The epidemiological patterns of respiratory tract infections (RTIs) have experienced substantial changes due to the influence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with a particular focus on acute respiratory infections (ARIs). Challenges in early diagnosis, inadequate triage strategies, and the inappropriate use of antimicrobials or antivirals have compounded the difficulties in accurately diagnosing and managing ARIs in the post-pandemic context. This study aimed to investigate the efficacy of fever clinics equipped with nucleic acid testing capabilities in the precise triage of ARIs. In a cohort of 604 individuals presenting with symptoms of ARIs, we utilized real-time reverse transcription polymerase chain reaction (RT-PCR) technology available in the fever clinic to perform nucleic acid testing for SARS-CoV-2, influenza A virus (Flu A), influenza B virus (Flu B), respiratory syncytial virus, adenovirus, human rhinovirus, and Mycoplasma pneumoniae. Subsequently, statistical methods were employed to analyze the distribution and types of ARIs associated with these pathogens. In fever clinics, most patients presenting with respiratory pathogen infections were diagnosed with non-SARS-CoV-2 respiratory pathogens, with a higher incidence noted among pediatric patients compared to adults. In contrast, SARS-CoV-2 primarily affected the adult population and was linked to more severe clinical outcomes. Consequently, the swift triage of patients exhibiting ARI symptoms in a fever clinic equipped with nucleic acid testing enables the rapid identification and precise treatment of pathogens. This approach alleviates patient discomfort and enhances the efficiency of healthcare resource utilization.

Persistent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection differs from long coronavirus disease (COVID-19) (acute symptoms ≥ 12 weeks post-clearance). The Omicron BA.5 variant has a shorter median clearance time (10-14 days) than the Delta variant, suggesting that the traditional 20-day diagnostic threshold may delay interventions in high-risk populations. This study integrated multi-threshold analysis (14/20/30 days), whole-genome sequencing, and machine learning to investigate diagnostic thresholds for persistent SARS-CoV-2 infection and developed a generalizable risk prediction model.

This retrospective study analyzed data from 1,216 patients with COVID-19 hospitalized at Aerospace Center Hospital between January 2021 and October 2024. We used whole-genome sequencing to genotype all COVID-19 cases and to identify major variants (such as Omicron BA. 5, Delta). The outcome, "persistent SARS-CoV-2 infection," was defined as viral nucleic acid positivity ≥ 14 days. Risk factors associated with persistent infection were identified through subgroup analysis with multiple logistic regression (adjusted for age, comorbidities, vaccination status, and virus strain) and machine learning models (70% training, 30% testing dataset).

Persistent SARS-CoV-2 infection was identified in 15.5% (188/1,216) of hospitalized COVID-19 patients. Key predictors included comorbidities-hypertension, diabetes, and active malignancy-and immune dysfunction, marked by reduced B-cell and CD4 + T-cell counts. Unvaccinated patients exhibited an 82% higher risk of persistent infection. Elevated inflammatory markers (C-reactive protein and interleukin-6) and bilateral lung infiltrates on computed tomography further distinguished persistent cases. The predictive model demonstrated strong discrimination with an area under the curve (AUC) of 0.847 (95% confidence interval: 0.815-0.879) and an AUC of 0.81 externally in external validation, underscoring its clinical utility for risk stratification.

Hypertension, diabetes, malignancy, immunosuppression (low B/CD4 + cells), and non-vaccination are independent risk factors for persistent SARS-CoV-2 infection. Integrating these factors into clinical risk stratification may optimize management of high-risk populations.

Introduction: Severe acute respiratory syndrome Coronavirus-2 (SARS-CoV-2) has been associated with the development of COVID-19. COVID-19 may cause endothelial cell dysfunction (ECD), which can lead to cardiometabolic diseases and podocytopathy. In this study, we explored whether presence of hyperglycemia predisposes to SARS-CoV-2 infection, in vitro, and whether COVID-19 can put an individual at a higher risk of persistent renal damage in the long-term following acute COVID infection. To estimate renal damage, we evaluated albuminuria and podocytopathy. Podocytopathy was estimated by measuring podocyte-specific protein levels in urine-derived exosomes from patients who were admitted with acute COVID-19 at 10 days, 6 months, and 12 months post-acute SARS-CoV-2 infection. Methods: Blood and urine samples from patients with SARS-CoV-2 post-infection were procured from the George Washington University COVID repository. Peripheral blood mononuclear cells and urine exosomes were isolated. Podocyte-specific proteins Podocalyxin (PODXL) and Nephrin (NEPH) were identified from urine exosomes. Results: Urine exosomal podocalyxin levels were significantly high at 10 week (n = 18; P = 0.001), 6 month (n = 25; P = 0.003) and 12 month (n = 14; P = 0.0001) time points. Nephrin levels were also noted to be high at 10 week (n = 18; P = 0.001) and 12 month (n = 14; P = 0.007) time points, compared with urine samples obtained from type 2 diabetes subjects who never had COVID-19. Though urinary podocyte-specific proteins were high, compared to control, there were no significant differences noted on urine albumin:creatinine ratios (UACR) between the groups. Conclusion: Persistent high levels of podocyte-specific proteins noted in urinary exosomes even at 12 months post-Covid may lead to the development of chronic kidney disease.

COVID-19 vaccines have been pivotal in the management of the recent pandemic. However, despite their safety and efficacy, apprehension regarding possible adverse effects has always been raised. Most of the vaccine-related side effects are mild. However, serious complications like anaphylaxis and thromboembolic events have also been reported. Various hematological disorders, including hypereosinophilia, have been reported following COVID-19 vaccination, the exact mechanisms of which remain unclear.

We report a 66-year-old male who developed hypereosinophilia (absolute eosinophil count: 4063 cells/µL) and lymphadenopathy two months after receiving the third dose of the BBIBP-CorV (Sinopharm) COVID-19 vaccine. Extensive investigations failed to identify an alternative cause for these findings.

This case report underscores the potential for unexpected hematological adverse events following COVID-19 vaccination, even with inactivated vaccines. While a definitive causal relationship cannot be established, the temporal association between vaccination and symptom onset warrants further investigation. This case emphasizes the importance of continued surveillance for rare adverse events and additional research to elucidate the potential mechanisms underlying vaccine-associated eosinophilia.

Contributions of leukocytes to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) defense have been reported extensively. However, it remains unclear whether there are different leukocyte responses to ancestral SARS-CoV-2 and its variants.

