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Background Obesity accompanied by excess ectopic fat storage has been postulated as a risk factor for severe disease in people with SARS‐CoV‐2 through the stimulation of inflammation, functional immunologic deficit and a pro‐thrombotic disseminated intravascular coagulation with associated high rates of venous thromboembolism. Methods Observational studies in COVID‐19 patients reporting data on raised body mass index at admission and associated clinical outcomes were identified from MEDLINE, Embase, Web of Science and the Cochrane Library up to 16 May 2020. Mean differences and relative risks (RR) with 95% confidence intervals (CIs) were aggregated using random effects models. Results Eight retrospective cohort studies and one cohort prospective cohort study with data on of 4,920 patients with COVID‐19 were eligible. Comparing BMI ≥ 25 vs <25 kg/m2, the RRs (95% CIs) of severe illness and mortality were 2.35 (1.43‐3.86) and 3.52 (1.32‐9.42), respectively. In a pooled analysis of three studies, the RR (95% CI) of severe illness comparing BMI > 35 vs <25 kg/m2 was 7.04 (2.72‐18.20). High levels of statistical heterogeneity were partly explained by age; BMI ≥ 25 kg/m2 was associated with an increased risk of severe illness in older age groups (≥60 years), whereas the association was weaker in younger age groups (<60 years). Conclusions Excess adiposity is a risk factor for severe disease and mortality in people with SARS‐CoV‐2 infection. This was particularly pronounced in people 60 and older. The increased risk of worse outcomes from SARS‐CoV‐2 infection in people with excess adiposity should be taken into account when considering individual and population risks and when deciding on which groups to target for public health messaging on prevention and detection measures. Systematic review registration: PROSPERO 2020: CRD42020179783.

Abstract Background The future of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic hinges on virus evolution and duration of immune protection of natural infection against reinfection. We investigated the duration of protection afforded by natural infection, the effect of viral immune evasion on duration of protection and protection against severe reinfection, in Qatar, between 28 February 2020 and 5 June 2022. Methods Three national, matched, retrospective cohort studies were conducted to compare the incidence of SARS-CoV-2 infection and coronavirus disease 2019 (COVID-19) severity among unvaccinated persons with a documented SARS-CoV-2 primary infection, to incidence among those infection-naïve and unvaccinated. Associations were estimated using Cox proportional hazard regression models. Results Effectiveness of pre-Omicron primary infection against pre-Omicron reinfection was 85.5% [95% confidence interval (CI): 84.8–86.2%]. Effectiveness peaked at 90.5% (95% CI: 88.4–92.3%) in the 7th month after the primary infection, but waned to ~ 70% by the 16th month. Extrapolating this waning trend using a Gompertz curve suggested an effectiveness of 50% in the 22nd month and < 10% by the 32nd month. Effectiveness of pre-Omicron primary infection against Omicron reinfection was 38.1% (95% CI: 36.3–39.8%) and declined with time since primary infection. A Gompertz curve suggested an effectiveness of < 10% by the 15th month. Effectiveness of primary infection against severe, critical or fatal COVID-19 reinfection was 97.3% (95% CI: 94.9–98.6%), irrespective of the variant of primary infection or reinfection, and with no evidence for waning. Similar results were found in sub-group analyses for those ≥50 years of age. Conclusions Protection of natural infection against reinfection wanes and may diminish within a few years. Viral immune evasion accelerates this waning. Protection against severe reinfection remains very strong, with no evidence for waning, irrespective of variant, for over 14 months after primary infection.

