Extracorporeal Membrane Oxygenation (ECMO) serves as a crucial intervention for patients with severe pulmonary dysfunction by facilitating oxygenation and carbon dioxide removal. While traditional ECMO systems are effective, their large priming volumes and significant blood-contacting surface areas can lead to complications, particularly in neonates and pediatric patients. Microfluidic ECMO systems offer a promising alternative by miniaturizing the ECMO technology, reducing blood volume requirements, and minimizing device surface area to improve safety and efficiency. This study investigates the oxygen transport performance of three membrane types- polydimethylsiloxane (PDMS), polypropylene, and a novel nanoporous silicon nitride (NPSiN) membrane-in a microfluidic ECMO platform. While nanoporous membranes rely on pore-mediated diffusion and PDMS on polymer lattice diffusion, results show no significant differences in device oxygenation efficiency (p > 0.05). Blood-side factors, including the diffusion rate of oxygen through the red blood cell (RBC) membrane, RBC residence time, and hemoglobin binding kinetics, were identified as primary bottlenecks. Even computational models of a hypothetical infinitely permeable membrane corroborate the limited impact of membrane material. These findings suggest a shift in ECMO design priorities from membrane material to blood-side enhancements. This research provides a foundation for optimizing ECMO systems.

Pregnant women are at higher risk for severe Coronavirus disease 2019 (COVID-19) infection, leading the Centers for Disease Control and Prevention to recommend vaccination. However, the frequency of vaccine side effects in pregnant women with autoimmune inflammatory rheumatic diseases (AIIRD) remains unknown. We investigated the frequencies of short-term (≤ 7 days) adverse reactions following the initial COVID-19 vaccination ever received by pregnant women with AIIRD.

A descriptive analysis of the incidence of side effects following the COVID-19 vaccination in pregnant women with AIIRD was conducted utilizing data from the MotherToBaby Study registry, a prospective cohort study designed to assess the safety of drug and vaccine exposure during pregnancy. This study enrolled pregnant women living in the United States or Canada between January 2021 and September 2022.

Of 1413 participants who received dose 1 of the COVID-19 vaccine in pregnancy, 79 had AIIRD. There was no large difference in the total number of adverse reactions between pregnant women with and without AIIRD (β = -0.01, 95 % Confidence Interval [CI]: -0.17, 0.17). Pregnant women with higher Health Assessment Questionnaire Disability Index (HAQ-DI) in AIIRD had a higher total number of systemic reactions (β = 0.56, 95 % CI: 0.04, 1.10) than those with lower HAQ-DI, although the total number of adverse reactions was not different (β = 0.27, 95 % CI: -0.08, 0.62).

We found no difference in the frequency of COVID-19 vaccine-related side effects between pregnant women with and without AIIRD. Patients with AIIRD who have higher levels of functional impairment may have a slightly higher frequency of short-term adverse effects. The results of this assessment may help provide information for pregnant women with AIIRD regarding COVID-19 vaccination.

The aim of this study is to investigate the differential expression and diagnostic value of ferroptosis-related genes in coronavirus-associated viral sepsis.

This study was conducted in two sequential phases: (1) identification of differentially expressed genes through comprehensive analysis of the experimental dataset (GSE164805); and (2) clinical validation of the candidate molecular markers using both test set samples and clinical samples, followed by rigorous evaluation of their diagnostic performance. Firstly, the microchips associated with coronavirus-associated viral sepsis were retrieved from the GEO database, a public data platform of NCBI (National Center for Biotechnology Information), and differentially expressed genes (DEGs) were obtained through differential analysis. The identified DEGs were then intersected with the ferroptosis gene dataset to obtain ferroptosis-related DEGs. Subsequently, molecular signaling pathways of ferroptosis-related genes in coronavirus-associated viral sepsis were analyzed using gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. CIBERSORT was employed to analyze immune cell infiltration in both the coronavirus-associated viral sepsis group and control group. Furthermore, a protein-protein interaction (PPI) network was constructed to identify hub genes involved in ferroptosis. Finally, the expression of ferroptosis hub genes in coronavirus-associated viral sepsis and its diagnostic value were analyzed in validation set GSE199816 and clinical case samples.

In test set GSE164805, a total of 15,059 differentially expressed genes (DEGs) were identified, comprising 7,458 up-regulated and 7,601 down-regulated genes. Subsequently, an intersection analysis with the ferroptosis gene dataset yielded 189 DEGs associated with ferroptosis. Functional enrichment analyses using GO and KEGG revealed significant enrichment in signaling pathways related to ferroptosis, oxidative stress, and HIF-1. Additionally, CIBERSORT immune-infiltration analysis revealed enhanced infiltration of innate immune cells but reduced infiltration of CD8+ T cells and natural killer (NK) cells in the coronavirus-associated viral sepsis group compared with healthy controls. Furthermore, analysis identified that the distribution of these immune cells correlated with the expression levels of IL1-β and HMOX1, suggesting that viral infection in the septic pathological state disrupts the balance between immune activation and suppression. Notably, PPI network analysis also identified IL1-β and HMOX1 as hub genes involved in ferroptosis. Finally, the results were verified in the validation set and clinical case samples, and the results showed that the expressions of IL1-β and HMOX1 in the coronavirus-associated viral sepsis group were decreased compared with the case control group and the healthy control group. In clinical samples, the expression levels were as follows: IL1-β (0.390 ± 0.068 vs. 1.101 ± 0.107), HMOX1 (0.629 ± 0.117 vs. 1.101 ± 0.107), and the differences were statistically significant (all p < 0.05). Further diagnostic performance analysis demonstrated that IL1-β and HMOX1 exhibited AUROCs of 0.892 and 0.765, respectively, indicating their robust diagnostic potential for coronavirus-associated viral sepsis.

The present study has successfully identified two hub genes, IL1-β and HMOX1, associated with ferroptosis in coronavirus-associated viral sepsis, and their expression and diagnostic value for the disease. These findings provide effective diagnostic biomarkers and potential therapeutic targets for coronavirus-associated viral sepsis. Notably, this study specifically focused on coronavirus-induced viral sepsis, distinct from previously characterized bacterial sepsis and other viral etiologies, thus warranting future studies with expanded sample sizes for stratified analyses.