We analyzed peripheral blood leukocyte and subtype concentrations from 575 COVID-19 patients and 950 non-COVID-19 subjects registered at the University of Connecticut John Dempsey Hospital between 2020 and 2022, which covers the ancestral strain, Delta, and Omicron variants.

We found that neutrophils, immature granulocytes, and monocytes were elevated, and lymphocytes were reduced after infection. These hyperactive neutrophils/immature granulocytes and suppressed lymphocytes/monocytes were associated with poorer prognosis in ancestral strain infection. Different from the ancestral strain, hyperactive immature granulocytes were not shown in the decedents of Delta infection, and immature granulocyte concentration was not observed to be associated with mortality. In Omicron infection, suppressed lymphocytes and monocytes were not shown in the decedents, and lymphocyte/monocyte concentrations were not associated with mortality.

Our findings provided insights into different leukocyte immune responses to ancestral SARS-CoV-2, Delta, and Omicron variants.

Xuebijing injection has been recommended as a therapeutic approach for individuals with severe and critical COVID-19. This study aims to explore the correlation of neutrophil to lymphocyte platelet ratio (NLPR) with the severity and prognosis of COVID-19, and the effect of XBJ on the prognosis of patients with COVID-19 in different inflammatory states.

This was a retrospective study conducted at Wuhan Union Hospital in China. COVID-19 patients admitted between November 1, 2022 and February 1, 2023 were included. In predicting prognosis for individuals with COVID-19, new inflammatory indicators were used, and their prognostic value was assessed by using Cox regression models and receiver operating characteristic curves. Furthermore, a calculation was made to determine the cutoff value for NLPR. Relative risk and Cox regression models were used to examine the effects of Xuebijing injection on prognosis in patient cohorts that had been stratified by the NLPR cutoff.

This research included 455 participants with COVID-19, with a mean age of 72 years. Several inflammatory indicators were found to be strongly correlated with prognosis, and NLPR shows the greatest predictive power. Patients with NLPR > 3.29 exhibited a mortality rate of 17.3%, which was 6.2 times higher than in patients with NLPR ≤ 3.29. Importantly, providing Xuebijing injection to patients with NLPR > 3.29 was associated with a lower risk of 60-day all-cause mortality. However, there was no discernible improvement in survival among patients with NLPR ≤ 3.29 who received Xuebijing injection.

NLPR is the most reliable inflammatory marker for predicting prognosis among individuals with COVID-19, and can accurately identify individuals who may benefit from Xuebijing injection. Please cite this article as: Liao M, Zhang LT, Bai LJ, Wang RY, Liu Y, Han J, Liu LH, Qi BL. Xuebijing injection reduces COVID-19 patients mortality as influenced by the neutrophil to lymphocyte platelet ratio. J Integr Med. 2025; Epub ahead of print.

Chronic rhinosinusitis with nasal polyps (CRSwNPs) involves persistent sinus inflammation, with emerging evidence suggesting a potential role of rhinovirus (RV) in its pathophysiology. However, whether RV exists in nasal tissues and affects the nasal mucosa after the resolution of infection symptoms remains unknown.

To investigate the prevalence and impact of silent RV infection in nasal tissues.

RV loads were detected in the nasal tissues of 47 controls and 101 patients with CRSwNP without respiratory infection. Participants were categorized into RV-positive (+), RV-negative (-), and the "gray zone" groups. Quantitative polymerase chain reaction, Western blotting, and immunofluorescence assays were used to analyze the impact of silent RV infection on the immune status of nasal tissues.

Silent RV infection was prevalent in both control (34%) and CRSwNP (30.7%) tissues, with higher viral loads observed in the nasal polyps. In controls, it was associated with high expression of types 1 and 2 interferon (IFN), type 2 inflammation, interleukin (IL)-17A, and IL-10. In patients with CRSwNP, silent RV infection was associated with lower levels of type 1 IFN, IL-17A, type 2 inflammation, and IL-10 but higher levels of type 2 IFN compared with those without RV infection. Meanwhile, RV (+) nasal polyps exhibited fewer tissue eosinophils and neutrophils than RV (-) nasal polyps.

Silent RV infection was prevalent in the nasal tissues, with a higher viral load detected in the nasal polyps. This silent RV infection is associated with distinct immune responses in healthy controls and patients with CRSwNP, involving differential modulation of IFNs, TH2 cytokines, IL-17A, IL-10, and eosinophil and neutrophil levels.

The entry and infection of the Severe Acute Respiratory Syndrome Coronavirus 2 virus (SARS-CoV-2) involve recognition and binding of the receptor-binding domain (RBD) of the virus surface spike protein to the peptidase domain (PD) of the host cellular Angiotensin-Converting Enzyme-2 (ACE2) receptor. ACE2 is also involved in normal blood pressure control. An association between hypertension and COVID-19 severity and fatality is evident, but how hypertension predisposes patients diagnosed with COVID-19 to unfavorable outcomes remains unclear. High temperature early during SARS-CoV-2 infection impairs binding to human cells and retards viral progression. Low body temperature can prelude poor prognosis. In this study, all-atom molecular dynamics simulations were performed to examine the effects of high pressure and temperature on RBD/PD binding. A high blood pressure of 940 mmHg enhanced RBD/PD binding. A high temperature above 315 K significantly weakened RBD/PD binding, while a low temperature of 305 K enhanced binding. The curvature of the PD α1-helix and proximity of the PD β3β4-hairpin tip to the RBM motif affected the compactness of the binding interface and, hence, binding affinity. These findings provide novel insights into the underlying mechanisms by which hypertension predisposes patients to unfavorable outcomes in COVID-19 and how an initial high temperature retards viral progression.

COVID-19 exhibits a variety of symptoms and may lead to multi-organ failure and death. This clinical complexity is exacerbated by significant immune dysregulation affecting nearly all cells of the innate and adaptive immune system. Granulocytes, including eosinophils, are affected by SARS-CoV-2.

Eosinophil responses remain poorly understood despite early recognition of eosinopenia as a hallmark feature of COVID-19 severity.

