The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has led to a significant burden on global healthcare systems. COVID-19-induced acute kidney injury (AKI) is among one of the complications, that has emerged as a critical and frequent condition in COVID-19 patients. This AKI among COVID-19 patients is associated with poor outcomes, and high mortality rates, especially in those with severe AKI or requiring renal replacement therapy. COVID-19-induced AKI represents a significant complication with complex pathophysiology and multifactorial risk factors. Indeed, several pathophysiological mechanisms, including direct viral invasion of renal cells, systemic inflammation, endothelial and thrombotic abnormalities as well as nephrotoxic drugs and rhabdomyolysis are believed to underlie this condition. Moreover, histopathological and immunohistopathological findings commonly observed in postmortem studies include acute tubular necrosis, glomerular injury, and the presence of viral particles within renal tissue and urine. Identified risk factors for developing AKI vary among studies, depending on regions, underlying conditions, and the severity of the disease. Moreover, histopathological and immunohistopathological findings commonly observed in postmortem studies include show acute tubular necrosis, glomerular injury, and viral particles within renal tissue and urine. While, identified risk factors for developing AKI vary among studies, according to regions, underlying conditions, and the gravity of the disease. This narrative review aims to synthesize current knowledge on the incidence, pathophysiology, risk factors, histopathology, and outcomes of AKI induced by COVID-19.

The impact of continued COVID-19 sequelae on singers' vocal function has yet to be determined. An online survey of singers who have contracted SARS-CoV-2 infection was designed and administered globally. Participants (n = 1,153) were recruited in Africa, the Americas, Asia, Australia, and Europe. Survey questions included demographics, peri- and post-SARS-CoV-2 infection symptoms, and self-reported sequelae attributed to long-COVID. The survey was made available in English, Portuguese, Spanish, and Traditional and Simplified Mandarin Chinese. Data were statistically analyzed to provide a useful summary of the sample and to evaluate associations between long-COVID and singers' vocal function. We found that age, gender, and vaccination status were not significantly correlated to a change in singing voice in our sample. However, severity of infection was statistically correlated with a change in singing voice. Of the 34 signs and symptoms presented, lingering cough, shortness of breath, and chronic fatigue were significantly correlated with a change in singing voice. These data and their analyses have added to our understanding of this growing population's unique vocal needs, and may inform strategies for singing voice habilitation in COVID-19 survivors.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), and SARS-CoV-2 has been linked to changes in DNA methylation (DNAm) patterns. Studies focused on post-SARS-CoV-2 infection and DNAm have been mainly carried out among severe COVID-19 cases or without distinguishing the severity of cases. However, investigations into mild and asymptomatic cases after SARS-CoV-2 infection are limited. In this study, we analyzed DNAm patterns of mild and asymptomatic cases seven months after SARS-CoV-2 infection in a household setting by conducting epigenome-wide association studies (EWAS).

We identified DNAm changes at 42 CpG sites associated with anti-SARS-CoV-2 antibody levels. We additionally report EWAS between COVID-19 cases and controls, with the case status being confirmed by either an antibody test or a PCR test. The EWAS with an antibody test case definition identified 172 CpG sites to be differentially methylated, while the EWAS with a PCR test case definition identified 502 CpG sites. Two common sites, namely cg17126990 (annotated to AFAP1L2) and cg25483596 (annotated to PC), were identified to be hypermethylated across the three EWAS. Both CpG sites have been reported to be involved in molecular pathways after SARS-CoV-2 infection. While AFAP1L2 has been found to be upregulated after SARS-CoV-2 infection, the pyruvate carboxylase (PC) activity seems to be affected by SARS-CoV-2 infection resulting in changes to the host cell metabolism. Additionally, an EWAS to assess persistent health restrictions among PCR-confirmed cases showed 40 CpG sites to be differentially methylated.

We detected associations between DNAm in individuals who had asymptomatic and mild SARS-CoV-2 infections as compared to their household controls. These findings contribute to our understanding of the molecular consequences of SARS-CoV-2 infection observed months after infection.

People with chronic illnesses are vulnerable to stress and psychopathology during population-level disasters, as a subset of individuals with disabilities. We aimed to examine the relationships between chronic illness, cumulative and specific stressors, and probable depression, probable anxiety, and post-traumatic stress in an under-resourced urban population in New York City during the COVID-19 pandemic. Using cross-sectional survey data collected in April 2020, we utilized bivariate chi-square analyses and multivariable logistic regression models to estimate differences in and adjusted odds of stressor endorsement and diagnostic prevalence between people with and without chronic illness. We also assessed effect modification of the relationship between stressor exposure and psychopathology by chronic illness status. Compared to people without chronic illness, those who reported having a chronic illness experienced increased odds of probable depression, probable anxiety, and post-traumatic stress. They were also more likely to report high cumulative COVID-19-related stress exposure, death of someone close to them due to coronavirus or COVID-19, family problems, feeling alone, supply shortages, and financial problems. Chronic illness was found to be an effect modifier in the relationship between the death of someone close due to coronavirus or COVID-19 and probable depression and between household job loss and probable anxiety.

Predictive models for determining coronavirus disease 2019 (COVID-19) severity have been established; however, the complexity of the interactions among factors limits the use of conventional statistical methods. This study aimed to establish a simple and accurate predictive model for COVID-19 severity using an explainable machine learning approach. A total of 3,301 patients ≥ 18 years diagnosed with COVID-19 between February 2020 and October 2022 were included. The discovery cohort comprised patients whose disease onset fell before October 1, 2020 (N = 1,023), and the validation cohort comprised the remaining patients (N = 2,278). Pointwise linear and logistic regression models were used to extract 41 features. Reinforcement learning was used to generate a simple model with high predictive accuracy. The primary evaluation was the area under the receiver operating characteristic curve (AUC). The predictive model achieved an AUC of ≥ 0.905 using four features: serum albumin levels, lactate dehydrogenase levels, age, and neutrophil count. The highest AUC value was 0.906 (sensitivity, 0.842; specificity, 0.811) in the discovery cohort and 0.861 (sensitivity, 0.804; specificity, 0.675) in the validation cohort. Simple and well-structured predictive models were established, which may aid in patient management and the selection of therapeutic interventions.