Modern society faces a variety of respiratory-related threats from the increased use of chemicals and periodic outbreaks of infectious diseases. This study investigates the connection between chemically-induced lung damage and SARS-CoV-2 infection, addressing a critical research gap. To investigate this connection, we conducted a study using a mouse model to assess SARS-CoV-2 infection symptoms in lungs injured by polyhexamethylene guanidine phosphate (PHMG-p). Our research revealed that PHMG-p-Induced Lung Injury (PILI) mice exhibited severe inflammatory responses and lung damage following infection. Cytokine storm-related factors were significantly elevated in the bronchoalveolar lavage fluids of infected PILI mice, indicating severe infection. RNA-seq analysis showed upregulated genes in infected PILI mice associated with respiratory tract diseases and increased inflammatory and immune responses. Downregulated genes were primarily involved in lipid metabolism processes. We also identified alterations in four _genes linked to asthma development in infected PILI mice, correlating with clinical observations in patients. Our findings suggest that SARS-CoV-2 infection in chemically damaged lungs may exacerbate symptoms and potentially lead to new-onset asthma. This study highlights the increased risk of infection severity in chemically damaged lungs and emphasizes the need for heightened awareness of respiratory health in individuals exposed to chemicals, especially during infectious disease outbreaks.

Coronavirus disease 2019 (COVID-19) is often associated with thrombosis. Elevated levels of soluble C-type lectin-like receptor 2 (sCLEC-2), a biomarker for platelet activation, have been reported in COVID-19. Therefore, we examined the behavior of sCLEC-2 levels and their relationship with thrombosis.The clinical course of inflammatory and thrombotic biomarkers was assessed in 271 patients with COVID-19.Inflammatory biomarkers such as C-reactive protein, procalcitonin, and presepsin levels were significantly increased in patients with COVID-19, and these behaviors differed among the clinical course or stages. The plasma D-dimer levels increased slightly and gradually. Platelet counts were within the normal range, and plasma sCLEC-2 levels were markedly increased in most patients with COVID-19. There were 17 patients with thrombosis in this study. Although there was no significant difference in various biomarkers between COVID-19 patients with and without thrombosis, the super formula of sCLEC-2xD-dimer/platelet count in patients with thrombosis was significantly higher than in those without thrombosis. Furthermore, this super formula was significantly higher in COVID-19 patients with severe or critical illness than in those with mild or moderate illness.Elevation of the super formula of sCLEC-2xD-dimer/platelet count was associated with the thrombosis in patients with COVID-19 suggesting the thrombosis in COVID-19 may be caused by the development of microthrombosis.

SARS-CoV-2 presents a hyperinflammatory scenario due to systemic inflammatory response syndrome with intense cytokine release, with consequent extrapulmonary involvement in 20 % of patients. The authors studied whether COVID-19 intestinal damage is a direct action of the virus on intestinal epithelial cells, with damage mainly at the tight junction. This is a retrospective observational study in a tertiary hospital emergency department. The authors studied 87 patients (46 patients over 61 years and 41 patients under 60 years old) with severe SARS-CoV-2 infection. The authors measured two plasma markers, LPS-Binding Protein (LBP) and ileal Fatty Acid-Binding Protein (iFABP). Furthermore, the authors evaluated the interaction between the two markers. TNF-α and IL-1 β were higher in bacterial co-infected patients and TNF-α was also higher in the older patients. Plasma iFABP levels were not statistically different in patients with bacterial co-infection; however, higher levels were found in the older population. Plasma LBP levels were higher in patients with bacterial co-infection when compared to patients without infection; however, when comparing plasma LBP levels in the older population with younger patients, no differences could be found. LBP, FABP, and cytokines can discriminate between bacterially infected patients and also discriminate elderly patients. The present study suggests that intestinal barrier dysfunction in SARS-CoV-2 infections is mainly due to damage to the intestinal tight junction complex with a disproportionately lower damage to enterocyte. In the older population, the authors also observed an increase in intestinal epithelial damage.

The COVID-19 pandemic, caused by the novel coronavirus SARS-CoV-2, has profoundly impacted global health, leading to over 74 million confirmed cases and 1.67 million deaths by December 2020. In Saudi Arabia, extensive measures were implemented to mitigate the spread of the virus. Kidney transplant recipients, due to their immunosuppressed status, are particularly vulnerable to severe COVID-19 outcomes. This study aims to identify risk factors associated with mortality in COVID-19-infected kidney transplant patients in Saudi Arabia. The primary objective is to identify mortality risk factors among COVID-19-infected kidney transplant patients. The secondary objective is to compare clinical management and outcomes between deceased and recovered patients.

This case-control study matched 82 deceased kidney transplant patients (cases) with 151 survivors (controls). Data were collected from the National Registry for COVID-19 Mortality and King Faisal Specialist Hospital and Research Centre (KFSH&RC) for patients diagnosed between March 2020 and January 2021. Key variables included demographic information, comorbidities, clinical symptoms, and treatment details. Statistical analyses involved chi-square tests and multivariable logistic regression to assess associations with mortality.

Among cases, 93.9% required ICU admission, and 95.1% were intubated. Males constituted 73.2% of cases, with 53.7% aged over 60. Cardiovascular comorbidities were more prevalent among cases (97% vs. 87.4%, p = 0.01). and presented more frequently with fever, cough, and respiratory distress. In multivariable analysis, fever, shortness of breath, and desaturation were associated with increased mortality odds. Notably, patients who discontinued immunosuppressive therapy had higher mortality odds (OR = 63.2, p = 0.083), whereas those who held or adjusted their therapy had significantly lower odds (OR = 0.1, p = 0.042; OR = 0.0, p = 0.007). Bacterial infections also increased mortality risk (OR = 56.6, p = 0.009).

This study identifies critical risk factors for mortality among kidney transplant patients infected with COVID-19 in Saudi Arabia. The findings underscore the need for tailored clinical management strategies to improve outcomes in this vulnerable population. Further research is warranted to explore long-term implications and effective treatment protocols.

SARS-CoV-2 infection frequently involves the respiratory system and may impact on pulmonary function tests (PFT) of recovered individuals. Studies which compare post-COVID-19 PFT to pre-illness measurements are scarce. The primary objective of this study was to assess the effect of COVID-19 on PFT soon after infection.

In this prospective observational study, PFT were measured early following recovery from COVID-19 among healthy military aircrew. Spirometry values were compared to pre-COVID-19 measurements, and abnormality rates of lung volumes and diffusion capacity for carbon monoxide (DLCO) were assessed.

The study included 252 aviators, 97.6% males, mean age 34.9-years, following recovery from SARS-CoV-2 infection. Participants manifested mild symptoms (79.4%) or were asymptomatic (20.6%). Post-COVID-19 spirometry results 10.79 ± 5.67 days following infection were compared to measurements performed 41.3 ± 28.59 months earlier. Pre- and post-COVID-19 results were comparable, with similar minimal abnormalities rates (2% and 4.4%, respectively). In addition, there were no restrictive abnormalities following infection, and just 7.7% of individuals had a marginally low DLCO of 70-80% of predicted.

