Severe Acute Respiratory Distress Syndrome Coronavirus 2 Research Articles

Divergent SARS-CoV-2 Omicron-reactive T and B cell responses in COVID-19 vaccine recipients.

The severe acute respiratory distress syndrome coronavirus-2 (SARS-CoV-2) Omicron variant (B.1.1.529) is spreading rapidly, even in vaccinated individuals, raising concerns about immune escape. Here, we studied neutralizing antibodies and T-cell responses targeting SARS-CoV-2 D614G (wildtype, WT), and the B.1.351 (Beta), B.1.617.2 (Delta), and B.1.1.529 (Omicron) variants of concern (VOC) in a cohort of 60 health care workers after immunization with ChAdOx-1 S, Ad26.COV2.S, mRNA-1273 or BNT162b2. High binding antibody levels against WT SARS-CoV-2 spike (S) were detected 28 days after vaccination with both mRNA vaccines (mRNA-1273 or BNT162b2), which significantly decreased after 6 months. In contrast, antibody levels were lower after Ad26.COV2.S vaccination but did not wane. Neutralization assays with infectious virus showed consistent cross-neutralization of the Beta and Delta variants, but neutralization of Omicron was significantly lower or absent (up to a 34-fold decrease compared to WT). Notably, BNT162b2 booster vaccination after either two mRNA-1273 immunizations or Ad26.COV.2 priming partially restored neutralization of the Omicron variant, but responses were still up to-17-fold decreased compared to WT. SARS-CoV-2-specific T-cells were detected up to 6 months after all vaccination regimens, with more consistent detection of specific CD4+ than CD8+ T-cells. No significant differences were detected between WT- and variant-specific CD4+ or CD8+ T-cell responses, including Omicron, indicating minimal escape at the T-cell level. This study shows that vaccinated individuals retain T-cell immunity to the SARS-CoV-2 Omicron variant, potentially balancing the lack of neutralizing antibodies in preventing or limiting severe COVID-19. Booster vaccinations are needed to further restore Omicron cross-neutralization by antibodies.

Recurrence of COVID-19 associated with reduced T-cell responses in a monozygotic twin pair.

Recurrence of COVID-19 in recovered patients has been increasingly reported. However, the immune mechanisms behind the recurrence have not been thoroughly investigated. The presence of neutralizing antibodies (nAbs) in recurrence/reinfection cases suggests that other types of immune response are involved in protection against recurrence. Here, we investigated the innate type I/III interferon (IFN) response, binding and nAb assays and T-cell responses to severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) with IFN gamma (IFNγ) enzyme-linked spot assay (ELISPOT) in three pairs of young adult monozygotic (MZ) twins with previous confirmed COVID-19, one of them presenting a severe recurrence four months after the initial infection. Twin studies have been of paramount importance to comprehend the immunogenetics of infectious diseases. Each MZ twin pair was previously exposed to SARS-CoV-2, as seen by clinical reports. The six individuals presented similar overall recovered immune responses except for the recurrence case, who presented a drastically reduced number of recognized SARS-CoV-2 T-cell epitopes on ELISPOT as compared to her twin sister and the other twin pairs. Our results suggest that the lack of a broad T-cell response to initial infection may have led to recurrence, emphasizing that an effective SARS-CoV-2-specific T-cell immune response is key for complete viral control and avoidance of clinical recurrence of COVID-19.

Temporal Patterns of COVID-19-Associated Pulmonary Pathology: An Autopsy Study.