Traditional vaccinology has primarily focused on neutralizing antibody titers as the main correlate of vaccine efficacy, often overlooking the multifaceted roles of antibody Fc effector functions in orchestrating protective immune responses. Fc-mediated immune responses play a pivotal role in immune modulation and pathogen clearance. Emerging evidence from natural infections and vaccine studies highlights the critical contribution of Fc effector functions in determining the quality and durability of immunity. This work explores the limitations of current vaccine evaluation paradigms that prioritize neutralization over Fc effector mechanisms. It also describes findings from a study showing an unexpected role for SARS-CoV-2 anti-spike antibodies: both convalescent plasma and patient-derived monoclonal antibodies (mAbs) lead to maximum phagocytic capacity by monocytes at low concentrations, whereas at higher concentrations the phagocytic capacity was reduced. Given that the severity of COVID-19 disease and antibody titers are strongly positively correlated, this work challenges the paradigm that high antibodies offer better protection against severe disease. It is proposed that humoral and cellular responses elicited by vaccination should never be higher than those produced by natural infection. By integrating antibody Fc effector functions into vaccine development, a paradigm shift is proposed that emphasizes synergic antibody responses. Such an approach could transform vaccine efficacy assessment, enhance protection against dangerous pathogens, and drive innovation in vaccine design.

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.

Despite the vast vaccination campaigns against SARS-CoV-2, vaccine-resistant variants have emerged, and COVID-19 is continuing to spread with the fear of emergence of new variants that are resistant to the currently available anti-viral drugs. Hence, there is an urgent need to discover potential host-directed - rather than virus-directed - therapies against COVID-19. SARS-CoV-2 enters host cells through binding of the viral spike (S)-protein to the host angiotensin-converting enzyme 2 (ACE2) receptor, rendering the viral port of entry an attractive therapeutic target. Accordingly, this study aimed to investigate FDA-approved drugs for their potential repurposing to inhibit the entry point of SARS-CoV-2. Accordingly, the FDA-approved drugs library was enrolled in docking simulations to identify drugs that bind to the Spike-ACE2 interface. The drugs list retrieved by the docking simulations was shortlisted to 19 drugs based on docking scores and safety profiles. These drugs were screened for their ability to prevent binding between ACE2 and S-protein using an ELISA-based Spike-ACE2 binding assay. Five drugs showed statistically significant inhibition of binding between ACE2 and S-protein, ranging from 4 % to 37 %. Of those five, argatroban, glimepiride and ranolazine showed potential antiviral activity at IC50 concentrations well below their CC50 assessed by the plaque assay. Their mode of antiviral action was then determined using the plaque assay with some modifications, which revealed that argatroban acted mainly through a direct virucidal mechanism, while glimepiride largely inhibited viral replication, and ranolazine exerted its antiviral impact primarily through inhibiting viral adsorption. In conclusion, this study has identified three FDA-approved drugs - argatroban, glimepiride and ranolazine - which could potentially be repurposed and used for the management of COVID-19.

Objective Thymus and activation-regulated chemokine (TARC) can predict severe disease in patients with coronavirus disease 2019 (COVID-19). However, no reports have addressed the predictive value of TARC with the widespread use of vaccines and medications for COVID-19 during the Omicron variant period of the pandemic. Methods This single-center prospective cohort study enrolled COVID-19 patients admitted to our institution between December 1, 2021, and August 15, 2022. Patients with respiratory failure due to diseases other than COVID-19 were also excluded. We measured the serum TARC levels of patients at admission. Results We enrolled 157 patients, with 89 in the severe group and 68 in the non-severe group. The severe group was more likely than the non-severe group to include older patients, those with no or one dose of vaccine, and those with interstitial lung disease. The cutoff level of TARC derived from a receiver operator characteristic curve analysis to predict severe disease was 174.0 pg/mL. The sensitivity, specificity, positive predictive value, and negative predictive value were 72.1%, 69.7%, 64.5%, and 76.5%, respectively. The area under the curve was 0.722 (95% confidence interval: 0.635-0.809). A multivariate analysis showed that 2 vaccination doses were associated with non-severe disease, and TARC ≤174 pg/mL was associated with severe disease. Conclusion TARC was a predictive factor for severe disease, but its cutoff value was higher and its predictive accuracy lower than those in previous reports. We surmised that during the Omicron variant period of the pandemic, the widespread use of vaccines and medications for COVID-19 decreased the predictive accuracy of TARC.

Since 2021, COVID-19 has had a substantial impact on global health and continues to contribute to serious health outcomes. In Taiwan, most research has focused on hospitalized patients or mortality cases, leaving important gaps in understanding the broader effects of the disease and identifying individuals at high risk. This study aims to investigate the risk factors for disease progression through a nationwide population-based cohort study on COVID-19 in Taiwan.

This study included 15,056 patients diagnosed with COVID-19 between January 1, 2021, and December 31, 2021, using the Taiwan National Health Insurance Research Database. Baseline and clinical characteristics were collected to verify the association with progression to severity outcomes, including hospital admission, intensive care unit (ICU) admission, invasive ventilatory support, fatal outcome, and the composite outcome of these four events. Patients were observed for 30 days for disease progression. Multivariable logistic regression models were used to calculate odd ratios and 95% confidence intervals (CIs) for each outcome, adjusting for age, sex, region, risk factors, and vaccination status.

Overall, 8,169 patients diagnosed during outpatient visits and 6,887 patients diagnosed during hospitalization were analyzed. Adjusting for age, sex, region, risk factors, and vaccination status, elderly patients had higher risks of hospital admission, ICU admission, invasive ventilatory support, fatal outcome, and composite outcome. Specifically, the risk of the fatal outcome was significantly higher for patients aged 75-84 (odds ratio: 6.11, 95% CI: 4.75-7.87) and those aged 85 years and older (12.70, 9.48-17.02). Patients with cardiovascular disease exhibited higher risks of hospital admission (1.60, 1.31-1.96), ICU admission (1.52, 1.31-1.78), invasive ventilatory support (1.57, 1.26-1.96), and fatal outcomes (1.26, 1.03-1.54) and the composite outcome (1.66, 1.20-1.54). Diabetes mellitus was identified as a significant risk factor for all clinical outcomes (hospital admission: 1.89, 1.53-2.35; ICU admission: 1.53, 1.30-1.79; invasive ventilatory support: 1.27, 1.01-1.60; the composite outcome: 1.45, 1.28-1.66), except for the fatal outcome.

This study indicated the impact of sex, age, and risk factors on the clinical outcomes of COVID-19 patients in Taiwan. Elderly patients and those with cardiovascular disease or diabetes mellitus had higher risks for severe outcomes, including hospitalization, ICU admission, invasive ventilatory support, and mortality. These findings can provide evidence for a better understanding of risk factors for disease progression and inform targeted intervention.