The heterogeneous nature of eosinophil responses categorizes them as dual-function cells with contradictory effects. Eosinophil activation can suppress virus-induced inflammation by releasing type 2 cytokines like IL-13 and granular proteins with antiviral action such as eosinophil-derived neurotoxins and eosinophil cationic protein, and also by acting as antigen-presenting cells. In contrast, eosinophil accumulation in the lungs can induce tissue damage triggered by cytokines or hormones like IFN-γ and leptin. Additionally, they can affect adaptive immune functions by interacting with T cells through direct formation of membrane complexes or soluble mediator action. Individuals with allergic disorders who have elevated levels of eosinophils in tissues and blood, such as asthma, do not appear to be at an increased risk of developing severe COVID-19 following SARS-CoV-2 infection. However, the SARS-CoV-2 vaccine appears to be associated with complications and eosinophilic infiltrate-induced immunopathogenicity, which can be mitigated by corticosteroid, anti-histamines and anti-IL-5 therapy and avoided by modifying adjuvants or excipients.

This review highlights the importance of eosinophils in COVID-19 and contributes to a better understanding of their role during natural infection and vaccination.

Eosinophils are immune cells that are crucial for the pathogenesis of allergic diseases, such as asthma. These cells play multifunctional roles in various situations, including infection. They are activated during viral infections and exert antiviral activity. Pattern recognition receptors, toll-like receptor 7 and retinoic acid inducible gene-I, are important for the recognition and capture of RNA viruses. In addition, intracellular granule proteins (eosinophil cationic protein and eosinophil-derived neurotoxin) and intracellular nitric oxide production inactivate and/or degrade RNA viruses. Interestingly, eosinophil-synthesizing specialized pro-resolving mediators possess antiviral properties that inhibit viral replication. Thus, eosinophils may play a protective role during respiratory virus infections. Notably, antiviral activities are impaired in patients with asthma, and eosinophil activities are perturbed in proportion with the severity of asthma. The exact roles of eosinophils in RNA virus (rhinovirus, respiratory syncytial virus, and influenza virus)-induced type 2 inflammation-based asthma exacerbation remain unclear. Our research demonstrates that interferons (IFN-α and IFN-γ) stimulate human eosinophils to upregulate antiviral molecules, including guanylate-binding proteins and tripartite motifs. Furthermore, IFN-γ specifically increases the expression of IL5RA, ICAM-1, and FCGR1A, potentially enhancing cellular responsiveness to IL-5, ICAM-1-mediated adhesion to rhinoviruses, and IgG-induced inflammatory responses, respectively. In this review, we have summarized the relationship between viral infections and asthma and the mechanisms underlying the development of antiviral functions of human and mouse eosinophils in vivo and in vitro.

The world is currently grappling with the potentially life-threatening coronavirus disease 2019 (COVID-19), marking it as the most severe health crisis in the modern era. COVID-19 has led to a pandemic, with the World Health Organization (WHO) predicting that individuals with diabetes are at a higher risk of contracting the virus compared to the general population. This review aims to provide a practical summary of the long-term impacts of COVID-19 on patients with diabetes. Specifically, it focuses on the effects of SARS-CoV-2 on different types of diabetic patients, the associated mortality rate, the underlying mechanisms, related complications, and the role of vitamin D and zinc in therapeutic and preventive approaches.

Relevant literature was identified through searches on PubMed, Web of Science, and Science Direct in English, up to April 2023.

COVID-19 can lead to distressing symptoms and pose a significant challenge for individuals living with diabetes. Older individuals and those with pre-existing conditions such as diabetes, coronary illness, and asthma are more susceptible to COVID-19 infection. Managing COVID-19 in individuals with diabetes presents challenges, as it not only complicates the fight against the infection but also potentially prolongs the recovery time. Moreover, the virus may thrive in individuals with high blood glucose levels. Various therapeutic approaches, including antidiabetic drugs, are available to help prevent COVID-19 in diabetic patients.

Diabetes increases the morbidity and mortality risk for patients with COVID-19. Efforts are globally underway to explore therapeutic interventions aimed at reducing the impact of diabetes on COVID-19.

Estimate the detection limits of the COVID-19 surveillance system (SS) in Chile, by estimating the SARS-CoV-2 true prevalence (TP) and the reported official positivity prevalence (OPP) gap.

Randomized cross-sectional.

Two sampling campaigns (SC) were conducted (October-November 2020 and December 2020-January 2021) in the cities of Temuco, Valdivia, and Osorno. Blood was collected from adults from randomly selected households. Sera were analyzed using a commercial later flow test (LFT). A meta-analysis was performed to estimate LFT-performance in asymptomatic-cases. Data were analyzed using a Bayesian latent class model (BLCM) to estimate TP. Finally, BLCM outputs were compared with the OPP, by calculating the TP/OPP rate.

1124 and 1017 households were visited during the 1st and 2nd SC, respectively. The BLCM rendered TP estimates of 6.5 %, 3.2 %, and 6.6 % for the cities of Temuco, Valdivia, and Osorno, respectively (1stSC), increasing to 9.4 %, 5.0 %, and 7.5 %, 60 days later (2ndSC). Depending on the city and SC, TP/OPP rates varied between 2.3 and 5.7.

The national SS was unable to detect 70-79 % of all infected cases, suggesting that mild and asymptomatic cases were scarcely detected.

The 2019 coronavirus illness (COVID 2019) first manifests as a newly identified pneumonia and may quickly escalate to acute respiratory distress syndrome, which has caused a global pandemic. Except for individualized supportive care, no curative therapy has been steadfastly advised for COVID-19 up until this point. T cells and virus-specific T lymphocytes are required to guard against viral infection, particularly COVID-19. Delayed immunological reconstitution (IR) and cytokine storm (CS) continue to be significant barriers to COVID-19 cure. While severe COVID-19 patients who survived the disease had considerable lymphopenia and increased neutrophils, especially in the elderly, their T cell numbers gradually recovered. Exhausted T lymphocytes and elevated levels of pro-inflammatory cytokines, including IL6, IL10, IL2, and IL17, are observed in peripheral blood and the lungs. It implies that while convalescent plasma, IL-6 blocking, mesenchymal stem cells, and corticosteroids might decrease CS, Thymosin α1 and adaptive COVID-19-specific T cells could enhance IR. There is an urgent need for more clinical research in this area throughout the world to open the door to COVID-19 treatment in the future.

The COVID-19 pandemic has profoundly affected mental health, with many survivors experiencing psychological challenges, including Post-Traumatic Stress Disorder (PTSD). This study assessed PTSD symptoms and Post-Traumatic Growth (PTG) among 62 individuals recovering from COVID-19 infection, all of whom were under the care of the Department of Pneumonology, Oncology, and Allergology at the Medical University of Lublin. Results revealed that 40.32% of participants exhibited PTSD symptoms. Key predictors of PTSD severity included cognitive symptoms and post-COVID self-rated health, with cognitive symptoms positively associated and self-rated health negatively associated with PTSD severity. A positive correlation was also found between PTSD severity and PTG, suggesting that while individuals endure significant psychological distress, they may also experience personal growth, such as enhanced resilience and a redefined life perspective. These findings highlight the dual psychological impact of COVID-19 infection, particularly for individuals with preexisting pulmonary conditions. They underscore the importance of holistic, integrated care that addresses both the reduction of PTSD symptoms and the promotion of meaningful psychological growth in COVID-19 survivors.

