to repurpose intramuscular antigens for mucosal delivery. By integrating nanoscale rational design with innate targeting, NanoCF501 establishes a universal adjuvant for next-generation vaccines, advancing nanomedicine for pandemic preparedness.

Abstract Severe COVID-19 is characterized by profound immune dysregulation and excessive inflammation. Aberrant myeloid responses drive hyperinflammation, yet the precise mechanisms remain elusive. Here, we demonstrate that certain spike antibodies promote the formation of heterotypic syncytia between monocytes/macrophages and virus-infected pneumocytes, leading to excessive inflammatory cytokine release. This antibody-dependent syncytium formation requires FcγRI (CD64) and ADAM10, as well as the assembly of the six-helix bundle by the spike S2 subunit. Notably, these syncytia exhibit a stronger proinflammatory signature compared to virus-infected epithelial cells. In vivo , sub-neutralizing antibody concentrations amplified inflammation and exacerbated disease in SARS-CoV-2-infected mice without increasing viral burden. Furthermore, scRNA-seq of postmortem lung tissues from COVID-19 patients implicated the monocyte/macrophage-derived syncytia as a key cellular source of inflammatory cytokines. Together, these findings define a novel mechanism of antibody-dependent enhancement of inflammation that helps explain the hyperinflammatory responses in severe COVID-19 and suggest new therapeutic opportunities targeting this pathway.

Background: Few prospective cohort studies have explored the associations of PM2.5 mass and its chemical constituents with asthma incidence in older Chinese adults, and the regional and sex-specific effect modifications remain unclear. Methods: We obtained data from the World Health Organization's (WHO) Study on Global Ageing and Adult Health (SAGE) to quantitatively evaluate the associations between long-term exposure to PM2.5 mass and its chemical constituents and asthma incidence among 8490 Chinese adults aged 50 years and older during 2007-2018. A Cox proportional hazards model was applied to estimate the associations of PM2.5 mass and its chemical constituents on asthma incidence. Furthermore, we computed the population attributable fraction (PAF) of asthma incidence associated with PM2.5 mass exposure. Results: During follow-up, 586 (6.90 %) were newly diagnosed with asthma. For each interquartile range (IQR) increase in the concentrations of PM2.5 mass and its chemical constituents [organic matter (OM), black carbon (BC), sulfate (SO42-), nitrate (NO3-) and ammonium (NH4+)], the HR values of asthma incidence were 1.20 (95 % CI: 1.08, 1.34), 1.24 (95 % CI: 1.11,1.39), 1.24 (95 % CI: 1.11,1.39), 1.21 (95 % CI: 1.09,1.33), 1.16 (95 % CI: 1.04,1.28), and 1.17 (95 % CI: 1.05,1.30), respectively. Stratified analyses showed greater associationsof PM2.5 mass and chemical constituents in females and in participants resided in Northern China. The PAF of asthma attributable to long-term PM2.5 exposure was 26.69 % (95 % CI: 12.24 %, 39.40 %). Conclusions: Long-term exposure to elevated PM2.5 mass and chemical constituents is associated with an increased of asthma, with the impacts modified by sex and region.

