When the coronavirus case was originally reported in Wuhan, China, in December 2019, it quickly spread throughout the world and became a global public health problem. Evidence of the admission and outcomes of coronavirus disease among patients with chronic obstructive pulmonary disease (COPD) has not been reported in Africa. Consequently, this research protocol uses a systematic review and meta-analysis of the admission and outcomes of COVID-19 in patients with COPD in Africa. All observational studies published in the English language and reporting on the prevalence, admission and outcomes of COVID-19 among patients with COPD in Africa will be included. A search strategy will be implemented using electronic databases and the Preferred Reporting Items for Systematic Reviews and Meta-Analysis Protocol recommendations. The findings of this review will be reported to health program designers, decision-makers and healthcare providers.

Although the SARS-CoV-2 infection has established risk groups, identifying biomarkers for disease outcomes is still crucial to stratify patient risk and enhance clinical management. Optimal efficacy of COVID-19 antiviral medications relies on early administration within the initial 5 d of symptoms, assisting high-risk patients in avoiding hospitalization and improving survival chances. The complete blood count (CBC) can be an efficient and affordable option to find biomarkers that predict the COVID-19 prognosis due to infection-induced alterations in various blood parameters. This study aimed to associate hematological parameters with different COVID-19 clinical forms and utilizes them as disease outcome predictors. We performed a CBC in blood samples from 297 individuals with COVID-19 from Belo Horizonte, Brazil. Statistical analysis, as well as ROC Curves and machine learning Decision Tree algorithms were used to identify correlations, and their accuracy, between blood parameters and disease severity. In the initial 4 d of infection, traditional hematological COVID-19 alterations, such as lymphopenia, were not yet apparent. However, the monocyte percentage and granulocyte-to-lymphocyte ratio (GLR) proved to be reliable predictors for hospitalization, even in cases where patients exhibited mild symptoms that later progressed to hospitalization. Thus, our findings demonstrate that COVID-19 patients with monocyte percentages lower than 7.7% and a GLR higher than 8.75 are assigned to the hospitalized group with a precision of 86%. This suggests that these variables can serve as important biomarkers in predicting disease outcomes and could be used to differentiate patients at hospital admission for managing therapeutic interventions, including early antiviral administration. Moreover, they are simple parameters that can be useful in minimally equipped health care units.

The COVID-19 (SARS-CoV-2) epidemic has posed a major challenge to global public health, especially in children. Some children may experience secondary infection with Mycoplasma pneumoniae after SARS-CoV-2 infection, which has attracted widespread attention. Studies have shown that eosinophils play an important role in respiratory tract infections and are involved in regulating immune responses and inflammatory processes. However, there is a lack of systematic research on the specific manifestations and mechanisms of eosinophils in secondary infection with Mycoplasma pneumoniae after SARS-CoV-2 infection.

This study aims to explore the characteristics of immune response in children with SARS-CoV-2 infection and Mycoplasma pneumoniae infection, focusing on the changes in immune indicators such as eosinophils (EOS), immunoglobulin E (IgE), interleukin-6 (IL-6), C-reactive protein (CRP), and procalcitonin (PCT).

This study is a retrospective observational study, and a total of pediatric patients who were treated in our hospital from January 2023 to December 2023 were included. The study group included children who were diagnosed with SARS-CoV-2 infection and further infected with Mycoplasma pneumoniae, and the control group included children who were only infected with SARS-CoV-2 and had no other pathogens. The clinical data of the two groups of patients, including absolute eosinophil value, IgE quantification, IL-6, CRP and PCT levels, were collected and analyzed, and statistical comparisons were performed.

A total of 134 children were included, including 79 in the study group and 55 in the control group. The absolute eosinophil value [0.17 (0.09, 0.31) vs. 0.09 (0.06, 0.23), P < 0.01] and IgE level [59.28 (37.54, 256.88) vs. 22.00 (11.00, 113.10) P < 0.01] of the children in the study group were significantly higher than those in the control group, while IL-6 [16.81(4.72,31.86) vs. 9.5(3,57.3), P = 0.602], CRP [2.82(1.10,6.13) vs. 1.94(0.50,8.94), P = 0.528] and PCT[0.12(0.08,0.20) vs. 0.12(0.10,0.24), P = 0.329] were no significant difference between the two groups. Binary logistic regression analysis showed that the absolute value of eosinophils and IgE were independent risk factors for secondary infection of Mycoplasma pneumoniae after SARS-CoV-2 infection.

This study shows that after SARS-CoV-2 infection, the increase in eosinophils and the increase in related immune indicators IgE may be closely related to secondary infection with Mycoplasma pneumoniae. This study provides an important basis for understanding the immune response of children after SARS-CoV-2 infection and its related clinical management, suggesting that clinicians should closely monitor the eosinophil count and IgE level of children after SARS-CoV-2 infection, especially for children at risk of secondary infection, so as to take timely intervention measures to prevent secondary infection with Mycoplasma pneumoniae and improve the prognosis of children.