IntroductionThe novel coronavirus variant - severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) and the disease it causes clinically (novel coronavirus disease 2019 or COVID-19) have placed medical science into a frenzy due to the significant morbidity and mortality, as well as the myriad of clinical complications developing as a direct result of infection. The most notable and one of the most severe changes in COVID-19 develops in the lungs.Materials and methodsAll cases of real-time polymerase chain reaction (rtPCR)-proved COVID-19 subjected to autopsy were withdrawn from the central histopathology archive of a single tertiary medical institution - St. Marina University Hospital - Varna, Varna, Bulgaria. Pulmonary gross and histopathology changes observed on light microscopy with hematoxylin and eosin as well with other histochemical and immunohistochemical stains were compared with the time from patient-reported symptom onset to expiration, to compare the extent and type of changes based on disease duration.ResultsA total of 27 autopsy cases fit the established criteria. All cases clinically manifested with severe COVID-19. From the selected 27 cases, n=14 were male and n=13 were female. The mean age in the cohort was 67.44 years (range 18-91 years), with the mean age for males being 68.29 (range 38-80 years) and the mean age for females being 66.54 (range 18-91 years). Gross changes in patients who expired in the first 10 days after disease onset showed a significantly increased mean weight - 1050g, compared to a relatively lower weight in patients expiring more than 10 days after symptom onset - 940g. Histopathology changes were identified as intermittent (developing independent from symptom onset and persisting) - diffuse alveolar damage with hyaline membranes - acute respiratory distress syndrome, endothelitis with vascular degeneration and fibrin thrombi; early (developing within the first week, but persisting) - type II pneumocyte hyperplasia, alveolar cell multinucleation and scant interstitial mononuclear inflammation; intermediate (developing within the late first and second weeks) - Clara cell hyperplasia and late (developing after the second week of symptom onset) - respiratory tract and alveolar squamous cell metaplasia and fibrosis.ConclusionCOVID-19-associated pulmonary pathology, both gross and histopathology, show a time-related dynamic with persistent early and a myriad of later developing dynamic changes in patients with severe disease. These changes underline both the severity of the condition, as well as the mechanisms and the probability of long-lasting severe complications in patients with post-COVID syndrome.

A Study of Clinical Profile and Neutrophil-Lymphocyte Ratio in Clinical Outcome of Covid 19 Patients: Tertiary Care Centre in Bangalore

Introduction: Corona virus disease is ongoing global pandemic, caused by severe acute respiratory distress syndrome corona virus 2 (SARS-Cov2). The virus was first identified in Wuhan, China in December 2019. The World Health Organization declared the virus a Public Health Emergency of International Concern on 30 January 2020, and later a pandemic on 11 March 2020.The severity of COVID-19 symptoms can range from asymptomatic milder forms to life-threatening. Severe illness is more likely in elderly patients and also in patients with co morbid conditions. Disease can transmit through air contaminated by droplets and small airborne particles. Aims: we aimed to know the clinical profile of covid 19 patients and also to co relate the neutrophil-lymphocyte ratio with clinical outcome of the disease. Materials and methods: This Prospective study was conducted in Patients admitted from August 2020 to October 2020. COVID-19 infection was diagnosed by RT-PCR and rapid antigen test (RAT) technique. Patients demographic data, clinical history was collected. Clinical assessment was performed. Laboratory investigations was sent. Patients were followed during the hospital stay. Appropriate statistical analysis was used Results: Males were commonly affected than females. Mean age of the patient was 61years. Diabetes was the most common co morbid condition. Fever was the most common symptom followed by cough, breathlessness. Neutrophil-lymphocyte ratio was elevated in intubated patients than in patients maintaining room air saturation, which was statistically significant (p value 0.001). Conclusion: Neutrophil-lymphocyte ratio (NLR) can be used as reliable, early marker for the disease progression of covid 19 disease.

Serum HDL-c and LDL-c levels as the predictors of COVID-19 severity

Background: Coronavirus disease 2019 (COVID-19) is a highly contagious disease caused by severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) and comes with various degrees of severity from mild to critical conditions. This study aims to evaluate and clarify the roles of serum HDL-c and LDL-c levels in predicting the COVID-19 severity.

Is body temperature mass screening a reliable and safe option for preventing COVID-19 spread?

With the ongoing coronavirus disease 2019 (COVID-19) pandemic continuing worldwide, mass screening of severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) infection is a cornerstone of strategies for limiting viral spread within communities. Although mass screening of body temperature with handheld, non-contact infrared thermometers and thermal imagine scanners is now widespread in a kaleidoscope of social and healthcare settings for the purpose of detecting febrile individuals bearing SARS-CoV-2 infection, this strategy carries some drawbacks, which will be highlighted and discussed in this article. These caveats basically include high rate of asymptomatic SARS-CoV-2 infections, the challenging definition of "normal" body temperature, variation of measured values according to the body district, false negative cases due to antipyretics, device inaccuracy, impact of environmental temperature, along with the low specificity of this symptom for screening COVID-19 in patients with other febrile conditions. Some pragmatic suggestions will also be endorsed for increasing accuracy and precision of mass screening of body temperature. These encompass the regular assessment of body temperature (possibly twice) with validated devices, which shall be constantly monitored over time and used following manufacturer's instructions, the definition of a range of "normal" body temperatures in the local population, patients interrogation on usual body temperature, measurement standardization of one body district, allowance of sufficient environmental acclimatization before temperature check, integration with contact history and other clinical information, along with exclusion of other causes of increased body temperature. We also endorse the importance of individual and primary care physician's regular and repeated check of personal body temperature.