It is anticipated that Chronic Obstructive Pulmonary Disease (COPD) has greater risk in acquiring COVID-19 infection and poorer outcome. However, current worldwide data are conflicting.

This study primarily aims to compare the outcomes of COVID-19 patients with COPD and those without COPD in terms of length of hospital stay (LOS), recovery or mortality, treatment received, and predictors of mortality.

This is a retrospective cohort chart review of 1,017 admitted adult COVID-19 patients from July to December 2020. Age, gender, smoking status, current control and medications for COPD, COVID-19 severity, symptoms, treatment, and outcomes of the two study groups were compared.

Prevalence rate of COPD was 3.8%. COVID-19 patients with COPD were older (median age of 69 vs 54, p<0.001), male (87% vs 50%, p<0.001), hypertensive (72% vs 48%, p=0.004), and with tuberculosis (31% vs 11%, p=0.002). COVID-19 patients with COPD more commonly needed oxygen therapy, High Flow Nasal Cannula, Mechanical Ventilation, Tocilizumab, Convalescent Plasma Therapy and Dexamethasone, and had longer LOS. Significant risk factors for mortality are malignancy, investigational therapies, smoking, and older age. There was no difference in survival rates between the two groups.

COPD increases the risk for severe COVID-19 and lengthens LOS.

Hypertension is an increasing health problem; hence, efforts have been made to promote the disease's early detection and modify prognoses. We aim to evaluate the accuracy of body mass index (BMI), waist circumference (WC), and waist-height ratio (WHtR) in detecting hypertension among adults in Northern Sudan.

Adults were recruited for a multi-stage sampling survey in Northern Sudan. Sociodemographic and anthropometric index (BMI, WC, and WHtR) information were collected. A receiver operating characteristic (ROC) curve with its area under the curve (AUC) was obtained, and a multivariate binary analysis was performed.

Of the 301 included adults, 113 (37.5%) were females and 188 (62.5%) were males. The median (interquartile range, IQR) age was 45.0 (32.0‒59.0) years. The median (IQR) of BMI, WC, and WHtR was 25.6 (21.9‒29.7) kg/m2, 83.0 (73.0‒94.8) cm, and 0.51 (0.43‒0.58), respectively; these values were significantly higher in adults with hypertension compared with adults without hypertension. A total of 166 (55.1%) adults had hypertension. BMI (AUC = 0.69 at the cutoff 22.5 kg/m2, sensitivity = 0.89, specificity = 0.53, YI = 0.35) and WHtR for both males and females (AUC = 0.68 at the cutoff 0.48, sensitivity = 0.75, specificity = 0.60, YI = 0.35) were more accurate than WC (AUC = 0.66 at the cutoff 77.5 cm, sensitivity = 0. 77, specificity = 0.56, YI = 0.33). The multivariate binary analysis revealed that being female (adjusted odds ratio [AOR] = 2.23, 95.0% CI = 1.25‒3.97), having increased age (AOR = 1.04, 95% CI = 1.02‒1.05), and having a higher BMI (AOR = 1.10, 95% CI = 1.04‒1.16) were associated with hypertension.

BMI, WC, and WHtR showed moderate predictive power, suggesting that these indices have a limited role in diagnosing hypertension at the individual level and are more appropriate for population screening than for individual diagnosis. BMI performs better than WC in terms of hypertension detection.

On March 11, 2020, the World Health Organization declared Coronavirus disease 2019 (COVID-19) as a pandemic. The spread of the Delta variant of coronavirus started in June 2021 and accounted for the fifth peak of COVID-19 in Iran in July 2021. According to reports from other countries, vaccination protects against severe diseases caused by COVID-19, including the Delta variant. Studies have also shown that vaccination provides strong protection against SARS-CoV-2 infection, COVID-19-related hospitalization, and mortality. This retrospective cohort study was designed based on the medical care monitoring center database of Sayyad Shirazi Hospital.

COVID-19 confirmed patients' data were extracted for this study from June 22, 2021, to September 22, 2021 including demographic characteristics, signs and symptoms, ICU admission, need for aggressive oxygen therapy, including intubation, mortality, and vaccination status.

A total of 2962 patients were enrolled. Being vaccinated was associated with a 4.14-fold increase in survival (adjusted OR = 4.14; 95% CI: 2.22-7.69; p < 0.01), and individuals in a younger age group demonstrated a 5.58-fold higher likelihood of surviving (adjusted OR = 5.58; 95% CI: 4.25-8.14; p < 0.01). The risk of severe COVID-19 was significantly lower in vaccinated individuals, showing a 3.12-fold decrease in risk (adjusted OR = 3.12; 95% CI: 2.06-4.72; p < 0.01), and in younger age groups, the risk exhibited a 3.28-fold decrease (adjusted OR = 3.28; 95% CI: 2.66-4.04; p < 0.01).

The present results suggest that receiving at least one dose of COVID-19 vaccine had a significant relationship with decreased COVID-19 severity and mortality in vaccinated patients compared to unvaccinated patients.

Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a major concern due to its astonishing prevalence and high fatality rate, especially among elderly people. Patients suffering from COVID-19 may exhibit immunosuppression in the initial stage of infection, while a cytokine storm can occur when the disease progresses to a severe stage. This inopportune immune rhythm not only makes patients more susceptible to the virus but also leads to numerous complications resulting from the excessive production of inflammatory factors. A20, which is widely accepted as a pivotal regulator of inflammation, has been shown to be implicated in the processes of antiviral responses and immunosuppression. Thus, A20 may participate in regulating the pathological processes of COVID-19.

This narrative literature review summarizes recent evidence on the mechanisms of A20 in regulating the pathological processes of COVID-19. We also downloaded single-cell RNA-seq data sets from healthy individuals and patients with varying severities of COVID-19 from the NCBI GEO database to further dissect A20's regulatory mechanisms of these intricate cytokine pathways that are closely associated with SARS-CoV-2 infection.

A20 might be one of the most critical anti-infectious and anti-inflammatory factors involved in the pathogenesis of COVID-19. It effectively suppresses the immune damage and inflammatory storm caused by viral infection.

Understanding the relationship between A20-regulated signaling pathways and pathological processes of COVID-19 can provide insight into potential targets for intervention. Precise regulation of A20 to induce antiviral activity and an anti-inflammatory response could mediate the pathogenesis of COVID-19 and could become an effective treatment.