(1) Background: The implication of type 2 (T2) inflammatory response in COVID-19 remains controversial. This study aimed to evaluate the association of eosinophils, neutrophils expressing eosinophilic surface markers and T2 cytokines with the severity and outcome of COVID-19. (2) Methods: Patients who were admitted to hospital due to COVID-19 from 18 December 2022 to 31 January 2023 were enrolled. Peripheral blood WBC and differentials, T2 cellular markers (subsets of eosinophils and neutrophils expressing eosinophilic surface markers) and cytokines at admission were measured and compared between subjects with different disease severities and outcomes. (3) Results: Ten mild-to-moderate and 22 severe-to-very severe cases were enrolled for analysis. Of these patients, seven died of severe-to-very severe disease. The severe-to-very severe patients showed a higher number of neutrophils, but lower numbers of eosinophils, lymphocytes cells and neutrophils expressing eosinophilic surface markers. Similarly, deceased cases were also characterized by increased neutrophils, but decreased eosinophils and neutrophils expressing eosinophilic surface markers. The levels of T2 cytokines failed to demonstrate a significant correlation with the severity or outcome of COVID-19. (4) Conclusions: Eosinophils and neutrophils expressing eosinophilic surface markers were associated with milder disease and better outcomes of COVID-19, suggesting that a T2 inflammatory response may confer a potential protective effect against the disease.

Coinfections in patients with coronavirus disease 2019 (COVID-19) affect patient prognosis. Patients with hematologic malignancies (HMs) are usually immunosuppressed and may be at high risk of coinfection, but few related data have been reported. Here, we conducted a retrospective study to explore coinfections in patients with HMs and COVID-19 by next-generation sequencing (NGS) of bronchoalveolar lavage fluid (BALF).

The data of hospitalized patients with pneumonia who underwent NGS analysis of BALF were reviewed. COVID-19 patients with HMs were enrolled in the HM group, and those without HMs were enrolled in the non-HM group. The coinfections of the two groups identified by NGS were analyzed.

Fifteen patients were enrolled in the HM group, and 14 patients were enrolled in the non-HM group. The coinfection rates in the HM group and non-HM group were 80.0% and 85.7%, respectively. The percentage of coinfected bacteria in the HM group was significantly lower than that in the non-HM group (20.0% vs 71.4%, p = 0.005). The coinfection rates of fungi and viruses were 60.0% and 35.7%, respectively, in the HM group and 35.7% and 78.6%, respectively, in the non-HM group, with no significant differences. The most common coexisting pathogen in patients with HMs was Pneumocystis jirovecii (33.3%), and the most common coexisting pathogen in patients without HMs was human gammaherpesvirus 4 (50%). Coinfection with herpesviruses occurred frequently in both groups.

Our study showed that the majority of hospitalized patients with COVID-19 are likely to be co-infected with other pathogens. Pneumocystis jiroveci and herpesvirus are commonly coinfected pathogens in patients with HMs. Bacterial coinfection is rare in patients with HMs but is more common in patients without HMs.

The clinical spectrum of COVID-19 varies considerably, ranging from asymptomatic cases to severe disease and even death. This variability can partly be attributed to genetic differences in genes associated with inflammation and immune responses. Among these genes, Interferon Induced with Helicase C Domain 1 (IFIH1), which codes for a cytoplasmic sensor, plays a crucial role in detecting SARS-CoV-2 viral RNA and initiating the antiviral interferon (IFN) response, thereby constituting a key element of innate immune defense.

This study aims to examine the association between genetic variants in the IFIH1 gene and susceptibility to, as well as the severity of, COVID-19 in the Moroccan population.

We conducted a case-control study involving 299 COVID-19 positive patients (149 severe, 150 benign) and 145 uninfected-SARS-CoV-2 controls. We determined the genotypes of two functional variants, rs1990760 (Ala946Thr) and rs3747517 (His843Arg), in the IFIH1 gene using predesigned TaqMan real-time allelic discrimination assay.

Our results indicated that the TT genotype of rs1990760 was associated with increased susceptibility to SARS-CoV-2 under a recessive model (odds ratio [OR] = 2.22, 95 % confidence interval [CI] 1.28-3.84, P=0.003). Conversely, the CT genotype appeared to confer protection against SARS-CoV-2 infection (OR=0.58, 95 % CI 0.38-0.91, P=0.016) and COVID-19 severity (OR=0.56, 95 % CI 0.34-0.91, P=0.019). No significant association was found between rs3747517 and the risk of hospitalization or infection susceptibility.

These findings underscore the significance of genetic variability in the IFIH1 gene in shaping individual responses to SARS-CoV-2 in the Moroccan population.

Patients often experience multiple prolonged symptoms following acute coronavirus disease 2019 (COVID-19) recovery, defined as long coronavirus disease (COVID). Patients with long COVID may experience dyspnea during acute and post-acute phases. Therefore, this study aimed to identify specific risk factors for dyspnea in patients with long COVID.

Hospitalized patients with COVID-19, aged ≥18 years, were enrolled in this multicenter cohort study conducted at 26 medical institutions across Japan. Clinical data during hospitalization and patient-reported outcomes after discharge at the 3, 6, and 12-month follow-ups were retrieved from medical records and paper-based or smartphone application-based questionnaires, respectively.

Generalized linear mixed model (GLMM) analysis of prolonged dyspnea at each time point during follow-up showed that this symptom was associated with chronic obstructive pulmonary disease (COPD) (odds ratio [OR], 2.74; 95% confidence interval [CI], 1.31-5.74), asthma (OR, 2.21; 95%CI, 1.17-4.16), and ventilator management (OR, 3.10; 95%CI, 1.65-5.83). In addition, patients with COPD (44.4%) and ventilator management (25.0%) were more frequently associated with delayed dyspnea onset. The generalized estimating equations analysis results with multiple imputed datasets, conducted as a sensitivity analysis, confirmed the adjusted GLMM analysis results.