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.

Diabetes mellitus (DM) is recognized and classified as a group of conditions marked by persistent high blood glucose levels. It is also an inflammatory condition that may influence concurrent disease states, including Coronavirus Disease 2019 (COVID-19). Currently, no effective drug has been found to treat COVID-19, especially in DM patients. Many herbal medicines, such as the well-known Andrographis paniculata, have been explored as drugs and complementary therapies due to their antidiabetic, antibacterial, antiviral, anti-inflammatory, and immunomodulatory effects. This study aimed to examine the potential of herbal medicines as complementary therapy in DM patients with COVID-19 complications, drawing from in-vitro and in-vivo investigations. This study analyzed articles published within the last 15 years using keywords including "herbal medicines", "COVID-19", "Diabetes Mellitus", "antidiabetics", "antiviral", and "anti-inflammatory". The results showed that several herbal medicines could serve as complementary therapy for DM patients with COVID-19 complications. These include Andrographis paniculata, Ageratum conyzoides, Artocarpus altilis, Centella asiatica, Momordica charantia, Persea gratissima, Phyllanthus urinaria, Physalis angulata, Tinospora cordifolia, and Zingiber zerumbet. Herbal medicines may serve as a complementary therapy for DM patients with COVID-19, but these claims need experimental validation in infection models and among affected patients.

COVID-19 poses a significant threat to global public health. As the severity of SARS-CoV-2 infection varies among individuals, elucidating risk factors for severe COVID-19 is important for predicting and preventing illness progression, as well as lowering case fatality rates. This work aimed to explore risk factors for developing severe COVID-19 to enhance the quality of care provided to patients and to prevent complications.

A retrospective study was conducted in Saudi Arabia's eastern province, including all COVID-19 patients aged 18 years or older who were hospitalized at Prince Saud Bin Jalawi Hospital in July 2020. Comparative tests as well as both univariate and multivariate logistic regression analyses were performed to identify risk factors for developing severe COVID-19 and poor outcomes.

Based on the comparative statistical tests patients with severe COVID-19 were statistically significantly associated with older age and had higher respiratory rate, longer hospital stay, and higher prevalence of diabetes than non-severe cases. They also exhibited statistically significant association with high levels of potassium, urea, creatinine, lactate dehydrogenase (LDH), D-dimer, and aspartate aminotransferase (AST). The univariate analysis shows that having diabetes, having high severe acute respiratory infection chest X-ray scores, old age, prolong hospitalization, high potassium and lactate dehydrogenase, as well as using insulin, heparin, corticosteroids, favipiravir or azithromycin were all statistically significant associated with severe COVID-19. However, after adjustments in the multivariate analysis, the sole predictor was serum LDH (p = 0.002; OR 1.005; 95% CI 1.002-1.009). In addition, severe COVID-19 patients had higher odds of being prescribed azithromycin than non-severe patients (p = 0.001; OR 13.725; 95% CI 3.620-52.043). Regarding the outcomes, the median hospital stay duration was statistically significantly associated with death, intensive care unit admission (ICU), and mechanical ventilation. On the other hand, using insulin, azithromycin, beta-agonists, corticosteroids, or favipiravir were statistically significantly associated with reduced mortality, ICU admission, and need of mechanical ventilation.

This study sheds light on numerous parameters that may be utilized to construct a prediction model for evaluating the risk of severe COVID-19. However, no protective factors were included in this prediction model.

The rapid evolution of the COVID-19 pandemic and subsequent global immunization efforts have rendered early metabolomics studies potentially outdated, as they primarily involved non-exposed, non-vaccinated populations. This paper presents a predictive model developed from up-to-date metabolomics data integrated with clinical data to estimate early mortality risk in critically ill COVID-19 patients. Our study addresses the critical gap in current research by utilizing current patient samples, providing fresh insights into the pathophysiology of the disease in a partially immunized global population.

One hundred elderly patients with severe COVID-19 infection, including 46 survivors and 54 non-survivors, were recruited in January-February 2023 at the Second Hospital affiliated with Harbin Medical University. A predictive model within 24 h of admission was developed using blood metabolomics and clinical data. Differential metabolite analysis and other techniques were used to identify relevant characteristics. Model performance was assessed by comparing the area under the receiver operating characteristic curve (AUROC). The final prediction model was externally validated in a cohort of 50 COVID-19 elderly critically ill patients at the First Hospital affiliated with Harbin Medical University during the same period.

Significant disparities in blood metabolomics and laboratory parameters were noted between individuals who survived and those who did not. One metabolite indicator, Itaconic acid, and four laboratory tests (LYM, IL-6, PCT, and CRP), were identified as the five variables in all four models. The external validation set demonstrated that the KNN model exhibited the highest AUC of 0.952 among the four models. When considering a 50% risk of mortality threshold, the validation set displayed a sensitivity of 0.963 and a specificity of 0.957.

The prognostic outcome of COVID-19 elderly patients is significantly influenced by the levels of Itaconic acid, LYM, IL-6, PCT, and CRP upon admission. These five indicators can be utilized to assess the mortality risk in affected individuals.

As the COVID-19 pandemic nears resolution in 2024, the mechanisms by which SARS-CoV-2 and other viral infections induce spermatogenic dysfunction remain poorly understood. This review examines the mechanisms by which viral infections, particularly COVID-19, disrupt spermatogenesis and highlights the implications for male reproductive health. While reports suggest that spermatogenic dysfunction caused by COVID-19 is mild and transient, these findings may have broader applications in understanding and treating spermatogenic dysfunction caused by future viral infections.

The PubMed database was searched to identify original and review articles investigating the mechanisms by which viral infections, particularly SARS-CoV-2, contribute to spermatogenic dysfunction.

SARS-CoV-2 affects the testis through multiple mechanisms, including ACE2 receptor-mediated entry, direct viral damage, inflammatory response, blood-testis barrier disruption, hormonal imbalance, oxidative stress, and impaired spermatogenesis. The combination of these factors can disrupt testicular function and highlights the complexity of the effects of COVID-19 on male reproductive health.