Among vaccinated, healthy adults, mild COVID-19 had no significant impact on PFT early post-infection. The data suggest that systematic PFT testing might not be necessary for asymptomatic healthy individuals who recovered from mild COVID-19.

Paxlovid® (nirmatrelvir and ritonavir) is the only licensed oral antiviral for COVID-19. Ritonavir is a potent inhibitor of cytochrome P450 enzymes causing numerous drug-drug interactions (DDIs).

To describe the frequency, type, and severity of detected drug related problems (DRPs) associated with Paxlovid®.

This study involved a retrospective quantitative analysis including all patients prescribed Paxlovid® at a public hospital in Vienna, Austria. Data were collected from the patients' records by a clinical pharmacist. A customised, piloted data collection form was used. A sample of data was checked for consistency by an independent clinical pharmacist. Any DDI and severity classification was recorded using an established interaction checker tool. Dosage adjustments due to renal impairment were recorded.

One hundred twenty-two of 140 patients (87.1%) required interventions to prevent DRPs. Pharmacists' intervention at dispensing was needed in 63.6% (n = 89) of cases. In 3 (2.1%) patients, Paxlovid® was prescribed despite being contraindicated due to severe renal impairment. The most common were DDIs (n = 80; 57.1%). Renal impairment and DDIs were noted in 24.3% (n = 34) of cases. A total of 313 DDIs were recorded in 114 (81.4%) patients, with severe interactions in 24 (17%) patients.

Pharmacists' involvement in prescribing highly interacting drugs such as Paxlovid® is essential to enhance patient safety.

The objective was to investigate the implications of enteral nutrition for elderly patients with common-type coronavirus disease 2019 (COVID-19).

Data were retrospectively extracted from medical records. Enteral nutritional supplementation was recommended for patients with a nutritional risk score >3. The preferred method was oral administration, and preparations included Ensure and TPF-T. Continuous variables were compared using analysis of two-tailed Student's t-tests or one-way analysis of variance for normally distributed data and the rank sum test for non-normally distributed data. Categorical variables were compared using the χ2 test or Fisher's exact test. Values of p <0.05 were considered to be statistically significant.

The mortality rate in the whole cohort was 9.54%. A total of 474 patients tested negative and were discharged; among them, 173 patients received enteral nutrition while 301 patients did not. There were significant correlations between mortality and age, serum albumin concentration, prognostic nutritional index, underlying severe disease status and diet condition. In patients with a poor diet, early use of enteral nutrition is associated with faster conversion to a negative polymerase chain reaction test.

The prognosis of elderly patients with common-type COVID-19 was related to their nutritional status. Enteral nutritional supplementation is the preferred method of nutrition because it is the simplest and most widely accepted method for patients. For patients with poor diet conditions, enteral nutritional intervention should be performed early.

Chronic obstructive pulmonary disease (COPD) is associated with severe Coronavirus disease 2019 (COVID-19) outcomes. However, it is uncertain whether the risk of acute exacerbation of COPD (AECOPD) increases after recovering from COVID-19.

This study included 2,118 individuals with COPD from the Korea National Health Insurance Service database who were also diagnosed with COVID-19. Matched controls were chosen using 1:1 propensity score (PS) matching. We compared the risk of AECOPD after COVID-19 recovery between the COVID-19 cohort and matched controls between October 8, 2020, and December 31, 2021, using PS-matched Cox proportional hazard regression models.

During a median follow-up of 62 days (interquartile range, 29-179 days), including a median of 14 days of recovery time after COVID-19, 68 people (5.6%) in the COVID-19 cohort and 50 (3.9%) in the matched control group experienced AECOPD. Compared to the matched controls, the COVID-19 cohort had a significantly higher risk of overall AECOPD (hazard ratio [HR] = 1.45, 95% confidence interval [CI] = 1.09-1.92). This increased risk was particularly evident for severe AECOPD among individuals who had severe COVID-19 within the first 30days post-recovery (aHR = 8.14, 95% CI = 3.32-19.97). When classified by COVID-19 severity, while severe COVID-19 significantly increased this risk (aHR = 2.97, 95% CI = 2.15-4.11), non-severe COVID did not significantly influence the risk of AECOPD, regardless of time duration or exacerbation severity.

Individuals with COPD who had severe COVID-19 have increased risk of AECOPD after COVID-19 recovery, especially within the first 30 days after COVID-19 recovery.

Zinc plays an important role in the functioning of the immune system. Zinc deficiency leads to increased susceptibility to inflammatory and infectious diseases. There are few studies investigating the role of zinc in the development and progression of COVID-19 in children, and their findings remain inconsistent. This study aimed to determine the zinc levels in children with COVID-19 and assess their association with symptoms, inflammation markers, and disease progression.

A prospective cohort study included hospitalized patients under 18 years who had a confirmed diagnosis of SARS-CoV-2 infection. Serum zinc concentrations were measured using a colorimetric method. Based on zinc levels, the children were divided into two groups: the first group had concentrations below 10.7 μmol/L, indicating zinc deficiency, while the second group had levels above 10.7 μmol/L, which was considered within the optimal range.

In total, 140 hospitalized patients with COVID-19 were examined. Zinc deficiency was identified in 40 children (28.6%), while optimal levels were found in 100 children (71.4%). Zinc status did not depend on the age of the children. Among the symptoms of acute SARS-CoV-2 infection, children with zinc deficiency showed a trend toward more frequent fever occurrences (p = 0.0654). No significant impact of zinc status was observed on the severity of COVID-19 or the duration of hospitalization. Children with zinc deficiency had higher median values of the neutrophil-to-lymphocyte ratio (NLR) (1.84 vs. 1.09, p = 0.0010), C-reactive protein (CRP) levels (9.65 vs. 3.96 mg/L, p = 0.0053), and fibrinogen levels (2.88 vs. 2.07 g/L, p = 0.0057) compared to those with adequate zinc levels. Additionally, the percentage of patients with a NLR greater than 4, elevated CRP, and fibrinogen levels was higher in the zinc-deficient group (p = 0.0017, p = 0.0107, p = 0.0338, respectively).

Zinc deficiency was observed in 28.6% of children with COVID-19 and was not dependent on age. Children with hypozincemia had higher levels of inflammation markers, including the neutrophil-to-lymphocyte ratio and CRP.