Prolonged dyspnea was associated with COPD, asthma, and severe infection that required mechanical ventilation in the Japanese population with long COVID. Further investigation is needed to clarify its mechanism and develop prophylactic and therapeutic strategies for dyspnea in patients with long COVID.

Even after the development of vaccines, SARS-CoV-2 continues to cause severe pneumonia all over the world. Consequently, in order to improve the management of patients and optimize the use of resources, predictors of disease severity and lung complications after COVID-19 pneumonia are urgently needed. Blood cell count is an easily available and reproducible biomarker. With this study, we aimed to explore the role of eosinophils in predicting disease behavior and pulmonary sequelae at first follow-up with computed tomography (CT).

we evaluated blood cell count and other inflammatory markers, both at baseline and during hospitalization, in a large population of hospitalized COVID-19 patients.

327 patients were finally enrolled, 214 were classified as low-intensity medical care (LIMC) and 113 as high-intensity medical care. Eosinophils were higher at discharge in the HIMC group [0.1 (0-0.72) vs. 0.05 (0-0.34) × 109/L; p < 0.0001]. Moreover, in the multivariable analysis, age ≥ 62 years (OR 1.76 (1.05-2.8) p = 0.03) and Δ eosinophils ≥ 0.05 (OR 1.75 (1.05-2.9) p = 0.03) were two independent predictors of residual lung abnormalities in the whole patient population at first follow-up.

an eosinophil increase during hospitalization could be a potential predictor of pulmonary sequelae in surviving patients after COVID-19 pneumonia.

The purpose of this study was to identify independent risk factors affecting patient survival and explore predictors of severe cases of coronavirus disease 2019 (COVID-19).

We conducted a retrospective, observational, case-control study on adult patients with severe COVID-19 who were admitted to affiliated hospitals in Tianjin between December 18, 2022, and January 31, 2023. We used univariate and multifactorial logistic regression analyses to analyze demographic indicators, comorbidity profiles, and laboratory parameters in two groups of patients (deceased and surviving) to identify independent risk factors for death in patients with severe COVID-19.

Patients in the deceased group were older than those in the survival group (p = 0.018), and there were more cases of coexisting respiratory insufficiency in the deceased group (p = 0.002). Additionally, laboratory test results for white blood cell count (WBC) and creatine kinase (CK) showed significantly higher values in the deceased group (p = 0.047 and p = 0.029, respectively), while arterial oxygen partial pressure (PAO2) showed significantly lower values compared to the survival group (p = 0.021). Age, respiratory insufficiency, WBCH (highest WBC value), CKH (highest CK value), and PAO2F (first PAO2 value) had area under curve (AUC) values of 0.698, 0.838, 0.721, 0.744, and 0.633, respectively.

The main risk factors for mortality in patients with severe COVID-19 that we identified in this study were the advanced age of patients, coexisting respiratory insufficiency, elevated levels of WBC and CK, and decreased levels of PAO2. Elevated WBC and CK laboratory parameters, in particular, demonstrated good predictive value for in-hospital mortality risk.

In the Spring of 2020, the world was hit with unparalleled impact by the coronavirus pandemic. Antibiotics were widely used, even without good rationale. The aim of our study was to compare the use of antibiotics in patients with confirmed COVID-19 from three hospitals across Europe (Poland, the Netherlands and Spain) between two subsequent periods in the early days of the pandemic.

We analysed data (antibiotics used and variation in the use of antibiotics, patients, admission and disease-related characteristics) from 300 patients admitted in three hospitals (University Hospital in Cracow, University Medical Center in Utrecht and Vall d'Hebron University Hospital in Barcelona) with confirmed infection of SARS-CoV-2 during Q1 2020 and Q4 2020.

There was ample variation in terms of patient mix and outcomes across the 3 hospitals. The majority of patients (225 out of 300) in all 3 hospitals received at least 1 antibiotic during the hospitalisation period. A minority of patients (68 out of 300) had their bacterial test results positive during their hospitalisation period. Throughout the 2 study periods, third-generation cephalosporins (ceftriaxone in 170 out of 300 patients) emerged as the most commonly used class of antibiotics. There was an apparent shift towards more rational utilisation of antibiotics, in all three hospitals.

Our study shows that during the early stage of COVID-19 pandemic in 2020, antibiotics were frequently used in three European teaching hospitals despite the relatively low incidence of microbiologically confirmed bacterial infections. While in the early days of the COVID-19 pandemic antibiotic prescribing was full of trial and error, we could also confirm a learning curve over time.

