An analysis of the possible protective effect of antipsychotics for SARS-CoV-2 in patients under treatment for severe mental illnesses.
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ABSTRACT:
SUBMITTER: Prokopez CR
PROVIDER: S-EPMC8220941 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundThe crosstalk between the ubiquitin-proteasome and the immune system plays an important role in the health and pathogenesis of viral infection. However, there have been few studies of ubiquitin activation in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.MethodsWe investigated the effect of ubiquitination on SARS-CoV-2 infection and patient prognosis by integrating published coronavirus disease 2019 (COVID-19) multi-transcriptome data and bioinformatics methods.ResultsThe differential expression of COVID-19 samples revealed changed ubiquitination in most solid and hollow organs, and it was activated in lymphatic and other immune tissues. In addition, in the respiratory system of COVID-19 patients, the immune response was mainly focused on the alveoli, and the expression of ubiquitination reflected increasing immune infiltration. Ubiquitination stratification could significantly differentiate patients' prognosis and inflammation levels through the general transcriptional analysis of the peripheral blood of patients with COVID-19. Moreover, high ubiquitination levels were associated with a favourable prognosis, low inflammatory response, and reduced mechanical ventilation and intensive care unit. Moreover, high ubiquitination promoted a beneficial immune response while inhibiting immune damage. Finally, prognostic stratification and biomarker screening based on ubiquitination traits played an important role in clinical management and drug development.ConclusionUbiquitination characteristics provides new ideas for clinical intervention and prognostic guidance for COVID-19 patients.
| S-EPMC9708907 | biostudies-literature
Project description:Little is known on the end-of-life (EOL) care of terminal breast cancer in women with severe psychiatric disorder (SPD). The objective was to determine if women with SPD and terminal breast cancer received the same palliative and high-intensity care during their end-of-life than women without SPD. Study design, setting, participants. This population-based cohort study included all women aged 15 and older who died from breast cancer in hospitals in France (2014-2018). Key measurements/outcomes. Indicators of palliative care and high-intensity EOL care. Multivariable models were performed, adjusted for age at death, year of death, social deprivation, duration between cancer diagnosis and death, metastases, comorbidity, smoking addiction and hospital category. The analysis included 1742 women with SPD (287 with bipolar disorder, 1075 with major depression and 380 with schizophrenia) and 36,870 women without SPD. In multivariate analyses, women with SPD had more palliative care (adjusted odd ratio aOR 1.320, 95%CI [1.153-1.511], p < 0.001), longer palliative care follow-up before death (adjusted beta = 1.456, 95%CI (1.357-1.555), p < 0.001), less chemotherapy, surgery, imaging/endoscopy, and admission in emergency department and intensive care unit. Among women with SPD, women with bipolar disorders and schizophrenia died 5 years younger than those with recurrent major depression. The survival time was also shortened in women with schizophrenia. Despite more palliative care and less high-intensity care in women with SPD, our findings also suggest the existence of health disparities in women with bipolar disorders and schizophrenia compared to women with recurrent major depression and without SPD. Targeted interventions may be needed for women with bipolar disorders and schizophrenia to prevent these health disparities.
| S-EPMC8119688 | biostudies-literature
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| S-BSST379 | biostudies-other
Project description:The pandemic burden caused by the SARS-CoV-2 coronavirus constitutes a global public health emergency. Increasing understanding about predisposing factors to infection and severity is now a priority. Genetic, metabolic, and environmental factors can play a crucial role in the course and clinical outcome of COVID-19. We aimed to investigate the putative relationship between genetic factors associated to obesity, metabolism and lifestyle, and the presence and severity of SARS-CoV-2 infection. A total of 249 volunteers (178 women and 71 men, with mean and ± SD age of 49 ± 11 years) characterized for dietary, lifestyle habits and anthropometry, were studied for presence and severity of COVID-19 infection, and genotyped for 26 genetic variants related to obesity, lipid profile, inflammation, and biorhythm patterns. A statistically significant association was found concerning a protective effect of APOE rs7412 against SARS-CoV-2 infection (p = 0.039; OR 0.216; CI 0.084, 0.557) after correction for multiple comparisons. This protective effect was also ascribed to the APOɛ2 allele (p = 0.001; OR 0.207; CI 0.0796, 0.538). The genetic variant rs7412 resulting in ApoE2, genetic determinant of lipid and lipoprotein levels, could play a significant role protecting against SARS-CoV-2 infection.