Background:The ability to predict cardiometabolic multimorbidity (CMM) could significantly facilitate the identification of and intervention for middle-aged and older Chinese adults at risk. This study aimed to develop a prediction model for CMM progression trajectories based on multidimensional risk factors using an ensemble machine learning approach. Methods:Data from 4,518 participants were obtained from the World Health Organization's Study on Global AGEing and Adult Health (SAGE) in China, covering the period from 2007 to 2019. Information on the incidence of cardiometabolic diseases (CMDs) was collected via self-reported surveys. CMM was defined as the presence of at least two CMDs, including hypertension, diabetes, angina, stroke, and obesity. A multi-state model was used to examine the influence of multidimensional factors on the transition from health to a single CMD and subsequently to CMM. Predictive models for these transitions were then developed. Results:During follow-up, 52.19% of initially healthy individuals developed one cardiometabolic disease (CMD), among whom 15.61% progressed to CMM. Female, low GDP per capita, unhealthy behaviors, elevated PM2.5 concentrations, low humidity, and low temperatures were identified as shared risk factors across the progression from health to CMD and from CMD to CMM. Moreover, in the health-to-CMD transition, older age, low educational level, and physical fitness impairment emerged as independent risk factors. Distinctively, in the CMD-to-CMM transition, IC impairment was identified as an independent influencing factor. Using these key predictors, a stacking ensemble model incorporating five machine learning algorithms was developed, and the model demonstrated area under the curve (AUC) values of 0.89 (95% CI: 0.88-0.91) for predicting the transition from health to CMD, and 0.76 (95% CI: 0.72-0.82) for predicting progression from CMD to CMM. Conclusion:In conclusion, this study demonstrates that a stacking ensemble model based on multidimensional factors can effectively predict the progression of CMM. Our study not only identified distinct risk factors for different transitional stages but also highlighted the potential of machine learning to improve early risk stratification and inform targeted interventions for preventing CMM in the aging.

The objective of this study was to investigate the gene-breastfeeding interaction on BMI based on the Chinese National Twin Register (CNTR). The study included 4,573 pairs of same-sex twins aged 2-18 from CNTR. Data were collected using a self-reported questionnaire, and a structural equation model was used to analyze the gene-environment interaction of breastfeeding with BMI in six age groups. Our findings indicate that as age increases, the heritability of BMI shows an increasing trend, being the lowest (h2: 0.08; 95% CI [0.00, 0.19]) in the 6- to 8-year age group and the highest (h2: 0.57, 95% CI [0.44, 0.72]) in the 12- to 14-year age group. Additionally, breastfeeding significantly modified the additive genetic component of BMI in the 6- to 8-year age group and 12- to 14-year age group. In the 6- to 8-year age group, breastfeeding decreased the impact of genes on BMI, with a genetic effect modification coefficient (βa) of -0.19 (-0.25, -0.13). In the 12- to 14-year age group, breastfeeding increased the impact of genes on BMI, with a genetic effect modification coefficient (βa) of 0.08 (0.02, 0.15). In conclusion, as age increases, the genetic influence on children's BMI becomes more pronounced. Breastfeeding may modulate genetic effects at the ages of 6-8 and 12-14. Given the metabolic diversity of obesity, our findings offer insight into how breastfeeding interacts with genetic background, helping to unravel the complex gene-environment interplay influencing obesity.

Background: Metabolic syndrome, a cardiovascular risk cluster, is recognized as a global health priority influenced by gene-diet interactions. The rs2794720 polymorphism has not been previously reported in relation to metabolic syndrome. This study examined the associations between dietary iron, SNP rs2794720, and metabolic syndrome in Chinese metropolitan population, with a focus on sex-specific and genotype-specific effects. Methods: A community-based cross-sectional study enrolled 2639 adults (1254 males, 1385 females) from Shanghai, China. Anthropometric measurements, laboratory analyses, and genotyping for the participants were performed. Dietary assessment utilized the 3-day 24 h dietary recall method. Metabolic syndrome was identified by the presence of at least three out of five metabolic abnormalities according to the NCEP-ATP III criteria. Results: After adjusting for confounders, in males, metabolic syndrome risk was associated with dietary iron (p = 0.002) but not with rs2794720 (p = 0.731). In females, metabolic syndrome risk was associated with rs2794720 (p = 0.014) and dietary iron (p = 0.016), with a significant interaction observed between rs2794720 and dietary iron (p = 0.047). Stratified by rs2794720, among females lacking the C allele, there was a linear trend between dietary iron and metabolic syndrome risk (p = 0.048). Compared to the reference group (lowest-intake GG homozygotes), the Q2-Q4 Ors (95% CI) were 5.31 (1.08, 39.52), 5.50 (1.16, 40.28), and 8.40 (1.80, 41.44)), while the major allele carriers did not show this trend (p = 0.704); compared to the reference group, the Q1-Q4 ORs(95% CI) were 6.13 (1.68, 39.66), 7.53 (2.06, 48.86), 8.10 (2.20, 52.60), and 7.84 (2.07, 51.70)). Conclusions: Our study first identified rs2794720 as a novel SNP associated with metabolic syndrome in Chinese females. The association between dietary iron and metabolic syndrome risk was unique to GG homozygotes (the minority), whereas CC/CG genotypes (the majority) showed no such association.