Background/Objectives: To elucidate the factors that contribute to individual variability in the progression of COVID-19, experiments on endothelial nitric oxide synthase polymorphisms have been reported. Nitric oxide synthase (NOS3) is located in the endothelium and is involved in the regulation of inflammation and vascular homeostasis. In this study, we investigated the association between COVID-19 severity and NOS3 G894T and NOS3 27-bp VNTR 4b/a genetic polymorphisms. Methods: Patients with COVID-19 (n = 178) were divided into Group 1 (mild disease) and Group 2 (severe disease) based on oxygen saturation levels in room air (Group 1, SpO2 ≥ 93%, n = 107; and Group 2, SpO2 < 93%, n = 73) and hospitalization requirements. Genotyping was performed using polymerase chain reaction-restriction fragment length polymorphism analysis. Results: Overall, genotype and allele frequencies of the NOS3 genetic polymorphisms were similar across the two study groups (p > 0.05). However, the subgroup analysis showed a notable trend for the 4b/4a allele distribution between Groups 1 and 2. In the younger subgroup of patients (≤50 years old) without chronic obstructive pulmonary disease, Group 2 tended to have a higher frequency of the 4b allele than Group 1 (97.4% vs. 85.4% p = 0.06) and a higher occurrence of 4b/4b genotype (94.7% vs. 74.0%, p = 0.05). Additionally, a rarely observed 4c allele was detected only in two subjects within Group 2 but not in Group 1. Conclusions: These findings suggest a trend of association between COVID-19 severity and NOS3 27-bp VNTR 4b/a genetic polymorphism. Genetic analysis may reveal patient susceptibility to disease, prognosis risk factors, and drug responsiveness.

Acute respiratory failure is the predominant presentation of intensive care unit (ICU) patients with COVID-19, and lung protective strategies are recommended to mitigate additional respiratory complications such as air-leak syndrome. The aim of this study is to investigate the prevalence, type, and timing of air-leak syndrome with regards to associated factors and patient outcome in patients with COVID-19 in ICUs at a large Swedish emergency hospital.

This retrospective study included all adult patients admitted to an ICU for COVID-19-related respiratory failure at Södersjukhuset between March 6, 2020, and June 6, 2021. Primary outcomes were proportion of patients diagnosed with air-leak syndrome and its different types of manifestations, and timing of diagnoses in relation to ICU admission and initiation of invasive ventilation. Secondary outcomes included the highest level of respiratory support prior to the diagnosis of air-leak syndrome, patient characteristics and treatment variables associated with air-leak syndrome, and 90-day mortality for patients with air-leak syndrome compared to those without.

Out of a total of 669 patients, 81 (12%) were diagnosed with air-leak syndrome. Air-leak syndrome manifested as pneumomediastinum (PMD) (n = 58, 72%), pneumothorax (PTX) (n = 43, 53%), subcutaneous emphysema (SCE) (n = 28, 35%) and pneumatocele (PC) (n = 4, 4.9%). Air-leak syndrome was diagnosed at a median of 14 days (IQR 6-22) after ICU admission and 12 days (IQR 6-19) following the initiation of invasive ventilation. The highest respiratory support prior to diagnosis was invasive ventilation (IV) in 64 patients (79%), non-invasive ventilation in two patients (2.5%), and low- or high-flow oxygen in 15 patients (19%). Multiple logistic regression showed that pulmonary disease at baseline (OR 1.87, 95% CI 1.07-3.25), a lower body mass index (OR 0.95, 95% CI 0.9-0.99), admission later compared with earlier in the pandemic (OR 3.89, 95% CI 2.14-7.08), and IV (OR 3.92, 95% CI 2.07-7.44) were associated with an increased risk of air-leak syndrome. Compared with patients not diagnosed with air-leak syndrome, patients with air-leaks had a higher mortality at 90 days after ICU admission, 46% versus 26% (p <.001). However, the mortality rate differed with different air-leak manifestations, 47% for PMD, 47% for PTX, 50% for the combination of both PMD and PTX and 0% in patients with only SCE and/or PC, respectively.

In 669 ICU patients with COVID-19, 12% had one or more manifestations of air-leak syndrome. Notably, PMD, rather than PTX, was the most common manifestation, suggesting a potentially distinctive feature of COVID-19-related air-leak syndrome. Further research is needed to determine whether COVID-19 involves different pathophysiological or iatrogenic mechanisms compared with other critical respiratory conditions.

Clinicaltrials.gov, identifying number, NCT05877443.

This single-centre cohort study of air leakage into soft tissue in ventilated COVID cases presents findings for associated factors and clinical manifestations, including with different COVID-19 periods and treatments.

Triglyceride-rich lipoproteins (TRLs) play essential roles in human health and disease by transporting bulk lipids into the circulation. This review summarizes the fundamental mechanisms and diverse factors governing lipoprotein production, secretion, and regulation. Emphasizing the broader implications for human health, we outline the intricate landscape of lipoprotein research and highlight the potential coordination between the biogenesis and transport of TRLs in physiology, particularly the unexpected coupling of metabolic enzymes and transport machineries. Challenges and opportunities in lipoprotein biology with respect to inherited diseases and viral infections are also discussed. Further characterization of the biogenesis and transport of TRLs will advance both basic research in lipid biology and translational medicine for metabolic diseases.

Background: The US Food and Drug Administration (FDA) and International Organization for Standardization (ISO) clearance standards for the clinical use of smart device pulse oximetry require in-laboratory human hypoxemia testing in healthy human individuals using arterial blood gas analysis. Methods: We evaluated the SpO2 measurements of the Samsung smartphone (Galaxy S9/10) and smartwatch (Galaxy 4) at stable arterial oxygen saturations (SaO2) between 70 and 100% in 24 healthy participants. Testing followed FDA/ISO-stipulated procedures for pulse oximetry performance validation, which include questionnaire estimation of skin tone based on Fitzpatrick estimation of skin types I-VI. During testing, inspired oxygen, nitrogen, and carbon dioxide partial pressures were monitored and adjusted via partial rebreathing circuits to achieve stable target arterial blood oxygen (SaO2) plateaus between 70% and 100%. Arterial blood samples were taken at each plateau, with device SpO2 readings taken at each sample extraction. An ABL-90FLEX blood gas analyzer determined arterial blood sample SaO2. Bias, calculated from device readings minus corresponding arterial blood measurements, was reported as root mean square deviation (RMSD). Results: Combined Participants demographics were: 62.5% female; median age 26 years (range 21-46); and race/ethnicity 16.7% African American, 33.3% Asian, 12.5% multi-ethnic, and 37.5% Caucasian. Fitzpatrick Skin Scale-identified skin tones were: white-fair (I&II), 20.8%; average-light brown (III-IV), 54% and brown-black (V-VI), 25%. There were no adverse events. The RMSD values of SpO2 measurements were: smartphone 2.6% (257 data pairs) and smartwatch 1.8% (247 data pairs). Conclusions: Device SpO2 demonstrated RMSD < 3.0% to SaO2, meeting FDA/ISO clearance standards at the time of study. However, additional testing in persons with darker skin tones is necessary. Smartphones and paired wearables, when cleared for clinical use following revision of FDA clearance standards, may expand access to remote pulse oximetry.