Vitamin D is a steroid hormone that is naturally produced in the body or obtained through dietary sources, primarily under the influence of UVB radiation. This essential nutrient has a vital role in numerous physiological processes, encompassing immune function, cell growth, differentiation, insulin regulation, and cardiovascular well-being, along with its pivotal role in sustaining the delicate equilibrium of calcium and phosphate concentrations in the body. Moreover, vitamin D reinforces mucosal defense and bolsters the immune system through immunomodulation, making it a critical component of overall health. Numerous studies have unveiled the profound connection between vitamin D and the predisposition to respiratory tract infections, including well-known viruses such as influenza and the novel severe acute respiratory syndrome coronavirus 2. Vitamin D deficiency has been consistently linked to increased severity of coronavirus disease 2019 (COVID-19) and a heightened risk of mortality among afflicted individuals. Retrospective observational studies have further substantiated these findings, indicating that levels of vitamin D are linked with both the occurrence and severity of COVID-19 cases. Vitamin D has its influence on viral infections through a multitude of mechanisms, such as promoting the release of antimicrobial peptides and fine-tuning the responses of the immune system. Additionally, vitamin D is intertwined with the intricate network of the renin-angiotensin system, suggesting a potential impact on the development of complications related to COVID-19. While further clinical trials and extensive research are warranted, the existing body of evidence strongly hints at the possible use of vitamin D as a valuable tool in the prophylaxis and management of COVID-19 and other viral infectious diseases.

The Food and Drug Administration (FDA) authorized the administration of ritonavir (RIT)-boosted nirmatrelvir (NMV) on May 25, 2023, for the treatment of mild to moderate COVID-19 in patients who are at high risk of developing severe COVID-19. In accordance with sustainability and environmental friendliness, simple, eco-friendly, and sustainable spectrophotometric methods were established for concurrently estimating RIT and NMV in newly launched copackaged pills. The suggested solutions for resolving the spectral overlap between RIT and NMV involve the following mathematical methods: the first derivative method (1D), second derivative method (2D), and dual-wavelength zero-order method (DWZ). When ethanol was used as a green dilution solvent, the linearity range was adjusted (10-250 µg/mL) for both drugs. The procedures resulted in a high correlation coefficient (not less than 0.9996) and satisfactory levels of detection and quantification. Additionally, method validation was performed in accordance with International Council for Harmonization norms. Moreover, a detailed ecological and sustainability evaluation protocol was established to confirm the greenness and whiteness of the methods. Finally, the proposed method, along with previously reported methods for analysing NMV and RIT, were reviewed analytically and ecologically.

Rationale: Diaphragm muscle weakness might underlie persistent exertional dyspnea, despite normal lung and cardiac function in individuals who were previously hospitalized for acute coronavirus disease (COVID-19) illness. Objectives: The authors sought, first, to determine the persistence and pathophysiological nature of diaphragm muscle weakness and its association with exertional dyspnea 2 years after hospitalization for COVID-19 and, second, to investigate the impact of inspiratory muscle training (IMT) on diaphragm and inspiratory muscle weakness and exertional dyspnea in individuals with long COVID. Methods: Approximately 2 years after hospitalization for COVID-19, 30 individuals (11 women, 19 men; median age, 58 years; interquartile range [IQR] = 51-63) underwent comprehensive (invasive) respiratory muscle assessment and evaluation of dyspnea. Eighteen with persistent diaphragm muscle weakness and exertional dyspnea were randomized to 6 weeks of IMT or sham training; assessments were repeated immediately after and 6 weeks after IMT completion. The primary endpoint was change in inspiratory muscle fatiguability immediately after IMT. Measurements and Main Results: At a median of 31 months (IQR = 23-32) after hospitalization, 21 of 30 individuals reported relevant persistent exertional dyspnea. Diaphragm muscle weakness on exertion and reduced diaphragm cortical activation were potentially related to exertional dyspnea. Compared with sham control, IMT improved diaphragm and inspiratory muscle function (sniff transdiaphragmatic pressure, 83 cm H2O [IQR = 75-91] vs. 100 cm H2O [IQR = 81-113], P = 0.02), inspiratory muscle fatiguability (time to task failure, 365 s [IQR = 284-701] vs. 983 s [IQR = 551-1,494], P = 0.05), diaphragm voluntary activation index (79% [IQR = 63-92] vs. 89% [IQR = 75-94], P = 0.03), and dyspnea (Borg score, 7 [IQR = 5.5-8] vs. 6 [IQR = 4-7], P = 0.03). Improvements persisted for 6 weeks after IMT completion. Conclusions: To the best of the authors' knowledge, this study is the first to identify a potential treatment for persisting exertional dyspnea in long COVID and provide a possible pathophysiological explanation for the treatment benefit. Clinical trial registered with www.clinicaltrials.gov (NCT04854863, NCT05582642).

The clinical course of COVID-19 is variable and often unpredictable. To test the hypothesis that disease progression and inflammatory responses associate with alterations in the microbiome and metabolome, we analyzed metagenome, metabolome, cytokine, and transcriptome profiles of repeated samples from hospitalized COVID-19 patients and uninfected controls, and leveraged clinical information and post-hoc confounder analysis. Severe COVID-19 was associated with a depletion of beneficial intestinal microbes, whereas oropharyngeal microbiota disturbance was mainly linked to antibiotic use. COVID-19 severity was also associated with enhanced plasma concentrations of kynurenine and reduced levels of several other tryptophan metabolites, lysophosphatidylcholines, and secondary bile acids. Moreover, reduced concentrations of various tryptophan metabolites were associated with depletion of Faecalibacterium, and tryptophan decrease and kynurenine increase were linked to enhanced production of inflammatory cytokines. Collectively, our study identifies correlated microbiome and metabolome alterations as a potential contributor to inflammatory dysregulation in severe COVID-19.