Our study aimed to systematically analyse the risk factors of coronavirus disease 2019 (COVID-19) patients with severe disease. An electronic search in eight databases to identify studies describing severe or critically ill COVID-19 patients from 1 January 2020 to 3 April 2020. In the end, we meta-analysed 40 studies involving 5872 COVID-19 patients. The average age was higher in severe COVID-19 patients (weighted mean difference; WMD = 10.69, 95%CI 7.83–13.54). Patients with severe disease showed significantly lower platelet count (WMD = −18.63, 95%CI −30.86 to −6.40) and lymphocyte count (WMD = −0.35, 95%CI −0.41 to −0.30) but higher C-reactive protein (CRP; WMD = 42.7, 95%CI 31.12–54.28), lactate dehydrogenase (LDH; WMD = 137.4, 95%CI 105.5–169.3), white blood cell count（WBC), procalcitonin（PCT）, D-dimer, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and creatinine（Cr）. Similarly, patients who died showed significantly higher WBC, D-dimer, ALT, AST and Cr but similar platelet count and LDH as patients who survived. These results indicate that older age, low platelet count, lymphopenia, elevated levels of LDH, ALT, AST, PCT, Cr and D-dimer are associated with severity of COVID-19 and thus could be used as early identification or even prediction of disease progression.

For each outcome, forest plot, 95% confidence interval (CI), p value (< 0.05 considered statistically significant), and I2 statistic (> 50% considered as substantial heterogeneity) was generated using Open Meta Analyst (CEBM, Oxford, UK). The pathophysiology behind hypoalbuminemia in disease state (such as pancreatitis, infection, trauma, burn, and organ dysfunction) is thought to be secondary to increased capillary permeability, decreased protein synthesis, decreased half-life of serum albumin, decreased serum albumin total mass, increased volume of distribution, and increase expression of vascular endothelial growth factor [14]. Zhou Y, Zhang Z, Tian J, Xiong S. Risk factors associated with disease progression in a cohort of patients infected with the 2019 novel coronavirus.

Aspergillosis complicating severe influenza infection has been increasingly detected worldwide. Recently, coronavirus disease-associated pulmonary aspergillosis (CAPA) has been detected through rapid reports, primarily from centers in Europe. We provide a case series of CAPA, adding 20 cases to the literature, with review of pathophysiology, diagnosis, and outcomes. The syndromes of pulmonary aspergillosis complicating severe viral infections are distinct from classic invasive aspergillosis, which is recognized most frequently in persons with neutropenia and in other immunocompromised persons. Combined with severe viral infection, aspergillosis comprises a constellation of airway-invasive and angio-invasive disease and results in risks associated with poor airway fungus clearance and killing, including virus- or inflammation-associated epithelial damage, systemic immunosuppression, and underlying lung disease. Radiologic abnormalities can vary, reflecting different pathologies. Prospective studies reporting poor outcomes in CAPA patients underscore the urgent need for strategies to improve diagnosis, prevention, and therapy.

Patients with severe or critical coronavirus disease 2019 (COVID-19) remain at a high risk of mortality. Although nirmatrelvir/ritonavir has demonstrated efficacy in non-severe COVID-19 patients with high-risk factors, its effectiveness in hospitalized patients with severe or critical COVID-19 remains unclear. This study evaluates the effectiveness of nirmatrelvir/ritonavir in this specific population. In this multicenter retrospective cohort study, we included adults hospitalized with severe or critical COVID-19 at three tertiary hospitals in Shaanxi Province between December 2022 and November 2023. Participants were non-randomly categorized into either the nirmatrelvir/ritonavir group or the non-antiviral group based on whether they received nirmatrelvir/ritonavir during hospitalization. The primary outcome was 28-day mortality, and secondary outcomes included in-hospital mortality and post-baseline hospitalization duration. Among the 386 patients (nirmatrelvir/ritonavir group,  = 173, and non-antiviral group,  = 213), those in the nirmatrelvir/ritonavir group had significantly lower 28-day mortality than those in the non-antiviral group (6.9% vs. 15.5%;  = 0.002). Additionally, the nirmatrelvir/ritonavir group had reduced in-hospital mortality rates (8.1% vs. 16.0%;  = 0.003). After multivariable adjustment, the use of nirmatrelvir/ritonavir remained independently associated with a reduced risk of 28-day mortality (adjusted hazard ratio (aHR) = 0.346, 95% confidence interval (CI): 0.175-0.687;  = 0.002) and in-hospital mortality (aHR = 0.374, 95% CI: 0.196-0.716;  = 0.003). Subgroup analyses suggested that the reduced mortality risk was particularly evident in patients aged ≥65 years, non-smokers, those without chronic lung disease or hypertension, those with critical illness, and those who initiated treatment within 5 days of symptom onset. The median post-baseline hospitalization duration was longer in the nirmatrelvir/ritonavir group than in the non-antiviral group (11.0 vs. 9.0 days;  = 0.019). Nirmatrelvir/ritonavir was associated with significantly reduced mortality in patients hospitalized with severe or critical COVID-19, supporting its clinical use in this population.