Introduction Obstructive sleep apnea (OSA) is characterized by repetitive upper airway collapse resulting in episodes of apnea and hypopnea. Studies have shown worsened coronavirus disease 2019 (COVID-19) severity due to coexisting respiratory conditions and suggest increased severity of COVID-19 in patients with or at high risk of OSA. However, the extent of this correlation is unclear. This retrospective study aimed to evaluate the association between OSA severity and COVID-19 severity and assess the impact of continuous positive airway pressure (CPAP) compliance. Methods This single-center retrospective study was conducted at King Abdulaziz University Hospital (KAUH), a tertiary care center in Jeddah, Saudi Arabia. Data were collected from 62 adult patients with OSA who were diagnosed via polysomnography (PSG) and had a positive documented severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) polymerase chain reaction (PCR) test result. COVID-19 severity was categorized into mild, moderate, and severe. Results There was no significant correlation between OSA severity as measured by the apnea-hypopnea index (AHI), low oxyhemoglobin desaturation (LSAT), arousal index (AI), respiratory disturbance index (RDI), or the type of treatment used, including adherence to CPAP, and the outcomes of COVID-19. However, higher arousal with respiratory index (ARI) and a lower percentage of time with SpO2 < 90% (T90) values were linked to moderate COVID-19 severity with significant p-values of 0.046 and 0.007, respectively. Conclusion There was no significant correlation between the severity or types of OSA treatment and the severity of COVID-19. Further research including multicenter studies with bigger populations and extensive sleep study data is warranted. Understanding the OSA-COVID-19 link may improve risk stratification and patient management.

While the CURB-65 score predicts mortality in community-acquired pneumonia (CAP), its performance in COVID-19 CAP is suboptimal. Hyperglycaemia correlates with an increased mortality in COVID-19. This analysis aims to enhance predictive accuracy for in-hospital mortality among COVID-19 patients by augmenting the CURB-65 score with objective variables, including markers of dysglycaemia.

A single-centre retrospective observational analysis assessed the effectiveness of the CURB-65 score in predicting in-hospital mortality among adult patients with moderate to severe COVID-19 from March to September 2020. Using a binary logistic regression model, two extended CURB-65 scores which include markers of dysglycemia are proposed to enhance the predictive capability of the CURB-65 score for in-hospital mortality.

Among 517 patients admitted, 117 (22.6%) died. Using the CURB-65 score, 393 patients (76%) were classified as low risk, 91 (17.6%) as medium risk and 33 (6.4%) as high risk. 37 patients were diagnosed with new-onset dysglycaemia, of which 22 (59.5%) died (p<0.001). Of those with dysglycaemia who died, 41% and 23% were classified as low risk and high risk using the CURB-65 score. The CURB-65 score demonstrated a modest area under the receiver operator characteristic curve (AUC) of 0.75 (95% CI 0.70 to 0.81) for in-hospital mortality in COVID-19 CAP. An Extended CURB-65 Score 1, incorporating an admission of fasting plasma glucose (FPG) and neutrophil to lymphocyte ratio, showed improved prognostic performance with an AUC of 0.80 (95% CI 0.76 to 0.85). When lactate and lactate dehydrogenase were added to these parameters (Extended CURB-65 Score 2), the AUC was 0.82 (95% CI 0.78 to 0.86). The integrated discrimination index showed an 11% and 24% higher discrimination slope when using the Extended CURB-65 Scores 1 and 2, respectively.

The addition of common biochemical parameters including an admission FPG enhances the prognostic performance of CURB-65 for in-hospital mortality among patients with COVID-19.

This study aimed to estimate the COVID-19 lethality in the Mexican Indigenous population from 2020 to 2022, considering clinical characteristics and social conditions. Data were retrieved from the Epidemiological Surveillance System of Respiratory Diseases, identifying the COVID-19-positive cases among the Indigenous population. Lethality was evaluated per clinical conditions and vulnerability due to social deprivation. The number of COVID-19-positive cases in the Indigenous population represented 0.7% of the total number of cases. The case fatality rate in the Indigenous population was 9.8% against 4.6% in the non-Indigenous population. Lethality was higher in men. However, the association with diabetes, hypertension, chronic kidney disease, obesity, and smoking was lower in the Indigenous population than in the non-Indigenous population. A greater vulnerability to social conditions was identified among the Indigenous population than the non-Indigenous population, mainly regarding income, education, and access to health services.

Toxoplasma gondii is a parasite that affects over one billion people worldwide. COVID-19, caused by the SARS-CoV-2 virus, has resulted in over 4.8 million deaths worldwide. Both diseases activate the innate immune response via the same pathway. Studies have suggested that toxoplasmosis may either protect against or worsen the severity of COVID-19. This meta-analysis investigated the relationship between toxoplasmosis prevalence and COVID-19. The selection of studies was based on a systematic search using specific keywords in Scopus, Web of Science, PubMed, and Google Scholar databases between 2019 and 2023. The study findings were analyzed using STATA software version 17.0, and the prevalence of toxoplasmosis in people with COVID-19 and its confidence interval were extracted from the selected studies. The study's heterogeneity was assessed using the I2 test, and publication bias was evaluated using a funnel plot and Egger's test. A p value of 0.05 was considered significant. The meta-analysis included nine studies with a total of 1745 COVID-19-positive individuals, and the results showed a significant association between toxoplasmosis and COVID-19 severity. The I2 statistic was almost 99 %, indicating large heterogeneity among the studies. The Egger's test showed no publication bias. The pooled prevalence of toxoplasmosis in COVID-19-positive individuals was 0.48 (95 % CI: 0.30-0.66), which was significantly different from that of 0 % (P < 0.001). The meta-analysis found that the prevalence oftoxoplasmosis was significantly higher in individuals with COVID-19 than in the general population, indicating a possible association between the two infections. However, the significant heterogeneity among the studies underscores the need for further research to understand the underlying mechanisms and clinical implications of this association.

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.