COVID-19 may disrupt spermatogenesis through direct testicular infection, systemic inflammation, hormonal disruption, and oxidative stress. Ongoing research, vaccination efforts, and clinical vigilance are essential to address these challenges and develop effective treatment and prevention strategies.

The complex link between COVID-19 and immunometabolic diseases demonstrates the important interaction between metabolic dysfunction and immunological response during viral infections. Severe COVID-19, defined by a hyperinflammatory state, is greatly impacted by underlying chronic illnesses aggravating the cytokine storm caused by increased levels of Pro-inflammatory cytokines. Metabolic reprogramming, including increased glycolysis and altered mitochondrial function, promotes viral replication and stimulates inflammatory cytokine production, contributing to illness severity. Mitochondrial metabolism abnormalities, strongly linked to various systemic illnesses, worsen metabolic dysfunction during and after the pandemic, increasing cardiovascular consequences. Long COVID-19, defined by chronic inflammation and immune dysregulation, poses continuous problems, highlighting the need for comprehensive therapy solutions that address both immunological and metabolic aspects. Understanding these relationships shows promise for effectively managing COVID-19 and its long-term repercussions, which is the focus of this review paper.

Background: Understanding the interactions between age and comorbidities is crucial for assessing COVID-19 mortality, particularly in patients with cardiac and pulmonary conditions. This study investigates the relationship between comorbidities and mortality outcomes in a cohort of hospitalized COVID-19 patients, emphasizing the interplay of age, cardiac, and pulmonary conditions. Methods: We analyzed a cohort of 3005 patients hospitalized with COVID-19 between 2020 and 2022. Key variables included age, comorbidities (diabetes, cardiac, pulmonary, and neoplasms), and clinical outcomes. Chi-square tests and logistic regression models were used to assess the association between comorbidities and mortality. Stratified analyses by age, diabetes, and pulmonary conditions were conducted to explore interaction effects. Additionally, interaction terms were included in multivariable logistic regression models to evaluate the combined impact of age, comorbidities, and mortality. Results: Cardiac conditions such as hypertension, ischemic cardiopathy, and myocardial infarction showed significant protective effects against mortality in younger patients and in those without pulmonary conditions (p < 0.001). However, these protective effects were diminished in older patients and those with pulmonary comorbidities. Age was found to be a significant modifier of the relationship between cardiac conditions and mortality, with a stronger protective effect observed in patients under the median age (p < 0.001). Pulmonary comorbidities significantly increased the risk of mortality, particularly when co-occurring with cardiac conditions (p < 0.001). Diabetes did not significantly modify the relationship between cardiac conditions and mortality. Conclusions: The findings highlight the complex interactions between age, cardiac conditions, and pulmonary conditions in predicting COVID-19 mortality. Younger patients with cardiac comorbidities show a protective effect against mortality, while pulmonary conditions increase mortality risk, especially in older patients. These insights suggest that individualized risk assessments incorporating age and comorbidities are essential for managing COVID-19 outcomes.

(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.

The COVID-19 pandemic raised concerns about whether individuals with chronic respiratory diseases, such as asthma, were at higher risk of severe outcomes. Although several studies were published on this topic, not all included asthma as a risk factor. Therefore, describing the clinical characteristics of COVID-19-infected asthma patients in a specialized respiratory center is valuable as a real-life study.

To investigate the clinical characteristics and disease severity in SARS-CoV-2-infected adults with pre-existing asthma hospitalized at the National Institute of Respiratory Diseases (INER) in Mexico City.

We conducted a retrospective, observational study on adults with confirmed COVID-19 hospitalized from March 2020 to June 2021. Out of 2,249 reviewed medical records, we identified asthmatic patients and compared them with a matched non-asthmatic control group to assess asthma's impact on COVID-19 severity and outcomes.

Based on the clinical records, asthma prevalence among hospitalized patients was low (1.51%); of these, 73% had allergic and 27% had non-allergic asthma. COVID-19 severity did not vary significantly between asthma phenotypes, although there was higher mortality among patients with non-allergic asthma. Most patients in both groups developed a severe form of the disease and higher mortality rates than non-asthmatics, though the differences were not statistically significant.

Asthma prevalence among patients with COVID-19 was low, but mortality was higher in asthma patients. Although the small sample size limits the generalizability of these findings, this study in a Mexican population hospitalized in a reference hospital provides insights for improving asthma management in future pandemics.

The global outbreak of the coronavirus disease 2019 (COVID-19) has been enormously damaging, in which prolonged shedding of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, previously 2019-nCoV) infection is a challenge in the prevention and treatment of COVID-19. However, there is still incomplete research on the risk factors that affect delayed shedding of SARS-CoV-2.

In a retrospective analysis of 56,878 hospitalized patients in the Fangcang Shelter Hospital (National Convention and Exhibition Center) in Shanghai, China, we compared patients with the duration of SARS-CoV-2 viral shedding > 12 days with those days < 12 days. The results of real-time polymerase chain reaction (RT-PCR) tests determined the duration of viral shedding from the first day of SARS-CoV-2 positivity to the day of SARS-CoV-2 negativity. The extreme gradient boosting (XGBoost) machine learning method was employed to establish a prediction model for prolonged SARS-CoV-2 shedding and analyze significant risk factors. Filtering features retraining and Shapley Additive Explanations (SHAP) techniques were followed to demonstrate and further explain the risk factors for long-term SARS-CoV-2 infection.

We conducted an assessment of ten different features, including vaccination, hypertension, diabetes, admission cycle threshold (Ct) value, cardio-cerebrovascular disease, gender, age, occupation, symptom, and family accompaniment, to determine their impact on the prolonged SARS-CoV-2 shedding. This study involved a large cohort of 56,878 hospitalized patients, and we leveraged the XGBoost algorithm to establish a predictive model based on these features. Upon analysis, six of these ten features were significantly associated with the prolonged SARS-CoV-2 shedding, as determined by both the importance order of the model and our results obtained through model reconstruction. Specifically, vaccination, hypertension, admission Ct value, gender, age, and family accompaniment were identified as the key features associated with prolonged viral shedding.