Emergency cardiac imaging for coronavirus disease 2019 (COVID-19) in practice: a case of takotsubo stress cardiomyopathy

BackgroundCardiovascular complications of severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV2) are known to be associated with poor outcome. A small number of case series and reports have described cases of myocarditis and ischaemic events, however, knowledge on the aetiology of acute cardiac failure in SARS-CoV2 remains limited. We describe the occurrence and risk stratification imaging correlates of ‘takotsubo’ stress cardiomyopathy presenting in a patient with Coronavirus Disease 2019 (COVID-19) in the intensive care unit.Case summaryAn intubated 53-year old patient with COVID19 suffered acute haemodynamic collapse in the intensive care unit, and was thus investigated with transthoracic echocardiography (TTE), 12-lead electrocardiograms (ECG) and serial troponins and blood tests, and eventually coronary angiography due to clinical suspicion of ischaemic aetiology. Echocardiography revealed a reduced ejection fraction, with evident extensive apical akinesia spanning multiple coronary territories. Troponins and NT-proBNP were elevated, and ECG revealed ST elevation: coronary angiography was thus performed. This revealed no significant coronary stenosis. Repeat echocardiography performed within the following week revealed a substantial recovery of ejection fraction and wall motion abnormalities. Despite requirement of a prolonged ICU stay, the patient now remains clinically stable, and is on spontaneous breathing.ConclusionThis case report presents a case of takotsubo stress cardiomyopathy occurring in a critically unwell patient with COVID19 in the intensive care setting. Stress cardiomyopathy may be an acute cardiovascular complication of COVID-19 infection. In the COVID19 critical care setting, urgent bedside echocardiography is an important tool for initial clinical assessment of patients suffering haemodynamic compromise.

Diseased lungs may hinder COVID-19 development: A possible reason for the low prevalence of COPD in COVID-19 patients

Presently, it remains unclear why the prevalence of lung diseases, namely chronic obstructive pulmonary disease (COPD), is much lower than other medical comorbidities and the general population among patients with coronavirus disease 2019 (COVID-19). If COVID-19 is a respiratory disease, why is COPD not the leading risk factor for contracting COVID-19? The same odd phenomenon was also observed with other pathogenic human coronaviruses causing severe acute respiratory distress syndrome (SARS) and Middle East respiratory syndrome (MERS), but not other respiratory viral infections such as influenza and respiratory syncytial viruses. One commonly proposed reason for the low COPD rates among COVID-19 patients is the usage of inhaled corticosteroids or bronchodilators that may protect against COVID-19. However, another possible reason not discussed elsewhere is that lungs in a diseased state may not be conducive for the severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) to establish COVID-19. For one, COPD causes mucous plugging in large and small airways, which may hinder SARS-CoV-2 from reaching deeper parts of the lungs (i.e., alveoli). Thus, SARS-CoV-2 may only localize to the upper respiratory tract of persons with COPD, causing mild or asymptomatic infections requiring no hospital attention. Even if SARS-CoV-2 reaches the alveoli, cells therein are probably under a heavy burden of endoplasmic reticulum (ER) stress and extensively damaged where it may not support efficient viral replication. As a result, limited SARS-CoV-2 virions would be produced in diseased lungs, preventing the development of COVID-19.

Acute kidney injury in children with COVID-19: a retrospective study

BackgroundAcute kidney injury (AKI) is a complication of coronavirus disease 2019 (COVID-19). The reported incidence of AKI, however, varies among studies. We aimed to evaluate the incidence of AKI and its association with mortality and morbidity in children infected with severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) who required hospital admission.MethodsThis was a multicenter retrospective cohort study from three tertiary centers, which included children with confirmed COVID-19. All children were evaluated for AKI using the Kidney Disease Improving Global Outcomes (KDIGO) definition and staging.ResultsOf 89 children included, 19 (21 %) developed AKI (52.6 % stage I). A high renal angina index score was correlated with severity of AKI. Also, multisystem inflammatory syndrome in children (MIS-C) was increased in children with AKI compared to those with normal kidney function (15 % vs. 1.5 %). Patients with AKI had significantly more pediatric intensive care admissions (PICU) (32 % vs. 2.8 %, p < 0.001) and mortality (42 % vs. 0 %, p < 0.001). However, AKI was not associated with prolonged hospitalization (58 % vs. 40 %, p = 0.163) or development of MIS-C (10.5 % vs. 1.4 %, p = 0.051). No patient in the AKI group required renal replacement therapy. Residual renal impairment at discharge occurred in 9 % of patients. This was significantly influenced by the presence of comorbidities, hypotension, hypoxia, heart failure, acute respiratory distress, hypernatremia, abnormal liver profile, high C-reactive protein, and positive blood culture.ConclusionsAKI occurred in one-fifth of children with SARS-CoV-2 infection requiring hospital admission, with one-third of those requiring PICU. AKI was associated with increased morbidity and mortality, and residual renal impairment at time of discharge.