Since the outbreak of COVID-19, genome-wide association studies have tried to discover the role of genetic predisposition in the clinical variability of this viral infection. The findings of various investigations have led to several loci for COVID-19 genetic susceptibility. Among candidate regions, the 3p21.31 locus has been in the spotlight among scientists, as it can increase the risk of severe COVID-19 by almost two fold. In addition to its substantial association with COVID-19 severity, this locus is related to some common diseases, such as diabetes, malignancies, and coronary artery disease. This locus also harbors evolutionary traces of Neanderthal genomes, which is believed to be the underlying reason for its association with COVID-19 severity. Additionally, the inheritance of this locus from Neanderthals seems to be under positive selection. This review aims to summarize a collection of evidence on the 3p21.31 locus and its impact on COVID-19 outcomes by focusing on the risk variants originated from the Neanderthal genome. Moreover, we discuss candidate genes at this locus and the possible mechanisms by which they influence the progression of COVID-19 symptoms. Better insights into human genetic susceptibility to newly emerging diseases such as COVID-19 and its evolutionary origin can provide fundamentals for risk assessment of different populations as well as the development of personalized prevention and treatments based on genomic medicine.

There have been differential mortality rates from COVID-19 in different parts of the world. It is not clear whether the clinical presentation does also differ, thus the need for this study in a sub-Saharan African setting. The aim of this study was to describe the clinical manifestations and outcomes of patients diagnosed with COVID-19 in selected tertiary hospitals in Tanzania.

This was a retrospective analysis of hospitalised adults confirmed SAR-COV-2 infection in five tertiary-level hospitals in Tanzania. Data collected and analysed included sociodemographic, radiological and clinical characteristics of the patients as well as the outcome of the admission (discharge vs death).

Out of 1387 COVID-19 patients, 52% were males. The median age was 60 years ((IQR)=(19-102)). The most common symptoms were dyspnoea (943,68%), cough (889, 64%), fever (597,43%) and fatigue (570, 41%). In-hospital mortality was (476, 34%). Mortality significantly increased with increasing age, being the most in age >90 years (aHR (95% CI)=4.4 (2.52 to 28.82), p=0.02). Other predictors of mortality were not possessing a health insurance, (aHR (95% CI)=3.7 (1.09 to 14.25), p=0.04); chest pain, (aHR (95% CI)=2.27 (1.36 to 4.13), p=0.03); HIV positivity, (aHR (95% CI)=3.9 (1.46 to 8.15), p=0.03); neutrophilia, (aHR (95% CI)=1.12 (1.01 to 2.65), p=0.03); no use of ivermectin, (aHR (95% CI)=1.21 (1.04 to 1.57), p=0.04) and non-use of steroids, (aHR (95% CI)=1.36 (1.18 to 2.78), p=0.04). The retrospective nature of this study which based on documented patients' records, with a large number of patients left out of the analysis due to missed data, this might in a way affect the results of the present study.

In-hospital mortality was 34%. The independent predictors of mortality were advanced age, HIV infection, no possession of a health insurance, chest pain, neutrophilia and no use of steroids or ivermectin.

COVID-19 disease has spread rapidly worldwide, causing high mortality. Accessible biomarkers capable of early identification of patients at risk of severe form are needed in clinical practice. The aim of the study was to determine the biological markers that predict a critical condition.

Retrospective study including patients with confirmed COVID-19 hospitalized between September 2020 and June 2021. The primary endpoint was progression to critical status within 7 days from admission. We defined two groups:Critical group: Patients who developed a critical condition or died or transferred to the ICU before or at 7 th day.Non-critical group: Patients who remained in non-critical respiratory status until 7 th day or discharged before or at 7 th day.

Our study included 456 patients, with a sex ratio of 1.32 and an average age of 62 years. At the 7 th day of hospitalization, 115 (25.2%) patients were in the critical group and 341 (74.8%) patients were in the non-critical group. The univariate logistic regression indicated that laboratory findings between non-critical and critical groups showed that C-reactive protein (CRP) (p=0.047), D-Dimer (p=0.011), creatinine (0.026), creatine kinase (p=0.039), lactate dehydrogenase (p=0.04), and troponin (p=0.001) were all higher among patients in critical group. However, lymphocyte (p<0.001) and platelet (p<0.001) counts were significantly lower among the critical group. Multivariate logistic regression model, identified four independent risk factors: lymphopenia (OR=2.771, 95%CI=1.482-5.181, p=0.001), Neutrophil to Lymphocyte Ratio (NLR) (OR=2.286, 95%CI=1.461-3.578, p<0.001), thrombocytopenia (OR=1.944, 95%CI=1.092-3.459, p=0.024), and CRP>71.5 (OR=1.598, 95% CI=1.042-2.45, p=0.032) were associated to critical group.

Our results show the predictive value of lymphopenia, thrombocytopenia, high NLR and CRP levels to evaluate the prognosis of COVID-19 pneumonia. A prognostic score could be proposed for guiding clinical care and improving patient outcomes.

Omics approaches were extensively applied during the coronavirus disease 2019 (COVID-19) pandemic to understand the disease, identify biomarkers with diagnostic and prognostic value, and discover new molecular targets for medications. COVID-19 continues to challenge the healthcare system as the virus mutates, becoming more transmissible or adept at evading the immune system, causing resurgent epidemic waves over the last few years. In this study, we used saliva from volunteers who were negative and positive for COVID-19 when Omicron and its variants became dominant. We applied a direct solid-phase extraction approach followed by non-target metabolomics analysis to identify potential salivary signatures of hospital-recruited volunteers to establish a model for COVID-19 screening. Our model, which aimed to differentiate COVID-19-positive individuals from controls in a hospital setting, was based on 39 compounds and achieved high sensitivity (85%/100%), specificity (82%/84%), and accuracy (84%/92%) in training and validation sets, respectively. The salivary diagnostic signatures were mainly composed of amino acids and lipids and were related to a heightened innate immune antiviral response and an attenuated inflammatory profile. The higher abundance of thyrotropin-releasing hormone in the COVID-19 positive group highlighted the endocrine imbalance in low-severity disease, as first reported here, underscoring the need for further studies in this area.

For many diseases, including cancer, infections, and auto-immune diseases, the immune response is a major determinant of disease progression, response to therapy, and clinical outcome. Innate and adaptive immune responses are controlled by coordinated activity of different immune cell types. The functional activity state of immune cells is determined by Signal Transduction Pathways (STPs). A recently developed technology (Simultaneous Transcriptome-based Activity Profiling of Signal Transduction Pathways, STAP-STP) enables simultaneous and quantitative activity measurement of relevant STPs in immune cells based on mRNA-analysis. STAP-STP technology was used to analyze public transcriptome data of a variety of immune cell types in resting and activated functional state. In addition, a clinical study on rheumatoid arthritis (RA) was analyzed to illustrate utility of the technology. Per sample, activity of androgen and estrogen receptor, PI3K, MAPK, TGFβ, Notch, NFκB, JAK-STAT1/2, and JAK-STAT3 STPs was calculated, generating an STP activity profile (SAP) consisting of 9 activity scores. Each analyzed immune cell type, i.e. naive/resting and immune-activated CD4 + and CD8 + T cells, T helper cells, B cells, NK cells, monocytes, macrophages, and dendritic cells, had a reproducible and characteristic SAP, reflecting both cell type and its activity state. Analysis of clinical RA samples revealed increased TGFβ STP activity in whole blood samples. In conclusion, STAP-STP technology enables quantitative measurement of the functional activity state of immune cells of the innate and adaptive immune system. Aside from diagnostic applications, utility lies in unravelling abnormal immune function in disease and immunomodulatory drug development.