Antibody-dependent enhancement (ADE) of viral entry remains a mechanistically unresolved phenomenon in SARS-CoV-2 variants, with its variant-specificity and pathological consequences poorly defined. Through systematic profiling of 114 monoclonal antibodies (mAbs) across major variants of concern (VOCs), we discover that the Delta variant exhibits uniquely potent ADE mediated by mAbs targeting specific spike (S) epitopes. Crucially, ​​integrative single-cell RNA sequencing of Delta-infected patients provides direct in vivo evidence of ADE-associated immunopathology, revealing significant depletion of FcγR⁺ and C1qR⁺ immune cells (particularly CD16⁺ monocytes and dendritic cells) alongside pan-cellular cytokine hyperactivation, patterns that are absent in wildtype or Omicron infections. Functional dissection demonstrates epistatic interactions among Delta-specific S mutations (L452R, P681R, and D950N), wherein individual mutations enhance ADE in wildtype background but suppress it in Delta context. Longitudinal surveillance reveals fluctuating ADE patterns across variants, with BA.5 sub-lineage exhibiting L452R-mediated resurgence of enhancement. This study establishes ​​variant-specific ADE as an in vivo driver of immunopathology governed by epistatic constraints​​, necessitating continuous risk assessment in evolving variants.

The discovery of broadly neutralizing antibodies (bNAbs) that target conserved epitopes on the HIV-1 envelope glycoprotein (Env) has garnered significant attention for its potential in the development of effective therapeutic and vaccine strategies. In this study, we isolated and characterized a CD4 binding site (CD4bs) antibody, FD22, from an elite neutralizer in China who had been infected with a clade B virus through contaminated blood plasma for 23 years. The heavy chain of FD22 was derived from a rarely reported IGHV3-30 germline gene and exhibited an exceptionally high degree of somatic hypermutation (SHM) (37%), along with a long and unique CDRH3 loop of 20-amino acids. FD22 exhibited potent and broad neutralizing activity, comparable to that of the well-known bNAb VRC01. It effectively neutralized 82% of a panel of 145 diverse HIV-1 pseudoviruses, including the two major circulating strains in China, CRF01_AE and CRF07_BC. FD22 bound strongly to HIV-1-infected cell lines, efficiently engaged FcγRIIIa receptors, triggered NK cell degranulation and the release of key cytokines such as IFN-γ and β-chemokines, and robustly induced antibody-dependent cellular cytotoxicity (ADCC) against HIV-1-infected target cells. Structural prediction for FD22 and the HIV Env SOSIP trimer performed by AlphaFold3, site-mutagenesis, and autologous virus reverse mutation assays revealed that the epitope of FD22 spans key CD4 binding site, including Loop D, the CD4 binding loop (CD4 BLP), and the V5 Loop. The unique long CDRH3 loop of FD22 interacts with the CD4 binding site through its negatively charged residue R102, distinguishing it from other CD4bs antibodies. Our findings provide valuable insights into the mechanisms of FD22 in viral neutralization and ADCC. The dual functionality of FD22 enhances its potential as a promising therapeutic antibody and offers new avenues for designing CD4bs-targeting vaccines with enhanced ADCC capabilities.

Three studies published in this issue of Cell reveal that multiple MERS-related coronaviruses (MERSr-CoVs) utilize ACE2, rather than the canonical Merbecovirus receptor DPP4, for cell entry. These ACE2-dependent MERSr-CoVs pose a risk of zoonotic transmission to humans with high transmissibility potential like SARS-CoV-2, thus calling for global surveillance and countermeasures.

