Translational research : the journal of laboratory and clinical medicine
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Early in the pandemic, concern that cardiovascular effects would accompany COVID-19 was fueled by lessons from the first SARS epidemic, knowledge that the SARS-COV2 entry receptor (Angiotensin-converting enzyme 2, ACE2) is highly expressed in the heart, early reports of myocarditis, and first-hand accounts by physicians caring for those with severe COVID-19. Over 18 months, our understanding of the cardiovascular manifestations has expanded greatly, leaving more new questions than those conclusively answered. Cardiac involvement is common (∼20%) but not uniformly observed in those who require treatment in a hospitalized setting. ⋯ To provide proper context, paradigms of cardiovascular injury due to other inflammatory processes will also be discussed. Ongoing research and a deeper understanding COVID-19 may ultimately reveal new insight into the mechanistic underpinnings of cardiovascular disease. Thus, in this time of unprecedented suffering and risk to global health, there exists the opportunity that well conducted translational research of SARS-COV2 may provide health dividends that outlast the current pandemic.
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The worldwide pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected an estimated 200 million people with over 4 million deaths. Although COVID-19, the disease caused by the SARS-CoV-2 virus, is primarily a respiratory disease, an increasing number of neurologic symptoms have been reported. Some of these symptoms, such as loss of smell or taste, are mild and non-life threatening, while others, such as stroke or seizure, are more critical. ⋯ Neurological symptoms can be difficult to study due to the complexity of the central and peripheral nervous system. These neurologic symptoms can be difficult to identify and quantitate. This narrative review will describe approaches for assessing neurologic manifestations of COVID-19, with examples of the data they provide, as well as some directions for future research to aid in understanding the pathophysiology of COVID-19-related neurological implications.
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Impaired glucose regulation (IGR) is common world-wide, and is correlated with Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) the virus that causes Coronavirus disease 2019 (COVID-19). However, no systematic reviews are available on the topic, and little is known about the strength of the evidence underlying published associations. ⋯ It is uncertain whether interventions targeting dysglycemia to improve SARS-CoV-2 outcomes have potential to be effective, or if risk assessment should include biomarkers of diabetes risk (ie, insulin and glucose or HbA1c) among diabetes-free individuals. Future studies with robust risk factor data collection, among population-based samples with pre-pandemic assessments will be important to inform these questions.
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Impaired glucose regulation (IGR) is common world-wide, and is correlated with Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) the virus that causes Coronavirus disease 2019 (COVID-19). However, no systematic reviews are available on the topic, and little is known about the strength of the evidence underlying published associations. ⋯ It is uncertain whether interventions targeting dysglycemia to improve SARS-CoV-2 outcomes have potential to be effective, or if risk assessment should include biomarkers of diabetes risk (ie, insulin and glucose or HbA1c) among diabetes-free individuals. Future studies with robust risk factor data collection, among population-based samples with pre-pandemic assessments will be important to inform these questions.
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Type I interferons (IFN) are central players in the pathogenesis of systemic lupus erythematosus (SLE) and the up-regulation of interferon-stimulated genes (ISGs) in SLE patients is subjected to increasing scrutiny as for its use in diagnosis, stratification and monitoring of SLE patients. Determinants of this immunological phenomenon are yet to be fully charted. The purpose of this systematic review was to characterize expressions of ISGs in blood of SLE patients and to analyze if they associated with core demographic and clinical features of SLE. ⋯ Generalized linear models adjusted for prevalence of lupus nephritis and usage of hydroxychloroquine confirmed the observed association between African ancestry and IFI27, IFI44L, IFIT1, PRKR and RSAD2, whereas disease activity was associated with expression of IFI27 and RNASE2. In conclusion, this systematic review revealed that expression of ISGs often used for deriving an IFN signature in SLE patients were influenced by African ancestry rather than disease activity. This underscores the necessity of taking ancestry into account when employing the IFN signature for clinical research in SLE.