This study aimed to assess the severity and outcomes of COVID-19 in pregnant women, focusing on laboratory and radiological discrepancies between pregnant women and matched nonpregnant women. In this retrospective cross-sectional analysis, we matched 107 nonpregnant women with 66 pregnant women in terms of age, comorbidities, and the interval between symptom onset and hospital admission. Demographic, clinical, laboratory, and radiological data were collected, and chest CT scans were evaluated using a severity scale ranging from 0 to 5. Logistic regression and adjusted Cox regression models were used to assess the impact of various factors on pregnancy status and mortality rates. Differences in several laboratory parameters, including the neutrophil-to-lymphocyte ratio, liver aminotransferases, alkaline phosphatase, urea, triglycerides, cholesterol, HbA1c, ferritin, coagulation profiles, and blood gases, were detected. Radiologic exams revealed that nonpregnant women had sharper opacities, whereas pregnant women presented with hazy opacities and signs of crypt-organizing pneumonia. A notable difference was also observed in the pulmonary artery diameter. The mortality rate among pregnant women was 4.62%, which was comparable to the 5.61% reported in nonpregnant patients. Compared with nonpregnant patients, pregnancy did not significantly affect the severity or mortality of COVID-19. Our study revealed discernible differences in specific laboratory and imaging markers between pregnant and nonpregnant COVID-19 patients.

The COVID-19 pandemic has underscored the critical need for precise diagnostic methods to distinguish between similar respiratory infections, such as COVID-19 and Mycoplasma pneumoniae (MP). Identifying key biomarkers and utilizing machine learning techniques, such as random forest analysis, can significantly improve diagnostic accuracy. We conducted a retrospective analysis of clinical and laboratory data from 214 patients with acute respiratory infections, collected between October 2022 and October 2023 at the Second Hospital of Nanping. The study population was categorized into three groups: COVID-19 positive (n = 52), MP positive (n = 140), and co-infected (n = 22). Key biomarkers, including C-reactive protein (CRP), procalcitonin (PCT), interleukin- 6 (IL-6), and white blood cell (WBC) counts, were evaluated. Correlation analyses were conducted to assess relationships between biomarkers within each group. The random forest analysis was applied to evaluate the discriminative power of these biomarkers. The random forest model demonstrated high classification performance, with area under the ROC curve (AUC) scores of 0.86 (95% CI: 0.70-0.97) for COVID-19, 0.79 (95% CI: 0.64-0.92) for MP, 0.69 (95% CI: 0.50-0.87) for co-infections, and 0.90 (95% CI: 0.83-0.95) for the micro-average ROC. Additionally, the precision-recall curve for the random forest classifier showed a micro-average AUC of 0.80 (95% CI: 0.69-0.91). Confusion matrices highlighted the model's accuracy (0.77) and biomarker relationships. The SHAP feature importance analysis indicated that age (0.27), CRP (0.25), IL6 (0.14), and PCT (0.14) were the most significant predictors. The integration of computational methods, particularly random forest analysis, in evaluating clinical and biomarker data presents a promising approach for enhancing diagnostic processes for infectious diseases. Our findings support the use of specific biomarkers in differentiating between COVID-19 and MP, potentially leading to more targeted and effective diagnostic strategies. This study underscores the potential of machine learning techniques in improving disease classification in the era of precision medicine.

Coagulopathy and thromboembolic events are associated with poor outcomes in coronavirus disease 2019 (COVID-19) patients. There is conflicting evidence on the effects of chronic anticoagulation on mortality and severity of COVID-19 disease.

To summarize the body of evidence on the effects of pre-hospital anticoagulation on outcomes in COVID-19 patients.

A Literature search was performed on LitCovid PubMed, WHO, and Scopus databases from inception (December 2019) till June 2023 for original studies reporting an association between prior use of anticoagulants and patient outcomes in adults with COVID-19. The primary outcome was the risk of thromboembolic events in COVID-19 patients taking anticoagulants. Secondary outcomes included COVID-19 disease severity, in terms of intensive care unit admission or invasive mechanical ventilation/intubation requirement in patients hospitalized with COVID-19 infection, and mortality. The random effects models were used to calculate crude and adjusted odds ratios (aORs) with 95% confidence intervals (95%CIs).

Forty-six observational studies met our inclusion criteria. The unadjusted analysis found no association between prior anticoagulation and thromboembolic event risk [n = 43851, 9 studies, odds ratio (OR)= 0.67 (0.22, 2.07); P = 0.49; I 2 = 95%]. The association between prior anticoagulation and disease severity was non-significant [n = 186782; 22 studies, OR = 1.08 (0.78, 1.49); P = 0.64; I 2 = 89%]. However, pre-hospital anticoagulation significantly increased all-cause mortality risk [n = 207292; 35 studies, OR = 1.72 (1.37, 2.17); P < 0.00001; I 2 = 93%]. Pooling adjusted estimates revealed a statistically non-significant association between pre-hospital anticoagulation and thromboembolic event risk [aOR = 0.87 (0.42, 1.80); P = 0.71], mortality [aOR = 0.94 (0.84, 1.05); P = 0.31], and disease severity [aOR = 0.96 (0.72, 1.26); P = 0.76].

Prehospital anticoagulation was not significantly associated with reduced risk of thromboembolic events, improved survival, and lower disease severity in COVID-19 patients.