We developed a predictive model and identified six risk factors associated with prolonged SARS-CoV-2 viral shedding. Our study contributes to identifying and screening individuals with potential long-term SARS-CoV-2 infections. Moreover, our research also provides a reference for future preventive control, optimizing medical resource allocation and guiding epidemiological prevention, and guidelines for personal protection against SARS-CoV-2.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has a high transmissibility profile which favors the accumulation of mutations along its genome, providing the emergence of new variants. In this context, haplotype studies have allowed mapping specific regions and combining approaches and tracking phylogenetic changes. During the COVID-19 pandemic, it was notorious that home environments favored the circulation of SARS-CoV-2, in this study we evaluated 1,407 individuals positive for SARS-CoV-2, in which we located 53 families in the period from June 2021 to February 2023. The epidemiological data were collected in E-SUS notifica and SIVEP-gripe. Then, the genetic material was extracted using the commercial kit and the viral load was evaluated and the viral genomes were sequenced using the Illumina MiSeq methodology. In addition, the circulation of 3 variants and their respective subvariants was detected. The delta variant represented the highest number of cases with 45%, the Omicron variant 43% and the lowest number with 11% of cases the Gamma variants. There were cases of families infected by different subvariants, thus showing different sources of infection. The haplotype network showed a distribution divided into 6 large clusters that were established according to the genetic characteristics observed by the algorithm and 224 Parsimony informative sites were found. In addition, 92% of subjects were symptomatic and 8% asymptomatic. The secondary attack rate of this study was 8.32%. Therefore, we can infer that the home environment favors the spread of SARS-CoV-2, so it is of paramount importance to carry out genomic surveillance in specific groups such as intradomiciliary ones.

The Omicron variant's high transmissibility has made it the most widespread novel coronavirus variant. Elevated serum β2-MG levels from viral infections and EOS' role in viral clearance have garnered attention. However, their predictive value for Omicron's severity and prognosis needs further exploration.

This retrospective study included 424 patients with confirmed COVID-19 Omicron variant admitted to the Second Hospital of Jilin University in Changchun, China, of whom 128 experienced in-hospital mortality. Patients were divided into high and low groups according to β2-MG and EOS levels; the relationship between disease severity and patient prognosis was analyzed.

Our findings showed that severe-to-critical Omicron patients had higher β2-MG levels than mild-normal patients. Conversely, EOS levels were higher in mild-moderate cases. Both β2-MG and EOS levels normalized when Omicron patients tested negative for nucleic acid. Deceased Omicron patients had significantly lower pre-mortem EOS levels. Elevated β2-MG and lower EOS levels correlated with reduced overall survival. Multivariate COX regression analysis indicated that elevated β2-MG was an independent adverse prognostic factor for Omicron patients.

High serum β2-MG levels and low eosinophil levels upon admission correlate with omicron variant severity and prognosis. β2-MG is an independent risk factor for poor outcomes in omicron patients.

The aim of this study is to examine the prognostic role of initial chest computed tomography severity score index (CTSS) and its association with demographic, socio-epidemiological, and clinical parameters in COVID-19 hospitalized patients. A retrospective study included patients who were hospitalized in the COVID Hospital of the Clinical Hospital Center Kosovska Mitrovica from July 2020 to March 2022. We compared patient characteristics and outcome of their hospital stay with values of CT severity score (mild, moderate, and severe form of the disease). Patients with severe disease were statistically significantly older, they treated more days, and they presented statistically significant highest mortality rate compared to mild and moderate forms. Smokers and obese were significantly more frequent among patients with higher CT, while vaccinated patients were more common among those with a mild form. Biochemical parameters at admission also showed statistical significance between the examined groups. We can conclude that by employing the initial CT severity score as the strongest predictor of mortality, it is possible to predict the outcome in hospitalized patients. A comprehensive examination of the patient upon admission, including determining the extent of inflammatory changes in the lungs using computed tomography, the levels of oxygen saturation, and other laboratory parameters, can assist doctors in making an adequate clinical evaluation and apply appropriate therapeutic protocols in the treatment of COVID-19.

The relationship between BMI, inflammation, and mental health is complex. A high BMI, especially obesity, is associated with chronic inflammation, which can lead to mental disorders such as depression. Inflammatory cytokines affect neurotransmitters and the stress axis, worsening mental health. Obesity and mental disorders can mutually reinforce each other. New findings show that inflammation can lead to neurobiological changes, and the gut microbiota may play a key role. Obesity has been implicated as a factor in the high mortality and duration of influenza-like illnesses, even in people who do not have other chronic diseases that may increase the risk of complications. The aim of this study was to determine the associations between BMI and chronic inflammation, metabolic disorders, depression, and anxiety in patients hospitalized with COVID-19 up to 12 months after hospitalization.

The study included 248 participants previously hospitalized for SARS-CoV-2 infection up to 12 months after hospitalization. The study was conducted in a multistage design using a diagnostic survey, anthropometric measurements, and laboratory methods.

A statistically significantly higher BDI-II score was observed among women. Statistical analysis showed a statistically significant higher GAD-7 score among women and those over 75 years of age.

Higher BMI among subjects is often associated with elevated values of inflammatory markers and immune cells, such as WBC, neutrophils, monocytes, and CRP, as well as higher blood glucose levels. These associations may be related to the chronic inflammation and metabolic disorders that often accompany obesity. Lymphocytes and eosinophils may show more varied relationships depending on individual factors and specific health conditions. It is therefore important to continue research in this area.

The Human Epidemiology and Response to SARS-CoV-2 (HEROS) Study is a prospective, multicity, 6-month incidence study conducted from May 2020 to February 2021. The objectives were to identify risk factors for SARS-CoV-2 infection and household transmission among children and people with asthma and allergic diseases, and to use the host nasal transcriptome sampled longitudinally to understand infection risk and sequelae at the molecular level. To overcome challenges of clinical study implementation due to the coronavirus pandemic, this surveillance study used direct-to-participant methods to remotely enroll and prospectively follow eligible children who are participants in other National Institutes of Health-funded pediatric research studies and their household members. Households participated in weekly surveys and biweekly nasal sampling regardless of symptoms. The aim of this report is to widely share the methods and study instruments and to describe the rationale, design, execution, logistics, and characteristics of a large, observational, household-based, remote cohort study of SARS-CoV-2 infection and transmission in households with children. The study enrolled a total of 5598 individuals, including 1913 principal participants (children), 1913 primary caregivers, 729 secondary caregivers, and 1043 other household children. This study was successfully implemented without necessitating any in-person research visits and provides an approach for rapid execution of clinical research. Trial registration: ClinicalTrials.gov. Identifier: NCT04375761.