Chronic obstructive pulmonary disease (COPD) is a risk factor for severe COVID-19. However, mortality after COVID-19 recovery in this population remains unclear.

We retrospectively enrolled individuals with COPD from the Korean National Health Insurance database. We compared the mortality rate in individuals with COPD who recovered from COVID-19 between 8 October 2020 and 31 December 2021 (COVID-19 cohort, n=2499) with that in 1:1 propensity score-matched controls (n=2499). The study population was followed until either death or 30 September 2022, whichever came first.

The COVID-19 cohort had a 4.8% mortality rate vs 2.7% in matched controls during a median follow-up of 319 days (IQR, 293-422 days), including 14 days of recovery time. The COVID-19 cohort had a higher risk of death than matched controls (adjusted HR (aHR)=1.81, 95% CI=1.35 to 2.45). The risk of mortality was notably higher in individuals with severe COVID-19 (aHR=5.05, 95% CI=3.65 to 6.97), especially during the first 180 days of recovery (highest during the first 30 days (aHR=20.25, 95% CI=7.79 to 52.64)). Non-severe COVID-19 does not increase the risk of mortality compared with controls (aHR=0.85, 95% CI=0.57 to 1.28).

Individuals with COPD recovering from COVID-19 showed an increased risk of long-term mortality, particularly within the first 180 days post-recovery, especially those who experienced severe COVID-19.

Profound metabolomic alterations occur during COVID-19. Early identification of the subset of hospitalised COVID-19 patients at risk of developing severe disease is critical for optimal resource utilization and prompt treatment. This work explores the metabolomic profile of hospitalised adult COVID-19 patients with severe disease, and establishes a predictive signature for disease progression. Within 48 hours of admission, serum samples were collected from 148 hospitalised patients for nuclear magnetic resonance (NMR) spectroscopy. Lipoprotein profiling was performed using the 1H-NMR-based Liposcale test, while low molecular weight metabolites were analysed using one-dimensional Carr-Purcell-Meiboom-Gill pulse spectroscopy and an adaptation of the Dolphin method for lipophilic extracts. Severe COVID-19, per WHO's Clinical Progression Scale, was characterized by altered lipoprotein distribution, elevated signals of glyc-A and glyc-B, a shift towards a catabolic state with elevated levels of branched-chain amino acids, and accumulation of ketone bodies. Furthermore, COVID-19 patients initially presenting with moderate disease but progressing to severe stages exhibited a distinct metabolic signature. Our multivariate model demonstrated a cross-validated AUC of 0.82 and 72% predictive accuracy for severity progression. NMR spectroscopy-based metabolomic profiling enables the identification of moderate COVID-19 patients at risk of disease progression, aiding in resource allocation and early intervention.

The Coronavirus Disease 2019 (COVID-19), caused by virus SARS-CoV-2, is characterized by massive inflammation and immune system imbalance. Despite the implementation of vaccination protocols, the accessibility of treatment remains uneven. Furthermore, the persistent threat of new variants underscores the urgent need for expanded research into therapeutic options for SARS-CoV-2. Mesenchymal stem cells (MSCs) are known for their immunomodulatory potential through the release of molecules into the extracellular space, either as soluble elements or carried by extracellular vesicles (EVs). The aim of this study was to evaluate the anti-inflammatory potential of EVs obtained from human adipose tissue (ASC-EVs) against SARS-CoV-2 infection. ASC-EVs were purified by size-exclusion chromatography, and co-culture assays confirmed that ASC-EVs were internalized by human lung cells and could colocalize with SARS-CoV-2 into early and late endosomes. To determine the functionality of ASC-EVs, lung cells were infected with SARS-CoV-2 in the presence of increasing concentrations of ASC-EVs, and the release of cytokines, chemokines and viruses were measured. While SARS-CoV-2 replication was significantly reduced only at the highest concentrations tested, multiplex analysis highlighted that lower concentrations of ASC-EV sufficed to prevent the production of immune modulators. Importantly, ASC-EVs did not contain detectable inflammatory cytokines, nor did they trigger inflammatory mediators, nor affect cellular viability. In conclusion, this work suggests that ASC-EVs have the potential to attenuate inflammation by decreasing the production of pro-inflammatory cytokines in lung cells following SARS-CoV-2 infection.

Cepharanthine (CEP) is a natural remedy that potently inhibits SARS-CoV-2 activity both in vitro and in vivo. To evaluate the efficacy and safety of CEP compared with placebo in adults with asymptomatic or mild coronavirus disease 2019 (COVID-19), we conducted a proof-of-concept, double-blind, randomized, placebo-controlled trial. Patients were randomized to receive 120 mg/day of CEP, 60 mg/day CEP or placebo for 5 days. Main outcome was the time from randomization to negative nasopharyngeal swab and safety. Among 262 randomized participants, 188 completed the trial among group of 120 mg/day CEP (n = 65), 60 mg/day CEP (n = 68) and placebo (n = 55). Neither 120 mg/day or 60 mg/day CEP shortened the time to negative significantly compared with placebo. However, 60 mg/day CEP showed a slight trend (difference=-0.77 days, hazard ratio (HR) = 1.40, 95% CI 0.97-2.01, p = 0.072). In analysis of participants with good medication compliance, 60 mg/day CEP significantly shortened the time to negative (difference=-0.87 days, HR = 1.56, 95% CI 1.03-2.37, p = 0.035). Adverse events were not different among the three groups, and no serious adverse events occurred. In conclusion, treatment of asymptomatic or mild Covid-19 with 120 mg/day or 60 mg/day did not shorten the time to negative significantly. However, 60 mg/day CEP showed a slight trend which needs future confirmatory trials to validate. (NCT05398705).

A 61-year-old man with chronic renal failure had an embolic stroke of undetermined source that was treated with warfarin. Five weeks later, the patient contracted coronavirus disease (COVID-19). Six days after the onset of COVID-19, high blood pressure (>200 ‍mmHg) and consciousness disturbance were reported. CT demonstrated symmetrical hypodensity areas in the bilateral cerebellar hemispheres. MRI revealed hyperintensity lesions in the bilateral cerebellar hemispheres and pons on the T2-weighted and fluid-attenuated inversion recovery images. Moreover, cerebellar lesions appeared as hyperintensity areas on apparent diffusion coefficient mapping. Based on these findings, a diagnosis of posterior reversible encephalopathy syndrome (PRES) was made. The patient was treated with antihypertensive drugs, and the consciousness level improved gradually. MRI after one month showed that the lesions had disappeared. PRES should be considered if the brain CT of patients with COVID-19 shows a low-density lesion, especially in patients with risk factors for PRES such as chronic renal failure or hypertension.