SARS-CoV-2 Infection Related Diabetes Mellitus

Introduction: SARS-Cov-2 (severe acute respiratory distress syndrome- coronavirus 2) viral infection has a predilection for pancreatic beta cells causing insulin deficiency. Studies from the SARS-CoV outbreak in 2003 highlighted the relationship between SARS-CoV and ACE-2 (angiotensin-converting enzyme 2) receptors in pancreatic islet cells. We describe a pediatric patient who developed Diabetes Mellitus after exposure to the Sars-CoV-2 virus. Case Report: A previously healthy 13-year-old female of Mexican descent was found to be hyperglycemic at her annual visit. The patient endorsed polyuria and polydipsia for 3 weeks, and weight loss for 3months. 3 months prior to presentation, her mother became ill and tested positive for SARS-CoV-2 by PCR analysis. The patient had no SARS-CoV-2 associated symptoms.Her exam was notable for a BMI was in the 78%ile for age with no acanthosis nigricans. She had no family history of diabetes or autoimmune disease.Initial blood glucose was 729 mg/dL, with bicarbonate of 20.6 mEq/L, pH 7.45, and anion gap of 14 mEq/L. Large ketones were present in the urine. Her concomitant C-peptide level of 1.0 ng/ml was low in the setting of hyperglycemia. Her HbA1c was 14.3%. Diabetes-related autoantibodies, celiac, and thyroid antibodies were negative. Her Sars-CoV-2 antibody titer was positive with a negative PCR.The patient was treated with a basal-bolus regimen of subcutaneous insulin at a maximal total daily dose of 0.7 u/kg/day. 5 weeks later, her insulin requirement and HbA1C were both lower; at 0.5 u/kg/day and 9.3% respectively. Discussion: This patient’s symptoms of hyperglycemia started shortly after her exposure to the SARS-CoV-2 virus. She had no features consistent with Type 2 DM. She similarly had no serological evidence of DM related autoimmunity, thus being different from reports of new-onset Type 1 DM with confirmed autoimmunity presenting during the Sars-CoV-2 pandemic. Although Type 1B DM without evidence of humoral islet autoimmunity and monogenic DM could not be fully excluded, we postulate that the patient developed SARS-CoV-2 associated DM given her time course and documented exposure to SARS –CoV-2 with the presence of SARS-CoV antibodies. One similar case has previously been reported By Holstein et al. 1 While we share the lack of direct evidence of causation, we postulate that more patients with similar presentations will be reported during the current pandemic. Reference: 1.Hollstein, T et al. Autoantibody-negative insulin-dependent diabetes mellitus after SARS-CoV-2 infection: a case report [published online ahead of print, 2020 Sep 2]. Nat Metab. 2020;10.1038/s42255-020-00281-8. doi:10.1038/s42255-020-00281-8

Natural Products as Anti-COVID-19 Agents: An In Silico Study

Background: The coronavirus disease 2019 (COVID-19) is a life-threatening viral infection caused by a positive-strand RNA virus belonging to the Coronaviridae family called severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2). This virus has infected millions of peoples and caused hundreds of thousands of deaths around the world. Unfortunately, to date, there is no specific cure for SARS-CoV-2 infection, although researchers are working tirelessly to come up with a drug against this virus. Recently, the main viral protease has been discovered and is regarded as an appropriate target for antiviral agents in the search for the treatment of SARS-CoV-2 infection due to its role in polyproteins processing coronavirus replication. Methodology: This investigation (an in silico study) explores the effectiveness of 16 natural compounds from a literature survey against the protease of SARS-CoV-2 in an attempt to identify a promising antiviral agent through a molecular docking study. Results: Among the 16 compounds studied, apigenin, alpha-hederin, and asiatic acid exhibited significant docking performance and interacted with several amino acid residues of the main protease of SARS-CoV-2. Conclusion: In summary, apigenin, alpha-hederin, and asiatic acid protease inhibitors may be effective potential antiviral agents against the main viral protease (Mpro) to combat SARS-CoV-2.