Background and Objectives Early-life risk factors influence the aging process in the short term and shape its trajectory in the long term. We aim to (1) explore the association between childhood socioeconomic position (cSEP) and frailty trajectories and (2) test whether adult socioeconomic position (aSEP) mediates the association between cSEP and frailty trajectories.Research Design and Methods We analyzed 4 waves of the China Health and Retirement Longitudinal Study data. The frailty index was estimated based on the number of individual deficits across 40 indicator variables. Principal component analysis was used to generate cSEP and aSEP. Group-based trajectory models were used to identify the patterns of frailty trajectories over time. Causal mediation analysis was conducted to determine whether the aSEP mediated the association between cSEP and frailty trajectories.Results We identified 3 distinct trajectories of frailty progression. Low cSEP was significantly associated with "High and increasing frailty trajectory" (odds ratio [OR] = 1.76, 95% confidence intervals [95% CI]: 1.38-2.23; adjusted OR = 1.55, 95% CI: 1.22-1.97). About 30% of the cSEP effect on rising frailty trajectory was mediated through the aSEP, and there is a significant gender disparity in the mediating effect of aSEP (18% among men and 51% among women, respectively).Discussion and Implications Our findings suggest that policies that initially benefit children will yield well-being benefits as they reach adulthood. Promoting ongoing cSEP advantages increases the likelihood of delaying frailty progression in later life. This study underscores the critical importance of addressing social determinants of health throughout one's life course to foster healthy aging and diminish health disparities in later stages of life.

ABSTRACT In November 2023, there was a substantial increase in the incidence of Mycoplasma pneumoniae infections in China following waves of SARS-CoV-2 Omicron variant and influenza outbreaks. This study aimed to elucidate the epidemiological features and clinical implications of M. pneumoniae infections in children and explore the potential influence of SARS-CoV-2 Omicron variants and influenza A infections on the M. pneumoniae outbreak. Among 38,668 children with lower respiratory tract infections from January to December 2023, 11,919 tested positive for M. pneumoniae, predominantly between October and December. The majority of the children with M. pneumoniae were aged 5–10 years, with type 1 strains and macrolide-resistant M. pneumoniae strains having the highest prevalence rates. Statistical analysis revealed elevated C-reactive protein, neutrophil, and monocyte levels and decreased lymphocyte, basophil, and eosinophil counts in M. pneumoniae-positive children. M. pneumoniae-positive children also presented significantly increased neutralizing antibody levels against preceding influenza A (H3N2) but not against SARS-CoV-2 Omicron variants. A parallel trend was observed between M. pneumoniae and H3N2 prevalence from June to December 2023. The emergence of macrolide-resistant strains and prior influenza A (H3N2) epidemics notably contributed to the M. pneumoniae outbreak. These findings suggested that H3N2 infection facilitates M. pneumoniae infection through various mechanisms. This study underscores the complex interactions between respiratory pathogens and highlights the need for comprehensive surveillance and response strategies.IMPORTANCEThis study identified key factors contributing to an outbreak of Mycoplasma pneumoniae that affected 11,919 children. The influencing factors included a high prevalence of macrolide-resistant epidemic strains (94.2%) and significantly higher H3N2 neutralizing antibody levels (P < 0.0001) stimulated by the preceding H3N2 influenza epidemic. These findings highlight the complex relationship between the prevalence of M. pneumoniae and H3N2 infection in children, indicating that it is necessary to consider pathogen interactions in respiratory disease management by continuously monitoring respiratory pathogens. The emergence of macrolide-resistant strains in China and the previous H3N2 influenza epidemic significantly exacerbated the severity of the M. pneumoniae outbreak. H3N2 infection potentially amplifies Mycoplasma transmission. This study elucidates the epidemiological and clinical aspects of M. pneumoniae infections in children, yields insights regarding the cause of the outbreak, and provides guidance for improving respiratory infection management.