It is not always possible to differentiate between influenza and COVID-19 based on symptoms alone. This is a topic of significant importance as it aims to determine whether there are specific hematological parameters that can be used to distinguish between influenza and COVID-19 in children.

Two hundred thirty-one children between the ages of 1 month and 18 years who presented to the children's outpatient clinic between June 2021 and June 2022 with similar symptoms and were tested with an influenza test and a COVID-19 PCR test were included in the study. Of the patients included in the study, 130 tested positive for COVID-19 and 101 positive for influenza. The patients were evaluated for hematological parameters.

Age, eosinophils and monocyte factors were shown to be statistically significantly effective in COVID-19. The risk of COVID-19 increased 1,484-fold with age, 10,708-fold with increasing eosinophil count, and 1,591-fold with increasing monocyte count. The performance of the monocyte count and eosinophil count was assessed by receiver operating characteristic curve (ROC) analysis. According to the performed ROC analysis, the area under the curve (AUC) value was observed to be 0.990 for monocytes. According to the cutoff point >1.50, the sensitivity value was determined as 98.4% and the specificity value as 97.0%. AUC significance for eosinophils was found to be 0.989. According to the cutoff point >0.02, the sensitivity value was determined as 99.2% and the specificity value as 93.1%.

In the diagnosis of COVID-19, the eosinophil count and monocyte count are easily accessible, inexpensive, and important parameters in terms of differential diagnosis and can help in the differentiation of COVID-19 from influenza during seasonal outbreaks of the latter. Developing parameters for clinicians to use in diagnosing COVID-19 and influenza can facilitate their work in practice.

COVID-19 illness severity ranges from mild- to life-threatening cases necessitating critical care. Rapid prediction of disease severity and the need for critical care support in COVID-19 patients remain essential, not only for current management but also for preparedness in future pandemics. This study aimed to assess hematological parameters as predictors of intensive care unit (ICU) admission and survival in COVID-19 patients, providing insights applicable to a broad range of infectious diseases.

A case-control study was conducted at Hospital Raja Perempuan Zainab II, a tertiary referral hospital in Kelantan, Malaysia, from March 2020 to August 2021. Demographics, clinical, and laboratory data were retrieved from patients' medical records. Statistical analyses, including the Chi-square (χ2) test, independent t-tests, and simple and multiple logistic regressions, were used to analyze the data. A receiver operating characteristic (ROC) curve analysis was conducted to assess the accuracy of the predictors.

The median age was 51 years, with females comprising 56.7% (n=148) and males 43.3% (n=113). A total of 88.5% of patients were admitted to non-ICU wards, with a mortality rate of 5.7%. Significant differences were observed in the distribution of hematological parameters between ICU-admitted and non-admitted patients. Neutrophil (OR: 23.96, 95% CI: 7.296-78.675) and white blood cell (WBC) count (OR: 36.677, 95% CI: 2.086-644.889) were the most significant predictors for ICU admission and survival, respectively.

WBC and neutrophil counts exhibited high predictive value for ICU admission, while WBC, neutrophil, lymphocyte, and immature granulocyte (IG) counts were significant predictors of survival status among COVID-19 patients. These findings underscore the continued relevance of hematological markers in managing severe respiratory infections and improving critical care triage, with implications for current and future healthcare challenges.

At the beginning of the 2019 coronavirus disease (COVID-19) pandemic, airway allergic diseases such as asthma and allergic rhinitis (AR) were considered as risk factors for COVID-19, as they would aggravate symptoms. With further research, more and more literature has shown that airway allergic disease may not be a high-risk factor, but may be a protective factor for COVID-19 infection, which is closely related to its low-level expression of the ACE2 receptor and the complex cytokines network as underlying molecular regulatory mechanisms. In addition, steroid hormones and age factors could not be ignored. In this review, we have summarized some current evidence on the relationship between COVID-19 and allergic rhinitis to highlight the underlying mechanisms of COVID-19 infection and provide novel insights for its prevention and treatment. The key findings show that allergic rhinitis and its related molecular mechanisms may have a protective effect against COVID-19 infection.

Investigate the clinical/hematological characteristics of children infected with the Omicron variant of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) and identify an effective indicator to distinguish coronavirus disease 2019 (COVID-19) severity in children.

A retrospective study was conducted through electronic medical records from pediatric patients. The demographic, clinical, and routine blood test (RBT) features of children diagnosed by real-time PCR for SARS-CoV-2 were collected.

Data of 261 patients were analyzed. The most common abnormality shown by RBTs was increased monocyte count (68%). Children had "mild-moderate" or "severe" forms of COVID-19. Prevalence of abnormal neutrophil count (p = 0.048), eosinophil count (p = 0.006), mean corpuscular volume (p = 0.033), mean platelet volume (p = 0.006), platelet-large cell ratio (p = 0.043), and red blood cell distribution width-standard deviation (p = 0.031) were significantly different in the two types. A combination of the neutrophil: lymphocyte ratio (NLR) and eosinophil count for diagnosing severe COVID-19 presented the largest AUC (0.688, 95% CI = 0.599-0.777; p < 0.001), and the AUC increased with a decrease in age.

Combination of the NLR and eosinophil count might be a promising indicator for identifying severe COVID-19 in children at infection onset.