A global shift to bivalent mRNA vaccines is ongoing to counterbalance the diminishing effectiveness of the original monovalent vaccines due to the evolution of SARS-CoV-2 variants, yet substantial variation in the bivalent vaccine effectiveness (VE) exists across studies and a complete picture is lacking. We searched papers evaluating absolute or relative effectiveness of SARS-CoV-2 BA.1 type or BA.4/5 type bivalent mRNA vaccines on eight publication databases published from September 1st, 2022, to November 8th, 2023. Pooled VE against Omicron-associated infection and severe events (hospitalization and/or death) was estimated in reference to unvaccinated, ≥2 original monovalent doses, and ≥ 3 original monovalent doses. From 630 citations identified, 28 studies were included, involving 55,393,303 individuals. Bivalent boosters demonstrated higher effectiveness against symptomatic or any infection for all ages combined, with an absolute VE of 53.5 % (95 % CI: –22.2–82.3 %) when compared to unvaccinated and relative VE of 30.8 % (95 % CI: 22.5–38.2 %) and 28.4 % (95 % CI: 10.2–42.9 %) when compared to ≥ 2 and ≥ 3 original monovalent doses, respectively. The corresponding VE estimates for adults ≥ 60 years old were 22.5 % (95 % CI: 16.8–39.8 %), 31.4 % (95 % CI: 27.7–35.0 %), and 30.6 % (95 % CI: −13.2–57.5 %). Pooled bivalent VE estimates against severe events were higher, 72.9 % (95 % CI: 60.5–82.4 %), 57.6 % (95 % CI: 42.4–68.8 %), and 62.1 % (95 % CI: 54.6–68.3 %) for all ages, and 72.0 % (95 % CI: 51.4–83.9 %), 63.4 % (95 % CI: 41.0–77.3 %), and 60.7 % (95 % CI: 52.4–67.6 %) for adults ≥ 60 years old, compared to unvaccinated, ≥2 original monovalent doses, and ≥ 3 original monovalent doses, respectively. The bivalent boosters demonstrated superior protection against severe outcomes than the original monovalent boosters across age groups, highlighting the critical need for improving vaccine coverage, especially among the vulnerable older subpopulation.