Palliative medicine in intensive care unit during a pandemic.

The coronavirus disease-2019 (COVID-19) or severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) pandemic has changed the landscape of medical care. Efforts made to limit the spread of the deadly disease have impacted the specialty of palliative medicine in ways that could not have been completely predicted or appreciated. The consequences of these changes have been most evident in the care of COVID-19 patients and families within the intensive care unit. The policies meant to keep staff, patients, and families safe, greatly changed the way that palliative medicine could be provided. This article provides a more in-depth look at how the practice of palliative medicine adapted to such difficult and constantly changing times, particularly in aspects of family meetings, communication, paternalism, managing emotions, death, and grief. Despite the ongoing challenges presented by this virus, the specialty of palliative medicine may be well suited to adapt and flourish.

Serum HDL-c and LDL-c levels as the predictors of COVID-19 severity

Background: Coronavirus disease 2019 (COVID-19) is a highly contagious disease caused by severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) and comes with various degrees of severity from mild to critical conditions. This study aims to evaluate and clarify the roles of serum HDL-c and LDL-c levels in predicting the COVID-19 severity.

POS-033 Acute Kidney Injury in Children with COVID-19

Acute kidney injury (AKI) is a complication of coronavirus disease 2019 (COVID-19). The reported incidence of AKI, however, varies among studies. We aimed to evaluate the incidence of AKI and its association with mortality and morbidity in children infected with severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) who required hospital admission.

Time on previous renal replacement therapy is associated with worse outcomes of COVID-19 in a regional cohort of kidney transplant and dialysis patients.

Chronic renal replacement therapy by either a kidney transplant (KTX) or hemodialysis (HD) predisposes patients to an increased risk for adverse outcomes of COVID-19. However, details on this interaction remain incomplete. To provide further characterization, we undertook a retrospective observational cohort analysis of the majority of the hemodialysis and renal transplant population affected by the first regional outbreak of severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) in Germany. In a region of 250,000 inhabitants we identified a total of 21 cases with SARS-CoV-2 among 100 KTX and 260 HD patients, that is, 7 KTX with COVID-19, 14 HD with COVID-19, and 3 HD with asymptomatic carrier status. As a first observation, KTX recipients exhibited trends for a higher mortality (43 vs 18%) and a higher proportion of acute respiratory distress syndrome (ARDS) (57 vs 27%) when compared to their HD counterparts. As a novel finding, development of ARDS was significantly associated with the time spent on previous renal replacement therapy (RRT), defined as the composite of dialysis time and time on the transplant (non-ARDS 4.3 vs ARDS 10.6 years, P = .016). Multivariate logistic regression analysis showed an OR of 1.7 per year of RRT. The association remained robust when analysis was confined to KTX patients (5.1 vs 13.2 years, P = .002) or when correlating the time spent on a renal transplant alone (P = .038). Similarly, longer RRT correlated with death vs survival (P = .0002). In conclusion our data suggest renal replacement vintage as a novel risk factor for COVID-19-associated ARDS and death. The findings should be validated by larger cohorts.

COVID-19 and the new variant strain in England - What are the implications for those from ethnic minority groups?

Two new variants of Severe Acute Respiratory Distress Syndrome-Coronavirus-2 (SARS-CoV-2) have been reported over a matter of days in the United Kingdom (UK). The first variant, named VUI-202,012/01, originally detected in Kent and London, has an unusually large number of mutations that increase the virus’ affinity for human hosts [1]. The second, named 501Y.V2 was first detected in Nelson Mandela Bay in South Africa [2]. Epidemiological evidence of a sharp rise in Coronavirus disease-2019 (COVID-19) admissions to both UK and South African hospitals along with a rising attributable proportion of cases due to these two variants, suggests that both are significantly more transmissible than previous variants.

Cardiovascular biomarkers in patients with COVID-19.