SARS-CoV-2 emerged, and continues to evolve, to efficiently infect humans worldwide. SARS-CoV-2 evades early innate recognition, interferon signaling occurring only in bystander cells. How the virus continues to evolve in the face of innate responses has important consequences, but the pathways involved are incompletely understood. Here, we find that autophagy genes regulate innate immune signaling, impacting the basal set point of interferons and, thus, permissivity to infection. Mechanistically, autophagy (mitophagy) genes negatively regulate MAVS, and this low basal level of MAVS is efficiently antagonized by SARS-CoV-2 ORF9b, blocking interferon activation in infected cells. However, loss of autophagy increased MAVS and overcomes ORF9b-mediated antagonism. This has driven the evolution of SARS-CoV-2 to express more ORF9b, allowing SARS-CoV-2 to replicate under conditions of increased MAVS signaling. Altogether, we find a critical role of mitophagy in the regulation of innate immunity and uncover an evolutionary trajectory of SARS-CoV-2 ORF9b to overcome host defenses.

This study aimed to investigate the relationship of psychological empowerment and enjoyment of physical activity with changes in physical activity levels, sleep quality, and muscular endurance following a high-intensity interval training (HIIT) program in physically inactive young women.

A total of 61 physically inactive young women (age: 20.1 ± 2.7 y) were recruited to participate in a six-month HIIT intervention delivered via a smartphone app. Outcome measures included physical activity levels (MET-min/week), muscular endurance (plank test), and sleep quality through the Pittsburgh Sleep Quality Index (PSQI). The Healthy Lifestyle and Personal Control Questionnaire (HLPCQ) and the Physical Activity Enjoyment Scale (PACES) were used to assess psychological empowerment and enjoyment, respectively. Repeated measures ANOVA and covariate analyses were performed to evaluate the impact of the intervention and the role of psychological empowerment and enjoyment.

At 6 months, significant improvements in physical activity (p < 0.001; ηp²=0.336) and muscular endurance (p = 0.005; ηp²=0.085) were observed, with large and moderate effect sizes, respectively. The PACES showed a significant interaction with time for MET-min/week (F = 11.67, p = 0.001, ηp²=0.129), suggesting that enjoyment influenced the increase in physical activity. No significant differences in sleep quality were observed (p > 0.05).

Enjoyment plays a crucial role in the response to HIIT programs among physically inactive young women, particularly in improving weekly physical activity levels. Psychological training showed no significant relationship with the outcomes studied.

Measuring virus in biofluids is complicated by confounding biomolecules coisolated with viral nucleic acids. To address this, we developed an affinity-based microfluidic device for specific capture of intact severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Our approach used an engineered angiotensin-converting enzyme 2 to capture intact virus from plasma and other complex biofluids. Our device leverages a staggered herringbone pattern, nanoparticle surface coating, and processing conditions to achieve detection of as few as 3 viral copies per milliliter. We further validated our microfluidic assay on 103 plasma, 36 saliva, and 29 stool samples collected from unique patients with COVID-19, showing SARS-CoV-2 detection in 72% of plasma samples. Longitudinal monitoring in the plasma revealed our device's capacity for ultrasensitive detection of active viral infections over time. Our technology can be adapted to target other viruses using relevant cell entry molecules for affinity capture. This versatility underscores the potential for widespread application in viral load monitoring and disease management.

Introduction: Long-term lung sequelae in severe COVID-19 survivors, as well as their treatment, are poorly described in the current literature. Objective: To investigate lung fibrotic sequelae in survivors of severe/critical COVID-19 pneumonia and their fate according to a "non-interventional" approach. Methods: Prospective study of the above COVID-19 survivors after hospital discharge from March 2020 to October 2022. Re-evaluation lasted 3-12 months and included chest HRCT, PFTs, dyspnea, and overall health evaluation by modified Medical Research Council (mMRC) and St. George's Respiratory Questionnaire (SGRQ), respectively. Results: In this study, 198 patients (61.1% male) with a median age of 57 years (IQR 49-66). After 3 months, 187 (94.4%) patients were assessed; after 6 months, 82 (41.1%) patients were assessed; and after 12 months, 16 (8%) patients were assessed. At each time point, a significant reduction was observed in the extent of COVID-19-associated opacities (p < 0.001 and p = 0.002) and of parenchymal bands (p = 0.014 and p = 0.025). Persisting fibrotic-like changes were observed in 18 (9%) patients (apical findings in 2 patients, fibrotic non-specific interstitial pneumonia-like changes in 14 patients, minimal fibrotic changes in 2 patients). At 3 months, the predicted median FVC% was 93% (80-100%) and the predicted DLCO% was 65% (58-78%) with a statistically significant improvement at 6 months in both (p = 0.001). Moreover, 81.1% had mMRC ≤ 1 and the median SGRQ was 11.65 [0-24.3] with a significant reduction at 6 months in both dyspnea (p < 0.001) and SGRQ (p = 0.027) persisting at 12 months. Conclusions: This prospective study, including only survivors of severe/critical COVID-19 pneumonia, documented the significant improvement in all imaging, functional, and clinical parameters by applying the "non-interventional" approach. These data do not indicate any post-COVID-19 severe/critical pneumonia and "epidemic of widespread pulmonary fibrosis".

COVID-19 severity and high in-hospital mortality are often associated with severe hypoxemia, hyperlactatemia, and acidosis, yet the key players driving this association remain unclear. It is generally assumed that organ damage causes toxic acidosis, but since neutrophil numbers in severe COVID-19 can exceed 80% of the total circulating leukocytes, we asked if metabolic acidosis mediated by the glycolytic neutrophils is associated with lung damage and impaired oxygen delivery in critically ill patients.

Based on prospective mortality outcome, critically ill COVID-19 patients were divided into ICU- survivors and ICU-non-survivors. Samples were analyzed to explore if correlations exist between neutrophil counts, lung damage, glycolysis, blood lactate, blood pH, hemoglobin oxygen saturation, and mortality outcome. We also interrogated isolated neutrophils, platelets, and PBMCs for glycolytic activities.