The immune response dynamics in COVID-19 patients remain a subject of intense investigation due to their implications for disease severity and treatment outcomes. We examined changes in leukocyte levels, eosinophil activity, and cytokine profiles in patients hospitalized with COVID-19.

Serum samples were collected within the first 10 days of hospitalization/confirmed infection and analyzed for eosinophil granule proteins (EGP) and cytokines. Information from medical records including comorbidities, clinical symptoms, medications, and complete blood counts were collected at the time of admission, during hospitalization and at follow up approximately 3 months later.

Serum levels of eotaxin, type 1 and type 2 cytokines, and alarmin cytokines were elevated in COVID-19 patients, highlighting the heightened immune response (p < 0.05). However, COVID-19 patients exhibited lower levels of eosinophils and eosinophil degranulation products compared to hospitalized controls (p < 0.05). Leukocyte counts increased consistently from admission to follow-up, indicative of recovery.

Attenuated eosinophil activity alongside elevated chemokine and cytokine levels during active infection, highlights the complex interplay of immune mediators in the pathogenesis COVID-19 and underscores the need for further investigation into immune biomarkers and treatment strategies.

The emergence of coronavirus disease 2019 (COVID-19) as a global health emergency necessitates continued investigation of the disease progression. This study investigated the relationship between eosinophilia and the severity of COVID-19 in chronic obstructive pulmonary disease (COPD) patients.

This cross-sectional study was conducted on 73 COPD patients infected by COVID-19 in Afzalipour Hospital, Iran. Peripheral blood samples were collected for hematological parameter testing, including eosinophil percentage, using Giemsa staining. Eosinophilia was defined as≥ 2% and non-eosinophilia as< 2%. The severity of pulmonary involvement was determined based on chest CT severity score (CT-SS) (based on the degree of involvement of the lung lobes, 0%: 0 points, 1-25%: 1 point, 26-50%: 2 points, 51-75%: 3 points, and 76-100%: 4 points). The CT-SS was the sum of the scores of the five lobes (range 0-20).

The average age of patients was 67.90±13.71 years, and most were male (54.8%). Non-eosinophilic COPD patients were associated with more severe COVID-19 (P= 0.01) and lower oxygen saturation (P= 0.001). In addition, the study revealed a significant difference in the chest CT severity score (CT-SS) between non-eosinophilic (9.76±0.7) and eosinophilic COPD patients (6.26±0.63) (P< 0.001). Although non-eosinophilic COPD patients had a higher mortality rate, this difference was not statistically significant (P= 0.16).

Our study demonstrated that reduced peripheral blood eosinophil levels in COPD patients with COVID-19 correlate with unfavorable outcomes. Understanding this association can help us identify high-risk COPD patients and take appropriate management strategies to improve their prognosis.

During the early stages of the coronavirus disease 2019 (COVID-19) pandemic, those with severe COVID-19 infection were at risk for a number of opportunistic infections including COVID-19-associated pulmonary aspergillosis (CAPA). We initiated a randomized clinical trial to evaluate whether isavuconazole, a triazole antifungal, could prevent CAPA and improve survival in patients admitted to the ICU with severe COVID-19 infection.

We designed a phase III/IV randomized, double-blind, two-arm, placebo-controlled trial evaluating standard of care (SOC) plus isavuconazole versus SOC plus placebo and were to enroll participants admitted to the ICU with severe COVID-19 infection at three medical centers in California, United States. The projected sample size was 162 participants.

Due to poor enrollment and the declining number of COVID-19 cases over time, the study was terminated after 7 participants were enrolled, all enrolled at one study site (UC San Diego Health). CAPA was suspected in two participants and they were started on open-label isavuconazole. One was withdrawn due to possible isavuconazole-related adverse side effects.

Enrollment was slower-than-expected due to multiple factors, including competing COVID-19-related studies and hesitancy from potential study participants or their families to join the study. Our experience highlights some of the difficulties in planning and running a clinical trial focused on fungal superinfections involving severely ill patients during the height of the COVID-19 pandemic. Lessons learned from this study will help in the design of proposed studies examining antifungal prophylaxis against aspergillosis following other severe respiratory viral infections.

COVID-19 is a spectrum of clinical symptoms in humans caused by infection with SARS-CoV-2. The coalescence of SARS-CoV-2 with seasonal respiratory viruses, particularly influenza viruses, is a global health concern. To understand this, transgenic mice expressing the human ACE2 receptor (K18-hACE2) were infected with influenza A virus (IAV) followed by SARS-CoV-2 and the host response and effect on virus biology was compared to K18-hACE2 mice infected with IAV or SARS-CoV-2 alone. The sequentially infected mice showed reduced SARS-CoV-2 RNA synthesis, yet exhibited more rapid weight loss, more severe lung damage and a prolongation of the innate response compared to the singly infected or control mice. Sequential infection also exacerbated the extrapulmonary encephalitic manifestations associated with SARS-CoV-2 infection. Conversely, prior infection with a commercially available, multivalent live-attenuated influenza vaccine (Fluenz Tetra) elicited the same reduction in SARS-CoV-2 RNA synthesis, albeit without the associated increase in disease severity. This suggests that the innate immune response stimulated by IAV inhibits SARS-CoV-2. Interestingly, infection with an attenuated, apathogenic influenza vaccine does not result in an aberrant immune response and enhanced disease severity. Taken together, the data suggest coinfection ('twinfection') is deleterious and mitigation steps should be instituted as part of the comprehensive public health and management strategy of COVID-19.