In 2019,China had over 13.14 million dementia cases,with incidence rates of(56.47-207.08)/100,000[1].Early cognitive impairment—a key dementia symptom—reduces quality of life,increases care dependence,and lowers survival in older adults[2].A decline in physical function can also be observed in older adults with increasing age.Grip strength has been shown to be a marker of overall physiological function in older adults.

Background: With the accelerating population ageing globally, disability has become a major public concern. Residential greenness may be one of the influencing factors of disability, but epidemiological evidence in the associations of residential greenness exposures with disability is limited. We aimed to investigate the associations of residential greenness exposures with the risk of disability in the elderly. Methods: Data of 8408 residents were obtained from the World Health Organization Study on Global AGEing and Adult Health (WHO SAGE) implemented in China during 2007-2018. Participants were matched to the Normalized Difference Vegetation Index (NDVI) and Enhanced Vegetation Index (EVI) at their residential address. Disability was measured by the 12-item Chinese version of the World Health Organization Disability Assessment Schedule (WHODAS 2.0). The associations were examined using a generalized linear mixed model with stratified analyses by the covariates. Results: We observed significantly negative associations of greenness exposures with the summary WHODAS score [NDVI500m:-0.290, 95% Confidence Intervals (95%CI): -0.510, -0.070; EVI500m:-0.453, 95%CI: -0.757, -0.149], and with the score of cognition (EVI500m:-0.472, 95%CI: -0.881, -0.063), mobility (NDVI500m:-0.632, 95%CI: -0.965, -0.299; EVI500m:-0.739, 95%CI: -1.199, -0.280), and participation (NDVI500m:-0.388, 95%CI: -0.651, -0.125; EVI500m:-0.530, 95%CI: -0.893, -0.166). People living alone had a more pronounced association in cognition (NDVI500m:-1.546, 95%CI: -2.471, -0.621). The associations with summary WHODAS score were stronger among participants living in rural areas (NDVI500m:-0.420, 95% CI: -0.683, -0.157), having less education level (NDVI500m:-0.618, 95%CI: -0.982, -0.253), and living in northern China (NDVI500m:-0.381, 95%CI: -0.776, 0.013). Conclusions: Residential greenness may reduce the onset and worsening of disability, particularly for domains of cognition, mobility, and social participation. Because of its stronger influence among people with low socioeconomic status, increasing greenness levels in areas with lower socioeconomic status may promote health equity.

ObjectiveTo analyze the epidemiological characteristics and influencing factors of SARS-CoV-2 reinfection by conducting follow-up investigations among community residents who experienced their first SARS-CoV-2 infection between March and June 2022, so as to provide a scientific basis for predicting future epidemic trends and adjusting prevention and control strategies.MethodsA cohort study was conducted in Xuhui District, Shanghai. A total of 1 208 individuals with a documented primary SARS-CoV-2 infection between March and June 2022 were enrolled and followed-up longitudinally. Data were collected using structured questionnaire surveys to assess the reinfection rate, incidence density, and clinical manifestations of SARS-CoV-2 reinfection. A logistic regression model was used to analyze the influencing factors of SARS-CoV-2 reinfection.ResultsA total of 497 SARS-CoV-2 reinfection cases were observed among the 1 208 research subjects, with a reinfection rate of 41.14% and an incidence density of 0.63 cases per 1 000 person-days. The cumulative reinfection rates at 6, 9, 12, 15, and 18 months following the initial infection were 0.08%, 15.31%, 19.04%, 33.53%, and 38.25%, respectively. Compared with the primary infection, reinfection was more likely to be symptomatic, with a greater severity of fever, dry cough, sore throat, and runny nose. Being female, younger age, and symptom duration ≥7 days during the primary infection were identified as influencing factors for SARS-CoV-2 reinfection, while a higher socioeconomic status can reduce the risk of SARS-CoV-2 reinfection.ConclusionSARS-CoV-2 reinfection is relatively common and often symptomatic. Age, gender, income level, and the duration of symptoms during the primary infection are identified as infuencing factors for SARS-CoV-2 reinfection. Continuous monitoring of reinfection in the population is recommended, along with the development of effective strategies to mitigate the impact of reinfection.