Arterial blood gas analyses showed remarkable hypoxemia in non-survivors with no consistent differences in PCO2 or [HCO3 -]. The hemoglobin oxygen dissociation curve revealed a right-shift, consistent with lower blood-pH and elevated blood lactate in non-survivors. Metabolic analysis of different blood cells revealed increased glycolytic activity only when considering the total number of neutrophils.

This indicates the role of neutrophilia in hyperlactatemia and lung damage, subsequently contributing to mortality outcomes in severe SARS-CoV-2 infection.

Extracorporeal Membrane Oxygenation (ECMO) serves as a crucial intervention for patients with severe pulmonary dysfunction by facilitating oxygenation and carbon dioxide removal. While traditional ECMO systems are effective, their large priming volumes and significant blood-contacting surface areas can lead to complications, particularly in neonates and pediatric patients. Microfluidic ECMO systems offer a promising alternative by miniaturizing the ECMO technology, reducing blood volume requirements, and minimizing device surface area to improve safety and efficiency. This study investigates the oxygen transport performance of three membrane types- polydimethylsiloxane (PDMS), polypropylene, and a novel nanoporous silicon nitride (SiN) membrane-in a microfluidic ECMO platform. While nanoporous membranes rely on pore-mediated diffusion and PDMS on polymer lattice diffusion, results show no significant differences in device oxygenation efficiency (p > 0.05). Blood-side factors, including the diffusion rate of oxygen through the red blood cell (RBC) membrane, RBC residence time, and hemoglobin binding kinetics, were identified as primary bottlenecks. Even computational models of a hypothetical infinitely permeable membrane corroborate the limited impact of membrane material. These findings suggest a shift in ECMO design priorities from membrane material to blood-side enhancements. This research provides a foundation for optimizing ECMO systems.

The role of home oxygen therapy for patients recovering from Coronavirus Disease 2019 (COVID-19) pneumonia, characterized by impaired gas exchange, is not well-defined.

To compare the characteristics, duration, odds of receiving, and continuing to receive home oxygen prescriptions between patients discharged home after COVID-19 pneumonia hospitalization and those discharged after non-COVID-19 pneumonia.

From April 2020 to March 2021, 52,951 patients with COVID-19 pneumonia (53.6 % women, 64 % White) were identified, and from January 2019 to December 2019, 26,701 patients with non-COVID pneumonia (53.9 % women, 76.7 % White) were identified, using the Optum Clinformatics Data Mart Database. New oxygen prescriptions were identified through Healthcare Common Procedure Coding Systems codes. Propensity score matching adjusted for confounders, and Cox regression analysis was conducted to compare post-discharge oxygen use.

Following hospitalization, oxygen was prescribed to 52,951 patients with COVID-19 pneumonia and 26,701 patients with non-COVID pneumonia in the United States. The COVID-19 pneumonia group were four times more likely to be prescribed supplemental oxygen compared to the non-COVID-19 pneumonia group (OR 4.22; 95 % confidence interval [CI] 3.76-4.74). This trend persisted in sensitivity analyses: ICU patients (OR 4.05; 95 % CI 3.36-4.88) and those who received both ICU admission and mechanical ventilation (OR 3.84; 95 % CI 2.32-6.37). Hispanic patients had the highest likelihood of receiving a supplemental oxygen prescription after discharge (OR 6.75; 95 % CI 5.03-9.05).

Post-hospitalization, one in five patients with COVID-19 received prescriptions for supplemental oxygen, which was significantly higher than the proportion of patients with non-COVID-19 pneumonia.

COVID-19 pandemic research efforts have mainly focused on adults, but data in paediatric populations are sparse.

We used the German nationwide-inpatient-sample analysing all hospitalized children ≤18 years with confirmed COVID-19-diagnosis in Germany during the year 2020, stratified for intensive care unit (ICU) admission.

Overall, 3360 hospitalization-cases of children ≤18 years with COVID-19-infection were diagnosed in Germany 2020 (median age 7.0 [IQR 0.0-15.0] years, 49.8 % female); among them 4.3 % were admitted on an ICU. In-hospital death occurred in five patients with and three without ICU admission (3.5 % vs. 0.1 %, P < 0.001) and ICU admission was independently associated with increased case-fatality (OR 21.573 [95%CI 4.191-111.044], P < 0.001). Obesity (OR 3.419 [95%CI 1.300-8.993], P = 0.013), diabetes mellitus (OR 6.929 [95%CI 3.327-14.432], P < 0.001), pneumonia (OR 7.373 [95%CI 4.823-11.271], P < 0.001), acute respiratory distress syndrome (ARDS) (OR 48.058 [95%CI 11.689-197.588], P < 0.001) and multisystem inflammatory syndrome caused by COVID-19 (OR 9.573 [95%CI 3.036-30.191], P < 0.001), heart failure (OR 64.509 [95%CI 24.462-170.121], P < 0.001), myocarditis (OR 4.682 [95%CI 1.278-17.149], P = 0.020), acute and/or chronic kidney failure (OR 7.946 [95%CI 3.606-17.508], P < 0.001), cancer (OR 5.220 [95%CI 2.599-10.485], P < 0.001) and liver diseases (OR 5.501 [95%CI 2.177-13.899], P < 0.001) were associated with an ICU admission.

Proportion of hospitalized paediatric COVID-19-patients admitted on ICU in Germany was low with 4.3 % accompanied by 3.5 % case-fatality rate. Independent factors for ICU admission comprised cardio-vascular risk factors, comorbidities, and complications of COVID-19.

Bruton's Tyrosine Kinase (BTK), an important element for the production of several inflammatory cytokines, may play a role in the pathogenesis of COVID-19. This study aimed to assess BTK gene expression levels in COVID-19 cases based on disease severity and outcome.

In this study, 33 hospitalized patients with COVID-19 were recruited and divided into two groups based on the severity of the disease: "mild to moderate" and "severe to critical". A blood sample was taken from each patient, peripheral blood mononuclear cells (PBMCs) were extracted, and BTK gene expression was measured. The level of BTK gene expression was compared based on the demographic data, laboratory results, and the severity and outcome of the disease.

Among the 33 patients, 22 (66.7%) were male, with nearly half having at least one underlying condition. The severity groups comprised 12 patients in the "mild to moderate" category and 21 in the "severe to critical" category, with eight (24.2%) experiencing fatal outcomes. Age, weight, and BMI showed no significant associations with BTK expression. BTK expression was notably lower in "severe to critical" and ICU-admitted cases, as well as in individuals with low O2 saturation. However, no significant difference in BTK expression was observed between cured and deceased patients (p = 0.117).

BTK gene expression in PBMCs exhibited an inverse correlation with COVID- 19 severity. However, no difference was found between BTK expression and disease outcome.

