Prevalence, correlates, and network analysis of depression and its association with quality of life in survivors with myocardial infarction during the COVID-19 pandemic.

BACKGROUND: Depression is common among myocardial infarction (MI) survivors and is strongly associated with poor quality of life (QOL). The aim of this study was to examine the prevalence, correlates and the network structure of depression, and its association with QOL in MI survivors during the COVID-19 pandemic. METHODS: This cross-sectional study evaluated depression and QOL in MI survivors with the Chinese version of the nine-item Patient Health Questionnaire (PHQ-9) and the World Health Organization Quality of Life-BREF (WHOQOL-BREF), respectively. Univariable analyses, multivariable analyses, and network analyses were performed. RESULTS: The prevalence of depression (PHQ-9 total score ≥ 5) among 565 MI survivors during the COVID-19 pandemic was 38.1 % (95 % CI: 34.1-42.1 %), which was significantly associated with poor QOL. Patients with depression were less likely to consult a doctor regularly after discharge, and more likely to experience more severe anxiety symptoms and fatigue. Item PHQ4 "Fatigue" was the most central symptom in the network, followed by PHQ6 "Guilt" and PHQ2 "Sad mood". The flow network showed that PHQ4 "Fatigue" had the highest negative association with QOL. CONCLUSION: Depression was prevalent among MI survivors during the COVID-19 pandemic and was significantly associated with poor QOL. Those who failed to consult a doctor regularly after discharge or reported severe anxiety symptoms and fatigue should be screened for depression. Effective interventions for MI survivors targeting central symptoms, especially fatigue, are needed to reduce the negative impact of depression and improve QOL.

Nervous system manifestations related to COVID-19 and their possible mechanisms.

In December 2019, the novel coronavirus disease (COVID-19) due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection broke. With the gradual deepening understanding of SARS-CoV-2 and COVID-19, researchers and clinicians noticed that this disease is closely related to the nervous system and has complex effects on the central nervous system (CNS) and peripheral nervous system (PNS). In this review, we summarize the effects and mechanisms of SARS-CoV-2 on the nervous system, including the pathways of invasion, direct and indirect effects, and associated neuropsychiatric diseases, to deepen our knowledge and understanding of the relationship between COVID-19 and the nervous system.

Mutations in spike protein and allele variations in ACE2 impact targeted therapy strategies against SARS-CoV-2.

Coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread rapidly worldwide with high rates of transmission and substantial mortality. To date, however, no effective treatments or enough vaccines for COVID-19 are available. The roles of angiotensin converting enzyme 2 (ACE2) and spike protein in the treatment of COVID-19 are major areas of research. In this study, we explored the potential of ACE2 and spike protein as targets for the development of antiviral agents against SARS-CoV-2. We analyzed clinical data, genetic data, and receptor binding capability. Clinical data revealed that COVID-19 patients with comorbidities related to an abnormal renin-angiotensin system exhibited more early symptoms and poorer prognoses. However, the relationship between ACE2 expression and COVID-19 progression is still not clear. Furthermore, if ACE2 is not a good targetable protein, it would not be applicable across a wide range of populations. The spike-S1 receptor-binding domain that interacts with ACE2 showed various amino acid mutations based on sequence analysis. We identified two spike-S1 point mutations (V354F and V470A) by receptor-ligand docking and binding enzyme-linked immunosorbent assays. These variants enhanced the binding of the spike protein to ACE2 receptors and were potentially associated with increased infectivity. Importantly, the number of patients infected with the V354F and V470A mutants has increased with the development of the SARS-CoV-2 pandemic. These results suggest that ACE2 and spike-S1 are likely not ideal targets for the design of peptide drugs to treat COVID-19 in different populations.