The coronavirus disease 2019 (COVID-19) pandemic has increased awareness that severe acute respiratory distress syndrome coronavirus-2 (SARS-CoV-2) may have profound effects on the cardiovascular system. COVID-19 often affects patients with pre-existing cardiac disease, and may trigger acute respiratory distress syndrome (ARDS), venous thromboembolism (VTE), acute myocardial infarction (AMI), and acute heart failure (AHF). However, as COVID-19 is primarily a respiratory infectious disease, there remain substantial uncertainty and controversy whether and how cardiovascular biomarkers should be used in patients with suspected COVID-19. To help clinicians understand the possible value as well as the most appropriate interpretation of cardiovascular biomarkers in COVID-19, it is important to highlight that recent findings regarding the prognostic role of cardiovascular biomarkers in patients hospitalized with COVID-19 are similar to those obtained in studies for pneumonia and ARDS in general. Cardiovascular biomarkers reflecting pathophysiological processes involved in COVID-19/pneumonia and its complications have a role evaluating disease severity, cardiac involvement, and risk of death in COVID-19 as well as in pneumonias caused by other pathogens. First, cardiomyocyte injury, as quantified by cardiac troponin concentrations, and haemodynamic cardiac stress, as quantified by natriuretic peptide concentrations, may occur in COVID-19 as in other pneumonias. The level of those biomarkers correlates with disease severity and mortality. Interpretation of cardiac troponin and natriuretic peptide concentrations as quantitative variables may aid in risk stratification in COVID-19/pneumonia and also will ensure that these biomarkers maintain high diagnostic accuracy for AMI and AHF. Second, activated coagulation as quantified by D-dimers seems more prominent in COVID-19 as in other pneumonias. Due to the central role of endothelitis and VTE in COVID-19, serial measurements of D-dimers may help physicians in the selection of patients for VTE imaging and the intensification of the level of anticoagulation from prophylactic to slightly higher or even therapeutic doses.

Depression and anxiety in cancer patients before and during the SARS-CoV-2 pandemic: association with treatment delays.

PurposePandemics can be associated with anxiety and depression in cancer patients who are undergoing treatment. In the present study, we aimed to perform a comparative evaluation of the conditions of cancer patients before and during the severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) pandemic using the Beck Depression Inventory (BDI) and Beck Anxiety Inventory (BAI) to detect the impact of the pandemic on treatment delays that are associated with anxiety and depression in cancer patients. In addition, the effect of public transport use on treatment delays was examined.MethodsBDI and BAI were administered to 595 breast, ovarian, colon and gastric cancer patients before and during the pandemic. The questionnaires were administered by the physician blindly, who was unaware of the delay of the patients. The number of days by which the patients delayed their treatment due to the fear of contamination were recorded retrospectively. Correlation analyses were performed between the obtained scores and treatment delays.ResultsThe depression and anxiety levels in cancer patients were found to increase during the pandemic (p = 0.000), and this increase was positively correlated with the disruption of their treatment (p = 0.000, r = 0.81). Depression and anxiety levels and treatment delays were higher in elderly patients (p = 0.021). Depression and anxiety were more pronounced in female patients (p = 0.000). Moreover, treatment delays were more common in patients who had to use public transportation (p = 0.038).ConclusionSARS-CoV-2 pandemic may increase anxiety and depression in cancer patients. This can cause patients to experience treatment delays due to concerns about becoming infected. At this point, if necessary, assistance should be obtained from psychiatric and public health experts.Supplementary InformationThe online version contains supplementary material available at 10.1007/s11136-021-02795-4.

What Are the Clinical Implications of the SARS-CoV-2 Variants: 5 Things Every Cardiologist Should Know

New variants of the severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) are emerging around the world and causing widespread concern regarding their ability to escape natural or vaccine-induced immunity and available therapeutics. Here, we will briefly review the potential clinical implications of these new variants.

COVID-19, Angiotensin-Converting Enzyme 2 and Renin-Angiotensin System Inhibition: Implications for Practice.

Recent studies suggested that patients with coronavirus disease 2019 (COVID-19) who use renin-angiotensin system (RAS) inhibitors have an increased risk of respiratory failure and death. The hypothesis was that angiotensin-converting enzyme inhibitor (ACEIs) or angiotensin receptor blocker (ARBs) might up-regulate ACE2 expression that is used as a receptor for viral entry into cells. The purpose of this review is to discuss the existing evidence on the interaction between COVID-19 infection, ACE2 and ACEIs or ARBs and to examine the main implications for clinical practice. In addition, novel therapeutic strategies for blocking ACE2-mediated COVID-19 infection will be displayed. We performed a comprehensive review of the literature to identify data from clinical and experimental studies for the association between COVID-19 infection, ACE2 and RAS inhibition. The current clinical and experimental evidence for ACEIs or ARBs to facilitate severe acute respiratory distress syndrome-coronavirus-2 (SARS-CoV-2) is insufficient to suggest discontinuing these drugs. Several observational studies arrive at the conclusion that the continued use of RAS inhibitors is unlikely to be harmful in COVID-19-positive patients. Further randomized trials are needed to answer the question of whether RAS inhibitors are harmful or beneficial to patients with COVID-19.