The rapidly evolving pandemic of Coronavirus disease 2019 (COVID-19) has presented with clinical severity, which varies from asymptomatic cases to being fatal in others. The need of the hour is to find meaningful and cost-effective COVID-19 biomarkers out of conventional hematological and biochemical parameters, which will help in the early identification of patients with a poor prognosis, leading to timely intervention.

The aim was to analyze different biochemical and hematological parameters in COVID-19 patients and also to study the association of these parameters with disease severity.

Cross-sectional observational study was carried out on 100 COVID-19 patients from a hospital from July to October 2020. Based on saturation of oxygen (SpO2), admitted patients were grouped into mild-moderate (SpO2 ≥90%) and severe groups (SpO2 <90%). Hematological and biochemical parameters were studied in both groups, and association with disease severity was analyzed.

Out of 100 patients, 57 patients were seen in the mild-moderate group (SpO2 ≥90%), while 43 patients (SpO2 <90%) belonged to the severe category. Males were predominant in both mild-moderate and severe groups. Among the hematological parameters, statistically significant higher values of absolute neutrophil count (P = 0.046) and significantly lower absolute lymphocyte count (P = 0.003) values were observed. With regard to biochemical parameters, increased urea and decreased total protein were found in the severe category and this association was statistically significant.

To conclude, early identification and monitoring of hematological and biochemical parameters, especially those associated with higher disease severity, may contribute toward improving disease outcomes.

The COVID-19 pandemic, caused by SARS-CoV-2, led to 622,119,701 reported cases and 6,546,118 deaths. Most studies on COVID-19 patients in hospitals are from high-income countries, lacking data for developing countries such as Ethiopia.This study assesses clinical features, demographics, and risk factors for in-hospital mortality in Hawassa, Ethiopia. The research cohort comprises 804 cases exhibiting clinical diagnoses and/or radiological findings and indicative of symptoms consistent with COVID-19 at Hawassa University Comprehensive Specialized Hospital from September 24, 2020, to November 26, 2021. In-hospital mortality rate was predicted using Cox regression. The median age was 45 years, with males making up 64.1% of the population. 173 (21.5%) fatalities occurred, with 125 (72.3%) among males. Male patients had higher mortality rates than females. Severe and critical cases were 24% and 21%. 49.1% had at least one comorbidity, with 12.6% having multiple. Common comorbidities were diabetes (15.9%) and hypertension (15.2%). The Cox regression in Ethiopian COVID-19 patients found that factors like gender, advanced age group, disease severity, symptoms upon admission, shortness of breath, sore throat, body weakness, hypertension, diabetes, multiple comorbidities, and prior health facility visits increased the risk of COVID-19 death, similar to high-income nations. However, in Ethiopia, COVID-19 patients were young and economically active. Patients with at least one symptom had reduced death risk. As a conclusion, COVID-19 in Ethiopia mainly affected the younger demographic, particularly economically active individuals. Early detection can reduce the risk of mortality. Prompt medical attention is essential, especially for individuals with comorbidities. Further research needed on diabetes and hypertension management to reduce mortality risk. Risk factors identified at admission play a crucial role in guiding clinical decisions for intensive monitoring and treatment. Broader risk indicators help prioritize patients for allocation of hospital resources, especially in regions with limited medical facilities. Government's focus on timely testing and strict adherence to regulations crucial for reducing economic impact.

In the SARSCov2 virus epidemic, pregnant women are more susceptible to infectious diseases due to changes in biochemical parameters and are at higher risk of severe respiratory disease and pneumonia. This study aimed to evaluate the biochemical, inflammatory and coagulation parameters in pregnant women with severe disease conditions (as one of the high-risk groups) as well as prognosis and outcome.

This cross-sectional study was performed on 135 pregnant women with COVID-19 admitted to ICU. Demographic and clinical information and laboratory parameters of the patients were evaluated and recorded at the time of admission and in the next follow-up until discharge or death in addition to the outcome and also the pregnancy outcome.

The mortality rate of pregnant women with COVID-19 was 9.6%. The mortality rate decreases with increasing Hb (OR (95% CI): 0.68 (0.47-0.99); P value = 0.043) and lymphocytes (OR (95% CI): 0.92 (0.85-0.96); P value = 0.028) and will increase significantly with increasing PT (OR (95% CI): 1.24 (1.01-1.51); P value = 0.037), INR (OR (95% CI): 1.89 (1.26-2.25); P value = 0.004), D-dimer (OR (95% CI): 1.68 (1.10-2.08); P value = 0.027), and LDH (OR (95% CI): 1.20 (1.01-1.61); P value = 0.010).

According to the results of the present study, inflammatory factors such as leukocytes, neutrophils, NLR, CRP have an increasing and lymphocytes have a decreasing trend, so that lymphocytopenia is more common in non-survivors. In addition, increase of PT, INR, D-dimer and LDH and decrease of Hb were significantly associated with increased chance of mortality. But fibrinogen, ferritin, ALT and AST were not significantly associated with mortality in these women.

Diabetes Mellitus is a major predictor for severity and mortality that is increased by 50% in COVID-19 infection. The aim of this study is to estimate the prevalence of new-onset DM among patients with COVID-19 and examined the short clinical outcomes of the disease.

This is a retrospective study of revising electronic medical records to assess the prevalence of new-onset DM in COVID-19 patients and its impact on the severity of the disease. Adult patients with confirmed COVID-19 during the period from June 2020 to December 2021 were enrolled.

725 patients were included. 53.8% of them were males and 46.2 were females, the mean age was 43.35 ± 16.76. 13.2% were diabetics; 2.2% with preexisting DM and 11.0% had new-onset DM. 6.34% had coexisting medical conditions. DKA at presentation was observed in 6 patients (0.8%) of newly diagnosed DM. There is a significant correlation between age and family history (FH), and BMI and new-onset DM (P < 0.05). The overall mortality rate was 2.2%, and it was significantly higher in diabetics in comparison to non-diabetics (P < 0.001). 8.6% had persistent hyperglycemia after 4 months of follow-up.

The prevalence of COVID-19 related new-onset DM was correlated significantly with disease severity and mortality rate. Age, FH, and BMI, were the major predictors. We recommend that frequent monitoring of blood glucose for patients with COVID-19 infections to detect DM, therefore, prompt treatment can be initiated.