While COVID-19 becomes periodical, old individuals remain vulnerable to severe disease with high mortality. Although there have been some studies on revealing different risk factors affecting the death of COVID-19 patients, researchers rarely provide a comprehensive analysis to reveal the relationships and interactive effects of the risk factors of COVID-19 mortality, especially in the elderly. Through retrospectively including 1917 COVID-19 patients (102 were dead) admitted to Xiangya Hospital from December 2022 to March 2023, we used the association rule mining method to identify the risk factors leading causes of death among the elderly. Firstly, we used the Affinity Propagation clustering to extract key features from the dataset. Then, we applied the Apriori Algorithm to obtain 6 groups of abnormal feature combinations with significant increments in mortality rate. The results showed a relationship between the number of abnormal feature combinations and mortality rates within different groups. Patients with "C-reactive protein > 8 mg/L", "neutrophils percentage > 75.0 %", "lymphocytes percentage < 20%", and "albumin < 40 g/L" have a 2 × mortality rate than the basic one. When the characteristics of "D-dimer > 0.5 mg/L" and "WBC > 9.5 × 10 9 /L" are continuously included in this foundation, the mortality rate can be increased to 3 × or 4 × . In addition, we also found that liver and kidney diseases significantly affect patient mortality, and the mortality rate can be as high as 100%. These findings can support auxiliary diagnosis and treatment to facilitate early intervention in patients, thereby reducing patient mortality.

Fulminant myocarditis is an acute diffuse inflammatory disease of myocardium. It is characterized by acute onset, rapid progress and high risk of death. Its pathogenesis involves excessive immune activation of the innate immune system and formation of inflammatory storm. According to China's practical experience, the adoption of the "life support-based comprehensive treatment regimen" (with mechanical circulation support and immunomodulation therapy as the core) can significantly improve the survival rate and long-term prognosis. Special emphasis is placed on very early identification,very early diagnosis,very early prediction and very early treatment.

The cutting-edge combination of fluvoxamine (FVM) and ivermectin (IVM) has been presented as a proposed dosage form for the treatment of COVID-19 infections in early diagnosed patients. The main objective of this work is to develop simple, sensitive, and efficient methods for the synchronous quantification of FVM and IVM without any prior separation. Four green UV-methods were employed for the synchronous quantification, namely: Fourier functions convolution of absorption spectra, FFAS, Fourier functions convolution of derivative spectra of absorption curves, FFDS, Fourier function convolution of ratio spectra of absorption curves, FFRS and the dual-wavelength method, DWM. FFRS and DWM approaches can be able to reconcile the two components' significantly interfering spectrum presented in this commixture. Good linearity was checked in the range of 5-40, and 2.5-25 μg/mL for the FVM, and IVM, respectively. All approaches developed have been recommended in compliance with ICH principles. Furthermore, the approaches' greenness was predestined by "National Environmental Method Index" (NEMI), "Analytical GREEnness metric (AGREE)", the "Analytical Eco-Scale", and the "Green Analytical Procedure Index" (GAPI). In addition, spider diagram was utilized for the assessment of the greenness index of the solvent used. Beside greenness, the sustainability of our methods was investigated using the HEXAGON tool. Continuing the constant pursuit of greenness, drug-drug interactions (DDIs) between FVM & IVM were predicted by insilico tools to ensure the safety of the suggested mixture as a preliminary step before invitro and in vivo studies. Because they were deemed sustainable, affordable, and successful, the suggested UV-methods may be used for routine quality control investigations of the indicated formulations FVM & IVM.

We realize a nationwide population-based retrospective study to analyze the characteristics and risk factors of fungal co-infections in COVID-19 hospitalized patients as well as describe their causative agents in the Spanish population in 2020 and 2021. Data were obtained from records in the Minimum Basic Data Set of the National Surveillance System for Hospital Data in Spain, provided by the Ministry of Health, and annually published with two years lag. The assessment of the risk associated with the development of healthcare-associated fungal co-infections was assessed using an adjusted logistic regression model. The incidence of fungal co-infection in COVID-19 hospitalized patients was 1.41%. The main risk factors associated were surgery, sepsis, age, male gender, obesity, and COPD. Co-infection was associated with worse outcomes including higher in-hospital and in ICU mortality, and higher length of stay. Candida spp. and Aspergillus spp. were the microorganisms more frequent. This is the first study analyzing fungal coinfection at a national level in hospitalized patients with COVID-19 in Spanish population and one of the few studies available that demonstrate that surgery was an independent risk factor of Aspergillosis coinfection in COVID-19 patients.

This study aimed to characterize the changes in serum inflammatory mediators in hospitalized patients with COVID-19 correlating with death. The study includes 58 participants: i) inpatients (n = 37): patients suffering from severe acute respiratory syndrome due to COVID-19, who were admitted at Intensive Care Unit (ICU) recovered and who died and ii) control group (n = 21): community volunteers. Inflammatory mediators evaluated interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-10 (IL-10), interleukin-17 (IL-17), interferon-gamma (IFN-γ) and interferon-gamma protein levels (IFN-γ), as well as, Urea, LDH, D-dimer, TAP/INR, AST, ALT and lymphocytes. Our results suggest that high levels of inflammatory markers, such as pro-inflammatory cytokines, and laboratory parameters, such as low levels of lymphocytes and high levels of IL-6, are associated with disease severity, especially in individuals who died. Constant measurement and monitoring of these inflammatory parameters is an effective tool in clinical practice, and it can help choosing appropriate therapies during the course of the disease.