[Objective]To analyze the epidemiological characteristics of long COVID and to investigate its main influencing factors by examining individuals infected with SARS-CoV-2 between March and June 2022 in two communities in Shanghai,to lay the foundation for further research on the mechanism and clinical treatment of long COVID,and to provide the basis for the development of inexpensive,convenient,and feasible prevention and intervention strategies.[Methods]A cross-sectional study was conducted,enrolling 6 410 individuals infected with SARS-CoV-2.Data were collected through a questionnaire survey.The incidence and common symptoms of long COVID were analyzed,along with their associations with demographic characteristics,medical history,and behavioral factors.A logistic regression model was used to identify the major factors associated with the development of long COVID symptoms.[Results]The overall incidence rate of long COVID among the study population was 13.9%.The most commonly reported symptoms included fatigue(65.1%),attention disorders(23.1%),and cough(16.9%).The analysis showed that having underlying chronic diseases(OR=2.580,95%CI:2.165-3.074),a history of allergies(OR=1.418,95%CI:1.003-1.971),current smoking(OR=1.461,95%CI:1.013-2.079),ever smoking(OR=2.462,95%CI:1.687-3.551),a greater number of symptoms during the acute phase[1 symptom(OR=1.778,95%CI:1.459-2.162),2 symptoms(OR=2.749,95%CI:2.209-3.409),≥3 symptoms(OR=7.792,95%CI:6.333-9.593)]and aggravated symptoms during the acute phase(OR=1.082,95%CI:1.070-1.094)were factors associated with a higher risk of developing long COVID symptoms.Additionally,individuals who had consumed alcohol in the past year(OR=1.914,95%CI:1.344-2.684)were more prone to objective long COVID symptoms.Among individuals under 50 years of age,females(OR=1.427,95%CI:1.052-1.943)were more likely to develop objective long COVID symptoms.[Conclusion]This study has identified the diversity of long COVID symptoms,which involve multiple organs and systems,including fatigue,attention disorders,cough,and joint pain.It has also revealed associations between long COVID and various demographic factors(e.g.,age,gender),personal medical history(e.g.,underlying chronic diseases,history of allergies),acute-phase characteristics(e.g.,number and severity of symptoms),and behavioral factors(e.g.,smoking,alcohol consumption).These findings highlight the need for further research and ongoing surveillance of long COVID and may inform the development of more targeted health management strategies for specific populations.

Background/Objectives: The antibody-dependent enhancement (ADE) of viral entry has been documented for SARS-CoV-2 infection both in vitro and in vivo. However, the potential for the SARS-CoV-2 vaccination to elicit similar ADE effects remains unclear. Methods: In this study, we assessed the in vitro ADE potential of monoclonal antibodies (mAbs) derived from individuals vaccinated with the inactivated SARS-CoV-2 vaccine and compared them to those from one convalescent donor. Results: Our analysis revealed no significant difference in binding affinity or neutralizing capacity between the vaccinated and convalescent mAbs. However, the inactivated SARS-CoV-2 vaccination induced fewer ADE-inducing mAbs, particularly those targeting the Class III epitope on the receptor-binding domain (RBD) compared to those from the convalescent individual. Moreover, no significant in vitro ADE was detected in either vaccinated or convalescent sera, indicating low levels of ADE-inducing antibodies in the sera. Conclusions: An inactivated SARS-CoV-2 vaccination induces fewer ADE-inducing antibodies compared to natural infection, further emphasizing the safety of inactivated SARS-CoV-2 vaccines.