This study aimed to investigate the impact of different types of nasal inflammation on the regulation of entry-associated genes of respiratory viruses, including severe acute respiratory syndrome coronavirus 2 (SARS CoV-2), Middle East respiratory syndrome coronavirus (MERS-CoV), human coronavirus 229E (HCoV-229E), and influenza virus, in the nasal epithelium. Subjects were classified into three groups: control, eosinophilic chronic rhinosinusitis (ECRS), and noneosinophilic CRS (NECRS) groups. Angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine subtype 2 (TMPRSS2), alanyl aminopeptidase (ANPEP), dipeptidyl peptidase 4 (DPP4), and beta-galactoside alpha-2,6-sialyltransferase 1 (ST6GAL1), and beta-galactoside alpha-2,3-sialyltransferase 4 (ST3GAL4) were selected as key entry-associated genes for SARS-CoV-2, HCoV-229E, MERS-CoV, and influenza, respectively, and were evaluated. Brushing samples obtained from each group and human nasal epithelial cells cultured using an air-liquid interface system were treated for 7 days with typical inflammatory cytokines and analyzed using real-time polymerase chain reaction. Western blot analysis and confocal microscopy were performed. The entry-associated genes showed distinct regulation patterns in response to each interleukin-4 (IL-4), interleukin-13 (IL-13), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ). Specifically, ACE2 significantly decreased in type 2 cytokines (IL-4 and IL-13), while TMPRSS2 significantly decreased in type 1 cytokines (TNF-α and IFN-γ). ANPEP significantly decreased in both types of cytokines. Remarkably, DPP4 significantly increased in type 2 cytokines and decreased in type 1 cytokines. Moreover, ST6GAL1 and ST3GAL4 significantly increased in type 2 cytokines and decreased in type 1 cytokines, particularly IFN-γ. These findings were supported by western blot analysis and confocal imaging results, especially for ACE2 and DPP4. The findings regarding differential regulation suggest that patients with ECRS, primarily mediated by type 2 inflammation, may have lower susceptibility to SARS-CoV-2 and HCoV-229E infections but higher susceptibility to MERS-CoV and influenza infections.

Our study aimed to describe the group of severe COVID-19 patients at an institutional level, and determine factors associated with different outcomes.

A retrospective chart review of patients admitted with severe acute hypoxic respiratory failure due to COVID-19 infection. Based on outcomes, we categorized 3 groups of severe COVID-19: (1) Favorable outcome: progressive care unit admission and discharge (2) Intermediate outcome: ICU care (3) Poor outcome: in-hospital mortality.

Eighty-nine patients met our inclusion criteria; 42.7% were female. The average age was 59.7 (standard deviation (SD):13.7). Most of the population were Caucasian (95.5%) and non-Hispanic (91.0%). Age, sex, race, and ethnicity were similar between outcome groups. Medicare and Medicaid patients accounted for 62.9%. The average BMI was 33.5 (SD:8.2). Moderate comorbidity was observed, with an average Charlson Comorbidity index (CCI) of 3.8 (SD:2.6). There were no differences in the average CCI between groups(p = 0.291). Many patients (67.4%) had hypertension, diabetes (42.7%) and chronic lung disease (32.6%). A statistical difference was found when chronic lung disease was evaluated; p = 0.002. The prevalence of chronic lung disease was 19.6%, 27.8%, and 40% in the favorable, intermediate, and poor outcome groups, respectively. Smoking history was associated with poor outcomes (p = 0.04). Only 7.9% were fully vaccinated. Almost half (46.1%) were intubated and mechanically ventilated. Patients spent an average of 12.1 days ventilated (SD:8.5), with an average of 6.0 days from admission to ventilation (SD:5.1). The intermediate group had a shorter average interval from admission to ventilator (77.2 hours, SD:67.6), than the poor group (212.8 hours, SD:126.8); (p = 0.001). The presence of bacterial pneumonia was greatest in the intermediate group (72.2%), compared to the favorable group (17.4%), and the poor group (56%); this was significant (p<0.0001). In-hospital mortality was seen in 28.1%.

Most patients were male, obese, had moderate-level comorbidity, a history of tobacco abuse, and government-funded insurance. Nearly 50% required mechanical ventilation, and about 28% died during hospitalization. Bacterial pneumonia was most prevalent in intubated groups. Patients who were intubated with a good outcome were intubated earlier during their hospital course, with an average difference of 135.6 hours. A history of cigarette smoking and chronic lung disease were associated with poor outcomes.

Coronavirus disease 2019 (COVID-19) is a highly infectious disease caused by a novel human coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Diabetes is a well-known risk factor for infectious diseases with high prevalence and increased severity. Here, we elucidated the possible factors for the increased vulnerability of diabetic patients to SARS-CoV-2 infection and the more severe COVID-19 illness. The worsened prognosis of patients with both COVID-19 and diabetes may be attributable to host receptor angiotensin-converting enzyme 2-assisted viral uptake. Moreover, insulin resistance is often associated with impaired mucosal and skin barrier integrity, resulting in mic-robiota dysbiosis, which increases susceptibility to viral infections. It may also be associated with higher levels of pro-inflammatory cytokines resulting from an impaired immune system in diabetics, inducing a cytokine storm and excessive inflammation. This review describes diabetes mellitus and its complications, explains the risk factors, such as disease characteristics and patient lifestyle, which may contribute to the high susceptibility of diabetic patients to COVID-19, and discusses preventive and therapeutic strategies for COVID-19-positive diabetic patients.

The COVID-19 pandemic has had a significant impact globally, and understanding the relationship between inflammatory markers and disease progression is crucial for effective management. This retrospective study aimed to examine the association between various inflammatory markers, such as C-reactive protein (CRP), the erythrocyte sedimentation rate (ESR), lactate dehydrogenase (LDH), D-dimer, ferritin, and procalcitonin (PCT), and the characteristics of disease progression and outcomes in individuals affected by COVID-19.

This study collected raw data from 470 patients who tested positive for SARS-CoV-2 using RT-PCR.

The logistic regression analysis revealed that elevated LDH levels were associated with male gender, ICU admission, low oxygen saturation (O2 < 93%), the need for mechanical ventilation, death, and the presence of lung infiltrates. Higher D-dimer levels were associated with older age, diabetes mellitus, cardiac disease, and low oxygen saturation. Ferritin levels were significantly associated with older age, ICU admission, low oxygen saturation, mechanical ventilation, and lung infiltrates. In contrast, CRP was only significant regarding lung infiltrates and procalcitonin levels were not significantly associated with any of the examined factors.

This study highlights the importance of monitoring key inflammatory markers, such as LDH, D-dimer, and ferritin, as they are significantly associated with the severity of COVID-19 illness. These findings can inform clinical decision-making and guide the development of targeted interventions to improve patient outcomes.