This study investigated the influence of single nucleotide polymorphisms (SNPs) in genes associated with the interferon pathway (IFNAR2 rs2236757), antiviral response (OAS1 rs10774671, OAS3 rs10735079), and viral entry (ACE2 rs2074192) on COVID-19 severity and their association with nonalcoholic fatty liver disease (MAFLD). We did not observe a significant association between the investigated SNPs and COVID-19 severity. While the IFNAR2 rs2236757 A allele was correlated with higher creatinine levels upon admission and the G allele was correlated with lower band neutrophils upon discharge, these findings require further investigation. The distribution of OAS gene polymorphisms (rs10774671 and rs10735079) did not differ between MAFLD patients and non-MAFLD patients. Our study population's distribution of ACE2 rs2074192 genotypes and alleles differed from that of the European reference population. Overall, our findings suggest that these specific SNPs may not be major contributors to COVID-19 severity in our patient population, highlighting the potential role of other genetic factors and environmental influences.

During the pandemic period, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) mutated, leading to changes in the disease's severity and the therapeutic effect of drugs accordingly. This study aimed to present the actual use of therapeutics and clinical outcomes based on the prevalence of each variant using real-world data.

We analyzed the electronic medical records of adult patients admitted to Busan Medical Center after confirming coronavirus disease 2019 (COVID-19) from February 1, 2020, to June 30, 2022. Patients with mild-to-moderate COVID-19 who were at a high risk of disease progression were selected as study subjects, and the time period was classified according to the variants as ancestral strain, Delta variant, or Omicron variant. We compared drug use status and clinical outcomes by time period.

Among all 3,091 patients, corticosteroids were the most commonly used therapy (56.0%), being used most frequently in the Delta variant (93.0%), followed by the Omicron variant (42.9%) and ancestral strain (21.2%). Regdanvimab accounted for the majority of therapeutic use in the Delta variant (82.9%) and ancestral strain (76.8%), whereas remdesivir was most frequently used during the Omicron variant period (68.9%). The composite outcomes of death or disease aggravation were ranked in the order of the Delta variant, Omicron variant, and ancestral strain (14.5, 11.9, and 6.0%, respectively, P < 0.001).

Regdanvimab was primarily used during the ancestral strain period, regdanvimab plus corticosteroids during the Delta variant period, and remdesivir during the Omicron variant period. The rate of death or disease aggravation was highest in the Delta variant, followed by the Omicron variant and the ancestral strain.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection represented a disruptive pathology that emerged in late 2019 with profound implications ranging from individual health to health systems and world economy. Our study aimed to evaluate clinical, biochemical and computerized tomography (CT) parameters values in determining the severity of pulmonary embolism (PE) associated with COVID-19.

We performed an observational cohort study evaluating demographic, clinical, biochemical, coagulation markers, as well as CT imaging parameters.

In our study on 186 patients with COVID-19, we found that 31 patients (16,66%) had pulmonary embolism. Significant correlations for the patients with PE were detected in C-reactive protein, lactate dehydrogenase, serum ferritin, IL-6, serum myoglobin, NT-proBNP, D-dimers, serum proteins, transaminases as well as white cell blood counts. Patients with pulmonary embolism had a more severe lung involvement, with thrombi distribution mainly involving the lower lobes.

Early identification of PE is an important step for timely and efficient treatment in the intensive care management of COVID-19 patients. Our study showed that high plasmatic values of lactate dehydrogenase, ferritin, IL-6, white blood cells and D-dimers and low proteins serum levels are strongly linked with COVID-19-associated pulmonary embolism.

Obesity has been suggested to be associated with the coronavirus disease 2019 (COVID-19); however, it is unclear whether obesity or metabolic abnormalities accompanied by obesity have a stronger association with COVID-19 risk.

This study used the Korea Disease Control and Prevention Agency database, which includes information about the COVID-19 diagnosis and mortality dates of the entire Korean population between October 2020 and December 2021 (for diagnosis) or March 2022 (for mortality). A total of 24,310,283 adults were included and classified into four metabolic obesity phenotypes: (1) metabolically healthy and normal weight (MHNW), (2) metabolically unhealthy and normal weight (MUNW), (3) metabolically healthy and obese (MHO), and (4) metabolically unhealthy and obese (MUO). COVID-19 mortality and severity were compared according to metabolic obesity phenotypes in the total population and in each age group (20-<50 years, 50-<70 years, and ≥ 70 years). Additionally, major adverse cardiovascular events (MACE) after COVID-19 infection were compared according to metabolic obesity phenotypes.

A total of 3, 956, 807 participants (16.3%) were diagnosed with COVID-19 during the study period. Among them, metabolically unhealthy subjects had higher mortality rates than metabolically healthy subjects (0.81% for MUNW, 0.40% for MUO, 0.23% for MHNW, and 0.19% for MHO). The rates of severe hospitalized disease were also higher in metabolically unhealthy subjects than in healthy subjects (0.59% for MUNW, 0.55% for MUO, 0.19% for MHNW, and 0.31% for MHO). In the subgroup analyses by age, similar trends were observed in subjects aged 20-50 and 50-70 years, respectively. Additionally, the incidence of total MACE was increased in metabolically unhealthy individuals.

The study shows that metabolic health is more strongly associated with COVID-19 mortality and severity than obesity, particularly in adults aged < 70 years.

It is necessary to identify appropriate clinical, biochemical, epidemiological and genetic biomarkers to elucidate the underlying mechanisms of the coronavirus disease-2019 (COVID-19) disease. The study focused on not only the link between disease severity (non-intense unit care (non-ICU) versus intensive unit care (ICU) and genetic susceptibility in COVID-19 patients but also the connection between comorbidity and genetic susceptibility affecting the severity of COVID-19.

One hundred and sixty-two COVID-19 patients treated in the non-ICU and ICU in Kayseri City Hospital were included. All volunteers underwent a physical examination and biochemical evaluation. Angiotensin-converting enzyme (ACE p.T776T G > A(rs4343) and g.16471_16472delinsALU (also referred to as I/D polymorphism; rs1799752), angiotensin II receptor type-1 (AGTR1) c.*86A > C (also referred to as A1166C; rs5186), and plasminogen activator inhibitor-1 (PAI-1-844 G > A (rs2227631) polymorphisms were analysed as well.

To have ACE "ID" genotype did not change the severity of the disease (OR: 0.92, 95% CI: 0.41-2.1, p = 0.84), but decreased the mortality risk 2.9-fold (OR: 2.9, 95% CI: 1.1-7.0, p = 0.03). In PAI-1-844 G > A, having the "AA" genotype in the "A" recessive model increased the risk of the diabetes mellitus (DM) 2.3-fold (OR: 2.3 95%, CI: 1.16-4.66, p = 0.018). In the "G" recessive model, to have the GG genotype increased the risk of chronic kidney disease (CKD) 4.8-fold (OR:4.8, 95% CI: 1.5-15.5, p = 0.008). "GG" genotype in the DM group had a higher fibrinogen level compared to those with the "AG" genotype (AG:4847.2 mg/L (1704.3) versus GG:6444.67 mg/L (1861.62) p = 0.019) and "AA" genotype in the CKD group had lower platelet levels and those with "GG" had higher platelet levels (AA:149 µL (18-159) versus GG: 228 µL (146-357) p = 0.022).