Rationale: Lymphopenia in coronavirus disease (COVID-19) is associated with increased mortality. Objectives: To explore the association between lymphopenia, host response aberrations, and mortality in patients with lymphopenic COVID-19. Methods: We determined 43 plasma biomarkers reflective of four pathophysiological domains: endothelial cell and coagulation activation, inflammation and organ damage, cytokine release, and chemokine release. We explored if decreased concentrations of lymphocyte-derived proteins in patients with lymphopenia were associated with an increase in mortality. We sought to identify host response phenotypes in patients with lymphopenia by cluster analysis of plasma biomarkers. Measurements and Main Results: A total of 439 general ward patients with COVID-19 were stratified by baseline lymphocyte counts: normal (>1.0 × 109/L; n = 167), mild lymphopenia (>0.5 to ⩽1.0 × 109/L; n = 194), and severe lymphopenia (⩽0.5 × 109/L; n = 78). Lymphopenia was associated with alterations in each host response domain. Lymphopenia was associated with increased mortality. Moreover, in patients with lymphopenia (n = 272), decreased concentrations of several lymphocyte-derived proteins (e.g., CCL5, IL-4, IL-13, IL-17A) were associated with an increase in mortality (at P < 0.01 or stronger significance levels). A cluster analysis revealed three host response phenotypes in patients with lymphopenia: "hyporesponsive" (23.2%), "hypercytokinemic" (36.4%), and "inflammatory-injurious" (40.4%), with substantially differing mortality rates of 9.5%, 5.1%, and 26.4%, respectively. A 10-biomarker model accurately predicted these host response phenotypes in an external cohort with similar mortality distribution. The inflammatory-injurious phenotype showed a remarkable combination of relatively high inflammation and organ damage markers with high antiinflammatory cytokine levels yet low proinflammatory cytokine levels. Conclusions: Lymphopenia in COVID-19 signifies a heterogenous group of patients with distinct host response features. Specific host responses contribute to lymphopenia-associated mortality in COVID-19, including reduced CCL5 levels.

We aimed to investigate the safety and efficacy of nirmatrelvir/ritonavir (Paxlovid) therapy for hemodialysis-dependent patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Thirteen hemodialysis patients infected with the Omicron variant of SARS-CoV-2 from April 3 to May 30, 2022, were recruited. Laboratory parameters and chest CT (computed tomography) imaging were analyzed. The treatment group included six patients who received 150 mg/100 mg of Paxlovid orally once daily for 5 days, whereas the control group included seven patients who received basic treatment. No serious adverse reactions or safety events were recorded. Four control patients progressed to moderate disease, and none in the treatment group showed progression of chest CT findings (P < 0.05). Paxlovid therapy tended toward early viral clearance and low viral load on Day 8. Moreover, 83.3% of the patients in the treatment group and 57.1% of the patients in the control group turned negative within 22 days. In the Paxlovid treatment group, we found significantly increased levels of lymphocytes (P=0.03) and eosinophils (P=0.02) and decreased levels of D-dimer on Day 8 compared with those on Day 1. Paxlovid therapy showed a potential therapeutic effect with good tolerance in hemodialysis patients. The optimal dose and effectiveness evaluation must be further investigated in a largeer cohort.

Emerging results indicate that, in COVID-19, thromboembolic complications contribute to the high mortality and morbidity. Previous research showed that the prevalence of pulmonary embolism (PE) is between 25-50% in COVID-19 patients, however, most of these reports are based on data from patients with severe pneumonia, treated in intensive care units.

We conducted a retrospective, single-center, observational study to estimate the prevalence of PE in COVID-19 patients who underwent CT angiography and to identify the most important predictors. Adult outpatients with COVID-19, who presented at our COVID Outpatient Clinic between 1st and 31st of March in 2021 and underwent CTA examination were included in this study. Multiple linear regression analysis was used to identify predictors of PE in COVID-19 patients. The predictors were: age, gender, disease duration, CT severity index and log-transformed quantitative D-dimer (logQDDIM) value.

843 COVID-19 patients were included into the study. 82.56% (693 patients) of the infected patients had a pulmonary CTA examination and D-dimer levels (mean age: 59.82 years ± 15.66). 7.61% (53 patients) of the patients had PE. 2.02% (14 patients) of the patients had main branch or lobar PE. The multiple regression analysis found that only logQDDIM was a significant predictor. A logQDDIM cut-off value of 0.0169 (1.0171 ug/ml serum D-dimer) predicted PE with 99% sensitivity (p<0.0001, degree-of-freedom = 570, AUC = 0.72).

We demonstrated in a large cohort of COVID-19 patients that a cut-off value of QDDIM of 1ug/ml can exclude pulmonary embolism in an outpatient setting, implicating that QDDIM might potentially supersede CTA as a screening approach in COVID-19 outpatient clinics.