ABSTRACT
Összefoglaló. Az elmúlt években mind laikus, mind szakmai oldalról az internet vált az elso számú egészségügyi információforrássá, amit a COVID-19-pandémia tovább fokozott. Az online térben számos, különbözo jellegu platform áll rendelkezésre egészségkommunikációs célokra, melyek markánsan különböznek egymástól az átadható információ mennyiségében és minoségében, a létrehozásukhoz szükséges anyagi vagy idobeli ráfordításban, továbbá az ott létrehozott tartalom fogyasztási lehetoségeiben. Összefoglaló közleményünkben rendszerezve mutatjuk be a szöveg-, a hang-, illetve a videóalapú online egészségügyi edukációs formák elonyeit és hátrányait. Külön foglalkozunk a közösségi média (social media) egészségügyi vonatkozásaival, a benne rejlo lehetoségekkel, kiemelve a pandémia kapcsán felmerült problémákat. Az egyes platformok egészségüggyel kapcsolatos történelmének feldolgozása mellett gyakorlati oldalról mutatjuk be azok hasznosíthatóságát, elosegítve ezzel az online térbe terelt kollégák munkáját. Orv Hetil. 2022; 163(4): 132-139. Summary. In recent years, the internet has become the leading source of health-related information for both professionals and laymen, and this process has been further speeded up by the Covid-19 pandemic. There are many different platforms available for health communication purposes online, that vary greatly in the quantity and quality of transferable information; the time or financial input, which are necessary to create them; and the possibilities of the utilization of the created content. In our review, we present systematically the advantages and disadvantages of the text-, audio-, and video-based online health-related education platforms. We specify the health-related aspects of social media and its potential usability, focusing on the problems allied to the pandemic. We present the practical use of the different platforms from a healthcare perspective through the review of their respective histories, thus providing guidance to the colleagues working online. Orv Hetil. 2022; 163(4): 132-139.
Subject(s)
COVID-19 , Health Communication , Social Media , Humans , Hungary , Pandemics , SARS-CoV-2ABSTRACT
Increasing age is the strongest predictor of risk of COVID-19 severity and mortality. Immunometabolic switch from glycolysis to ketolysis protects against inflammatory damage and influenza infection in adults. To investigate how age compromises defense against coronavirus infection, and whether a pro-longevity ketogenic diet (KD) impacts immune surveillance, we developed an aging model of natural murine beta coronavirus (mCoV) infection with mouse hepatitis virus strain-A59 (MHV-A59). When inoculated intranasally, mCoV is pneumotropic and recapitulates several clinical hallmarks of COVID-19 infection. Aged mCoV-A59-infected mice have increased mortality and higher systemic inflammation in the heart, adipose tissue, and hypothalamus, including neutrophilia and loss of γδ T cells in lungs. Activation of ketogenesis in aged mice expands tissue protective γδ T cells, deactivates the NLRP3 inflammasome, and decreases pathogenic monocytes in lungs of infected aged mice. These data establish harnessing of the ketogenic immunometabolic checkpoint as a potential treatment against coronavirus infection in the aged.
Subject(s)
Coronavirus Infections/diet therapy , Diet, Ketogenic/methods , Murine hepatitis virus/pathogenicity , Age Factors , Aging , Animals , COVID-19/diet therapy , Coronavirus Infections/metabolism , Coronavirus Infections/mortality , Disease Models, Animal , Glycolysis , Humans , Inflammasomes/metabolism , Ketone Bodies/metabolism , Male , Mice , Mice, Inbred C57BL , Murine hepatitis virus/metabolism , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , SARS-CoV-2ABSTRACT
There are currently limited Food and Drug Administration (FDA)-approved drugs and vaccines for the treatment or prevention of Coronavirus Disease 2019 (COVID-19). Enhanced understanding of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection and pathogenesis is critical for the development of therapeutics. To provide insight into viral replication, cell tropism, and host-viral interactions of SARS-CoV-2, we performed single-cell (sc) RNA sequencing (RNA-seq) of experimentally infected human bronchial epithelial cells (HBECs) in air-liquid interface (ALI) cultures over a time course. This revealed novel polyadenylated viral transcripts and highlighted ciliated cells as a major target at the onset of infection, which we confirmed by electron and immunofluorescence microscopy. Over the course of infection, the cell tropism of SARS-CoV-2 expands to other epithelial cell types including basal and club cells. Infection induces cell-intrinsic expression of type I and type III interferons (IFNs) and interleukin (IL)-6 but not IL-1. This results in expression of interferon-stimulated genes (ISGs) in both infected and bystander cells. This provides a detailed characterization of genes, cell types, and cell state changes associated with SARS-CoV-2 infection in the human airway.