This study was shown that genetic predispositions that causes comorbidities were also likely to affect the prognosis of COVID-19.

Coronavirus disease 2019 (COVID-19) could induce the "cytokine storm" due to overactivation of immune system and accompanied by acute respiratory distress syndrome as a serious complication. Vitamin C has been effective in improving lung function of patients by reducing inflammation.

The aim was to explore the therapeutic effects of high-dose vitamin C supplementation for patients with COVID-19 using meta-analysis.

Published studies were searched from PubMed, Cochrane Library, Web of Science, EMBASE, and China National Knowledge Infrastructure databases up to August 2022 using the terms "vitamin C" and "COVID-19". Data analyses were performed independently by 2 researchers using the PRISMA guidelines.

Heterogeneity between the included studies was assessed using I2 statistics. When I2 ≥50%, the random-effects model was used; otherwise, a fixed-effects model was applied. Stata 14.0 software was used to pool data by standardized mean differences (SMDs) with 95% CIs or odds ratios (ORs) with 95% CIs.

The 14 studies had a total of 751 patients and 1583 control participants in 7 randomized controlled trials and 7 retrospective studies. The vitamin C supplement significantly increased ferritin (SMD = 0.272; 95% CI: 0.059 to 0.485; P = 0.012) and lymphocyte count levels (SMD = 0.376; 95% CI: 0.153 to 0.599; P = 0.001) in patients with COVID-19. Patients administered vitamin C in the length of intensive care unit staying (SMD = 0.226; 95% CI: 0.073 to 0.379; P = 0.004). Intake of vitamin C prominently alleviate disease aggravation (OR = 0.344, 95%CI: 0.135 to 0.873, P = 0.025).

High-dose vitamin C supplementation can alleviate inflammatory response and hinder the aggravation of COVID-19.

Severe COVID-19 can cause acute respiratory distress syndrome, hypoxia, systemic complications, and increased mortality. Pulmonary hypertension (PH) is a major global health issue associated with worsening symptoms and increased mortality. This systematic review aimed to assess the influence of PH onset among COVID-19 patients on all-cause mortality and intensive care unit (ICU) admission.

An unrestricted search of five databases up to June 2022 was undertaken. Pulmonary hypertension was assessed using transthoracic echocardiogram, computed tomography, or right heart catheterisation. After duplicate screening, data extraction, and risk of bias assessment, random effects meta-analyses of odds ratios (OR) and their 95% confidence intervals (CI) were performed for all-cause mortality and ICU admission.

From the 26 studies that were included (3,373 patients, 76% males, median age 62.6 years), PH in COVID-19 patients was significantly associated with higher odds for all-cause mortality (26 studies; OR 3.89; 95% CI 2.85-5.31; p<0.001) and higher odds for ICU admission (six studies; OR 2.50; 95% CI 1.69-3.70; p<0.001). Meta-regression/subgroup analyses by patient demographics, comorbidities, or therapeutic regimens, and sensitivity analyses did not find any differences.

Evidence from observational studies indicates that PH in COVID-19 patients is associated with increased odds of mortality and ICU admission.

In severe COVID-19 cases, an exacerbated inflammatory response triggers a cytokine storm that can worsen the prognosis. Compounds with both antiviral and anti-inflammatory activities show promise as candidates for COVID-19 therapy, as they potentially act against the SARS-CoV-2 infection regardless of the disease stage. One of the most attractive drug targets among coronaviruses is the main protease (MPro). This enzyme is crucial for cleaving polyproteins into non-structural proteins required for viral replication. The aim of this review was to identify SARS-CoV-2 MPro inhibitors with both antiviral and anti-inflammatory properties. The interactions of the compounds within the SARS-CoV-2 MPro binding site were analyzed through molecular docking when data from crystallographic structures were unavailable. 18 compounds were selected and classified into five different superclasses. Five of them exhibit high potency against MPro: GC-376, baicalein, naringenin, heparin, and carmofur, with IC50 values below 0.2 μM. The MPro inhibitors selected have the potential to alleviate lung edema and decrease cytokine release. These molecules mainly target three critical inflammatory pathways: NF-κB, JAK/STAT, and MAPK, all previously associated with COVID-19 pathogenesis. The structures of the compounds occupy the S1/S2 substrate binding subsite of the MPro. They interact with residues from the catalytic dyad (His41 and Cys145) and/or with the oxyanion hole (Gly143, Ser144, and Cys145), which are pivotal for substrate recognition. The MPro SARS-CoV-2 inhibitors with potential anti-inflammatory activities present here could be optimized for maximum efficacy and safety and be explored as potential treatment of both mild and severe COVID-19.

Telemedicine has shown benefits in continuous care during the COVID-19 pandemic. This article discusses its practice in elderly patients with COVID-19, considering its limitations and benefits.

Patients with COVID-19, aged 60 years or older, were followed up through phone calls three times a week for 10 days at the Telemedicine Section of the Clinical Center of the University of Caxias do Sul (UCS) in the south of Brazil. The outcomes evaluated were referrals to hospital, basic health unit (BHU)/emergency care unit (ECU), and psychology and physiotherapy services; instructions about vaccination, isolation period, tests for COVID-19, taking a specific medication, and measuring oxygen saturation; guidance to family members; and avoiding going to hospitals.

A total of 64 patients were followed up, the mean age was 69.28 years and 15.62% had at least one comorbidity. Among the patients, 7.81% were instructed about the vaccine, 23.43% about post-diagnostic tests, 25% about medication, 62.5% about isolation, 31.35% received guidance on saturation monitoring and 28.12% received guidance for family members, and 3.12% were referred to the hospital and 7.81% to the BHU/ECU (n = 5/64). Physiotherapy and psychology services were indicated for 4.68% of patients each, hospital visits were avoided in 31.25% and 93.75% recommended telemonitoring.

In this experience, it is suggested that the telehealth service maximizes patient care and the health care effectiveness for patients with COVID-19. Furthermore, the sample studied showed good adherence and suggested the need for more guidance than face-to-face consultation.