Background Malaria transmission has recently fallen in many parts of Africa, but systematic descriptions of infection and disease across all age groups are rare. Here, an epidemiological investigation of parasite prevalence, the incidence of fevers associated with infection, severe hospitalized disease and mortality among children older than 6 months and adults on the Kenyan coast is presented. Methods A prospective fever surveillance was undertaken at 6 out-patients (OPD) health-facilities between March 2018 and February 2019. Four community-based, cross sectional surveys of fever history and infection prevalence were completed among randomly selected homestead members from the same communities. Paediatric and adult malaria at Kilifi county hospital was obtained for the 12 months period. Rapid Diagnostic Tests (CareStart™ RDT) to detect HRP2-specific to Plasmodium falciparum was used in the community and the OPD, and microscopy in the hospital. Crude and age-specific incidence rates were computed using Poisson regression. Results Parasite prevalence gradually increased from childhood, reaching 12% by 9 years of age then declining through adolescence into adulthood. The incidence rate of RDT positivity in the OPD followed a similar trend to that of infection prevalence in the community. The incidence of hospitalized malaria from the same community was concentrated among children aged 6 months to 4 years (i.e. 64% and 70% of all hospitalized and severe malaria during the 12 months of surveillance, respectively). Only 3.7% (12/316) of deaths were directly attributable to malaria. Malaria mortality was highest among children aged 6 months–4 years at 0.57 per 1000 person-years (95% CI 0.2, 1.2). Severe malaria and death from malaria was negligible above 15 years of age. Conclusion Under conditions of low transmission intensity, immunity to disease and the fatal consequences of infection appear to continue to be acquired in childhood and faster than anti-parasitic immunity. There was no evidence of an emerging significant burden of severe malaria or malaria mortality among adults. This is contrary to current modelled approaches to disease burden estimation in Africa and has important implications for the targeting of infection prevention strategies based on chemoprevention or vector control.

Vaccines can reduce an individual's risk of infection and their risk of progression to severe disease given infection. The latter effect is less commonly estimated but is relevant for vaccine impact modeling and cost-effectiveness calculations. Using a motivating example from the COVID-19 literature, we note how vaccine effectiveness against progression to severe disease can appear to increase from below 0 % to over 70 % within 8 months. With true biological strengthening of this magnitude being unlikely, we use a mathematical modeling framework to identify parameter combinations where this phenomenon can occur. Fundamental features are an immunocompetent population with high initial protection against infection, contrasted with a vulnerable subpopulation with poor vaccine response against infection and progression. As a result, the earliest infections are among those with the weakest protection against severe disease. This work highlights methodological challenges in isolating a vaccine's effect on progression to severe disease after infection, and it signals the need for refined analytical methods to adjust for differences between the vaccinated infected and the unvaccinated infected populations.

Objective Systemic lupus erythematosus (SLE) patients are at risk during the COVID‐19 pandemic, yet the underlying molecular mechanisms remain incompletely understood. This study sought to analyze the potential molecular connections between COVID‐19 and SLE, employing a bioinformatics approach to identify effective drugs for both conditions. Methods The data sets GSE100163 and GSE183071 were utilized to determine share differentially expressed genes (DEGs). These DEGs were later analyzed by various bioinformatic methods, including functional enrichment, protein–protein interaction (PPI) network analysis, regulatory network construction, and gene–drug interaction construction. Results A total of 50 common DEGs were found between COVID‐19 and SLE. Gene ontology (GO) functional annotation revealed that “immune response,” “innate immune response,” “plasma membrane,” and “protein binding” were most enriched in. Additionally, the pathways that were enriched include “Th1 and Th2 cell differentiation.” The study identified 48 genes/nodes enriched with 292 edges in the PPI network, of which the top 10 hub genes were CD4, IL7R, CD3E, CD5, CD247, KLRB1, CD40LG, CD7, CR2, and GZMK. Furthermore, the study found 48 transcription factors and 8 microRNAs regulating these hub genes. Finally, four drugs namely ibalizumab (targeted to CD4), blinatumomab (targeted to CD3E), muromonab‐CD3 (targeted to CD3E), and catumaxomab (targeted to CD3E) were found in gene–drug interaction. Conclusion Four possible drugs that targeted two specific genes, which may be beneficial for COVID‐19 patients with SLE. (1) This study sought to analyze the potential molecular connections between COVID‐19 and systemic lupus erythematosus (SLE), employing a bioinformatics approach to identify effective drugs for both conditions. (2) Four drugs namely ibalizumab (targeted to CD4), blinatumomab (targeted to CD3E), muromonab‐CD3 (targeted to CD3E), and catumaxomab (targeted to CD3E) were found. (3) Four possible drugs that targeted two specific genes, which may be beneficial for COVID‐19 patients with SLE.