Receptor-interacting protein kinase 1 (RIPK1), a serine/threonine protein kinase, is mainly activated by pro-inflammatory cytokines and pathogens, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and its activation could result in apoptosis, necroptosis, or inflammation. This study was conducted to evaluate the safety and efficacy of a potent and selective inhibitor of RIPK1, SIR1-365, in hospitalized patients with severe coronavirus disease 2019 (COVID-19).

This multicenter, randomized, double-blind, phase 1b study screened patients from December 18, 2020 until November 27, 2021. Adults hospitalized with severe COVID-19 (diagnosed ≤2 weeks before screening) were randomized 1:1 to receive oral placebo or SIR1-365 100 mg three times daily for ≤14 consecutive days, with standard-of-care. The primary objective was to evaluate SIR1-365 safety and tolerability. Secondary objectives included an assessment of SIR1-365 efficacy. Descriptive statistics were used to summarize safety. The study was not powered for efficacy testing. Relevant inferential statistical tests were used to aid interpretation of differences in clinical efficacy.

Forty-five patients were randomized, 42 were treated. Eighteen patients experienced treatment-emergent adverse events (TEAEs) and 7 patients were ≥ grade 3. Fewer SIR1-365-treated vs. placebo-treated patients experienced TEAEs (30.4% vs. 57.9%) and serious TEAEs (13.0% vs. 26.3%) within 28 days of the first dose. There were no serious treatment-related TEAEs or deaths. Compare to placebo, SIR1-365 significantly increased arterial oxygenation from baseline to day 7 (least-squares mean change [standard error]: 109.4 [26.4] vs. -24.2 [23.6]; P=0.0095), significantly reduced hospitalization duration after treatment (mean±standard deviation: [4.7±3.7] days vs. [8.6±5.6] days; P=0.0145) and respiratory failure incidence (8.3% vs. 38.1%; two-sided P=0.0291) during the study, and numerically shortened the time to clinical improvement in World Health Organization ordinal scale (median: 5.0 days vs. 9.0 days, P=0.0766).

SIR1-365 was well tolerated and demonstrated a trend toward quicker recovery than placebo in hospitalized patients with severe COVID-19.Trial Registration ClinicalTrials.gov number: NCT04622332.

Severe disease due to COVID-19 has declined dramatically as a result of widespread vaccination and natural immunity in the population. With the emergence of SARS-CoV-2 variants that largely escape vaccine-elicited neutralizing antibody responses, the efficacy of the original vaccines has waned and has required vaccine updating and boosting. Nevertheless, hospitalizations and deaths due to COVID-19 have remained low. In this review, we summarize current knowledge of immune responses that contribute to population immunity and the mechanisms how vaccines attenuate COVID-19 disease severity.

Telemedicine is an innovative medical care system that facilitates visual communication between patients and healthcare workers (HCWs), mainly in a community-based setting. We investigated the clinical effectiveness of in-patient telemedicine care for patients in quarantine for the Coronavirus disease 2019 (COVID-19).

We conducted a prospective study to include patients with mild-to-moderate severity of COVID-19 and their primary-care HCWs. Patients were stratified into the "telemedicine" group and the "standard-care" group. The telemedicine group received additional telemedicine communications and wearable devices for vital signs monitoring during hospitalization. The primary endpoint was the usability of the telemedicine system assessed by the modified telehealth usability questionnaire (TUQ) on a 7-point ordinal Likert scale. The secondary endpoints were the outcomes of COVID-19.

Overall, we included 30 and 48 patients in the respective standard-care group and telemedicine group. In addition, 31 primary care residents and 56 nurses were included in the HCW groups. For all participants, the modified TUQ responses in the categories of usefulness (6.2), ease of use (6.1), effectiveness (6.0), and satisfaction (6.1) were significantly greater than 5 (somewhat agree), except for the reliability sectors (5.3). The telemedicine group liked the telemedicine system significantly more than the HCWs. The doctors scored significantly higher than the nurses in the categories of effectiveness and satisfaction of the telemedicine systems. The outcomes of COVID-19 were comparable between the telemedicine and the standard-care group.

Our study demonstrated the clinical effectiveness and satisfaction of the telemedicine for the care of quarantined COVID-19 patients during hospitalization.

SUMMARYDetection of the presence of infection and its etiology must be accurate and timely to facilitate appropriate antimicrobial use. Diagnostic strategies that rely solely on pathogen detection often are insufficient due to poor test characteristics, inability to differentiate colonization from infection, or protracted delay to result. Understanding the human response across different pathogens on a clinical and molecular level can provide more accurate, timely, and useful answers, especially in critical illness and diagnostic uncertainty. Improvements in understanding the human immune response including genomics, protein analysis, gene expression, and cellular morphology have led to rapid innovation of new host response-based diagnostic tests. This review describes the limitations of pathogen-focused technology and the benefits of examining the breadth of immune response to diagnose infection. It then explores biomarkers that have been studied for this purpose and scrutinizes the performance of host-based multianalyte testing. Currently cleared diagnostics and those in late-stage development are described in depth, with a focus on the purpose of testing and its utility for clinicians. Finally, it concludes by examining opportunities for further host response-derived diagnostic innovation.

The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has significantly impacted the global healthcare system, with particularly harmful effects on the human respiratory system. Beyond the acute symptoms, there is growing concern about persistent symptoms that last for weeks or months after the initial infection, known as long COVID syndrome. This study focuses on investigating the relationship between smoking, obesity, and the presence of post-COVID-19 sequelae, as well as their influence on the risk of hospitalization.

An observational and retrospective study was conducted using medical records of patients diagnosed with COVID-19 in Castilla y León, Spain, between November 1 and 30, 2020. The patients were divided into three groups: smoking (current and former), obesity/overweight, and control group. Various variables were analyzed, including age, sex, and the presence of post-COVID-19 sequelae, chronic pathologies, cardiovascular diseases, psychological conditions, and hospitalization. Descriptive statistics and Odds Ratio analysis were used for comparisons.

The results revealed that obesity was significantly associated with a higher risk of post-COVID-19 sequelae, particularly memory disorders and neurological, mental, or psychological symptoms. In contrast, smoking was correlated with an increase in memory problems but did not show a direct influence on post-COVID-19 sequelae or hospitalization. Additionally, women were found to have a higher prevalence of obesity in the studied population.

This study provides evidence that obesity increases the risk of post-COVID-19 sequelae, especially in terms of memory disorders and neuropsychological symptoms. On the other hand, smoking is related to memory problems. Regarding cardiovascular pathologies, there was not enough statistical evidence for analysis, while for hospitalization, it was determined that smoking and obesity do not have a direct influence on these post-COVID consequences.