The opportunity of long-term exposure to non-optimal temperature and relative humidity (RH) may increase which might contribute to elevations in blood pressure (BP). This study aimed to examine the joint effect of long-term exposure to temperature and RH on BP which help better adaption to climate change. Data were collected from 9272 participants in global AGEing and adult health cohort study across eight provinces in China from 2007 to 2019. Annual meteorological data were treated as indicators which derived from European Centre for Medium-Range Weather Forecasts atmospheric reanalysis (ERA5). Generalized linear mixed models (GLMM) and quantile-based g-computation models were employed to estimate the individual and joint associations between long-term exposure to temperature and RH with BP. In joint effect analysis, we found a U-shaped pattern. The minimum blood pressure percentile (MBPP) for both systolic blood pressure (SBP) and diastolic blood pressure (DBP) was observed at a temperature of approximately 15.4 °C and RH of 72.8

Background: It is unclear whether patients with Global Initiative for Chronic Obstructive Lung Disease stage 1 (mild) chronic obstructive pulmonary disease (COPD) have a higher risk of all-cause mortality than participants with normal spirometry results. Methods: We used the data from the National Health and Nutrition Examination Survey (NHANES) III and 2007-2012, which included participants aged 20-79 years, to investigate whether patients with mild COPD (whole population and subgroups) have a higher risk of all-cause mortality than participants with normal spirometry. Mild COPD was defined as prebronchodilator forced expiratory volume in 1 second /forced vital capacity <0.70 and FEV1 >= 80% of the predicted value. All-cause mortality risk is the total risk of death from all causes over a given period of time. We performed subgroup analyses by sex, age, smoking status, race, body mass index, and level of education. We also performed sensitivity analyses using the lower limit of normal to define COPD. Results: 1,760 patients (64.5% male; median aged 59 years) with mild COPD and 19,969 participants with normal spirometry (46.9% male; median aged 43 years) were followed up (median 308 months). Patients with mild COPD had a higher all-cause mortality risk than participants with normal spirometry (adjusted: Hazard Ratios 1.13, 95% Confidence Intervals 1.04-1.23; P = 0.005). The results remained robust in the sensitivity analyses. The subgroup analyses results for male sex, age >= 50 years, and current smokers were consistent with the main analysis. Conclusion: Patients with mild COPD had a higher all-cause mortality risk than those with normal spirometry, especially males, those aged >= 50 years, and current smokers. These results suggest the need for appropriate management of different subgroups with mild COPD.

Background We aimed to investigate the associations of long‐term exposure to ambient formaldehyde with hypertension and angina pectoris symptoms in Chinese adults. Methods and Results Participants' information was obtained from the WHO SAGE (World Health Organization Study on Global Aging and Adult Health) study. The Cox proportional hazards regression model was applied to estimate the associations of formaldehyde with hypertension and angina pectoris symptoms. Mediating effect analysis was used to investigate the mediating effect of hypertension between formaldehyde exposure and angina pectoris symptoms. Long‐term exposure to formaldehyde was positively associated with the risk of angina pectoris symptoms (hazard ratio [HR], 1.66 [95% CI, 1.29–2.13], per interquartile range [IQR], 3.33, 10 15 molecules/cm 2 ) and hypertension (HR, 1.17 [95% CI, 1.02–1.34], per IQR, 3.34, 10 15 molecules/cm 2 ). The associations between formaldehyde and angina pectoris symptoms were greater in participants aged ≥65 years (HR, 1.90 [95% CI, 1.29–2.80]) and in rural areas (HR, 2.71 [95% CI, 1.54–4.77]), whereas the associations of formaldehyde with hypertension were stronger in men (HR, 1.27 [95% CI, 1.02–1.58]), rural areas (HR, 1.22 [95% CI, 0.94–1.59]), and in ever smokers (HR, 1.33 [95% CI, 1.02–1.72]). The mediation effect analysis indicated that 18.44% (95% CI, 2.17–37.65) of the association between formaldehyde exposure and angina pectoris symptoms was mediated by hypertension. Conclusions Long‐term exposure to ambient formaldehyde was positively associated with hypertension and angina pectoris symptoms. The effects of formaldehyde may be modified by age, sex, urbanicity, and smoking status. Hypertension might play a mediating effect in formaldehyde‐induced angina pectoris symptoms.