| S-EPMC9065660 | biostudies-literature
Project description:Genetic and nongenetic factors associated with an increased inflammatory response may mediate a link between severe coronavirus disease 2019 (COVID‑19) and serious mental illness (SMI). However, systematic assessment of inflammatory response‑related factors associated with SMI that could influence COVID‑19 outcomes is lacking. In the present review, dietary patterns, smoking and the use of psychotropic medications are discussed as potential extrinsic risk factors and angiotensin‑converting enzyme (ACE) insertion/deletion (I/D) gene polymorphisms are considered as potential intrinsic risk factors. A genetics‑based prediction model for SMI using ACE‑I/D genotyping is also proposed for use in patients experiencing severe COVID‑19. Furthermore, the literature suggests that ACE inhibitors may have protective effects against SMI or severe COVID‑19, which is often linked to hypertension and other cardiovascular comorbidities. For this reason, we hypothesize that using these medications to treat patients with severe COVID‑19 might yield improved outcomes, including in the context of SMI associated with COVID‑19.
| S-EPMC8258463 | biostudies-literature
Project description:Background/objectivesWe investigated whether behavioral precautions adopted during Coronavirus disease (COVID-19) pandemic also influenced the spreading and multidrug resistance (MDR) of ESKAPEEc (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii [AB], Pseudomonas aeruginosa, Enterobacter spp and Escherichia Coli, [EC]) among Intensive Care Unit (ICU) patients.Subjects/methodsWe performed a single-center retrospective study in adult patients admitted to our COVID-19-free surgical ICU. Only patients staying in ICU for more than 48 hours were included. The ESKAPEEc infections recorded during the COVID-19 period (June 1, 2020 - February 28, 2021) and in the corresponding pre-pandemic period (June 1, 2019 - February 28, 2020) were compared. An interrupted time series analysis was performed to rule out possible confounders.ResultsOverall, 173 patients in the COVID-19 period and 132 in the pre-COVID-19 period were investigated. The ESKAPEEc infections were documented in 23 (13.3%) and 35 (26.5%) patients in the pandemic and the pre-pandemic periods, respectively (p = 0.005). Demographics, diagnosis, comorbidities, type of surgery, Simplified Acute Physiology Score II, length of mechanical ventilation, hospital and ICU length of stay, ICU death rate, and 28-day hospital mortality were similar in the two groups. In comparison with the pre-pandemic period, no AB was recorded during COVID-19 period, (p = 0.017), while extended-spectrum beta-lactamase-producing EC infections significantly decreased (p = 0.017). Overall, the ESKAPEEc isolates during pandemic less frequently exhibited multidrug-resistant (p = 0.014).ConclusionsThese findings suggest that a robust adherence to hygiene measures together with human contact restrictions in a COVID-19 free ICU might also restrain the transmission of ESKAPEEc pathogens.
| S-EPMC8646464 | biostudies-literature
Project description:BackgroundCoronavirus Disease 2019 (COVID-19) is a viral pandemic disease that may induce severe pneumonia in humans. In this paper, we investigated the putative implication of 12 vaccines, including BCG, OPV and MMR in the protection against COVID-19. Sequences of the main antigenic proteins in the investigated vaccines and SARS-CoV-2 proteins were compared to identify similar patterns. The immunogenic effect of identified segments was, then, assessed using a combination of structural and antigenicity prediction tools.ResultsA total of 14 highly similar segments were identified in the investigated vaccines. Structural and antigenicity prediction analysis showed that, among the identified patterns, three segments in Hepatitis B, Tetanus, and Measles proteins presented antigenic properties that can induce putative protective effect against COVID-19.ConclusionsOur results suggest a possible protective effect of HBV, Tetanus and Measles vaccines against COVID-19, which may explain the variation of the disease severity among regions.
| S-EPMC7995392 | biostudies-literature
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| S-EPMC6491096 | biostudies-literature
Project description:Severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is a newly emerging, highly transmitted and pathogenic coronavirus that has caused global public health events and economic crises. As of March 4, 2021, more than 100 million people have been infected, more than 2 million deaths have been reported worldwide, and the numbers are continuing to rise. To date, a specific drug for this lethal virus has not been developed to date, and very little is currently known about the immune evasion mechanisms of SARS-CoV-2. The aim of this review was to summarize and sort dozens of published studies on PubMed to explore the pathogenic features of SARS-CoV-2, as well as the possible immune escape mechanisms of this virus.
| S-EPMC8317057 | biostudies-literature