Subject(s)
Bronchi/pathology , COVID-19/diagnosis , Gene Expression , SARS-CoV-2/isolation & purification , Single-Cell Analysis/methods , Adult , Bronchi/virology , COVID-19/immunology , COVID-19/pathology , COVID-19/virology , Cells, Cultured , Epithelium/pathology , Epithelium/virology , Humans , Immunity, Innate , Longitudinal Studies , SARS-CoV-2/genetics , Transcriptome , Viral TropismABSTRACT
SARS-CoV-2 is the cause of a pandemic with growing global mortality. Using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS), we identified 309 host proteins that bind the SARS-CoV-2 RNA during active infection. Integration of this data with ChIRP-MS data from three other RNA viruses defined viral specificity of RNA-host protein interactions. Targeted CRISPR screens revealed that the majority of functional RNA-binding proteins protect the host from virus-induced cell death, and comparative CRISPR screens across seven RNA viruses revealed shared and SARS-specific antiviral factors. Finally, by combining the RNA-centric approach and functional CRISPR screens, we demonstrated a physical and functional connection between SARS-CoV-2 and mitochondria, highlighting this organelle as a general platform for antiviral activity. Altogether, these data provide a comprehensive catalog of functional SARS-CoV-2 RNA-host protein interactions, which may inform studies to understand the host-virus interface and nominate host pathways that could be targeted for therapeutic benefit.
Subject(s)
Host-Pathogen Interactions , RNA, Viral/genetics , SARS-CoV-2/genetics , Animals , COVID-19/virology , CRISPR-Cas Systems/genetics , Cell Line, Tumor , Chlorocebus aethiops , Female , Genome, Viral , Humans , Lung/virology , Male , Mass Spectrometry , Mitochondria/metabolism , Mitochondria/ultrastructure , Proteome/metabolism , RNA-Binding Proteins/metabolism , SARS-CoV-2/ultrastructure , Vero CellsABSTRACT
Although COVID-19 is considered to be primarily a respiratory disease, SARS-CoV-2 affects multiple organ systems including the central nervous system (CNS). Yet, there is no consensus on the consequences of CNS infections. Here, we used three independent approaches to probe the capacity of SARS-CoV-2 to infect the brain. First, using human brain organoids, we observed clear evidence of infection with accompanying metabolic changes in infected and neighboring neurons. However, no evidence for type I interferon responses was detected. We demonstrate that neuronal infection can be prevented by blocking ACE2 with antibodies or by administering cerebrospinal fluid from a COVID-19 patient. Second, using mice overexpressing human ACE2, we demonstrate SARS-CoV-2 neuroinvasion in vivo. Finally, in autopsies from patients who died of COVID-19, we detect SARS-CoV-2 in cortical neurons and note pathological features associated with infection with minimal immune cell infiltrates. These results provide evidence for the neuroinvasive capacity of SARS-CoV-2 and an unexpected consequence of direct infection of neurons by SARS-CoV-2.
Subject(s)
Angiotensin-Converting Enzyme 2 , Antibodies, Blocking/chemistry , COVID-19 , Cerebral Cortex , Neurons , SARS-CoV-2/metabolism , Angiotensin-Converting Enzyme 2/antagonists & inhibitors , Angiotensin-Converting Enzyme 2/metabolism , Animals , COVID-19/metabolism , COVID-19/pathology , Cerebral Cortex/metabolism , Cerebral Cortex/pathology , Cerebral Cortex/virology , Disease Models, Animal , Female , Humans , Male , Mice , Middle Aged , Neurons/metabolism , Neurons/pathology , Neurons/virology , Organoids/metabolism , Organoids/pathology , Organoids/virologyABSTRACT
BACKGROUNDThe effects of the novel coronavirus disease 2019 (COVID-19) in pregnancy remain relatively unknown. We present a case of second trimester pregnancy with symptomatic COVID-19 complicated by severe preeclampsia and placental abruption.METHODSWe analyzed the placenta for the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) through molecular and immunohistochemical assays and by and electron microscopy and measured the maternal antibody response in the blood to this infection.RESULTSSARS-CoV-2 localized predominantly to syncytiotrophoblast cells at the materno-fetal interface of the placenta. Histological examination of the placenta revealed a dense macrophage infiltrate, but no evidence for the vasculopathy typically associated with preeclampsia.CONCLUSIONThis case demonstrates SARS-CoV-2 invasion of the placenta, highlighting the potential for severe morbidity among pregnant women with COVID-19.FUNDINGBeatrice Kleinberg Neuwirth Fund and Fast Grant Emergent Ventures funding from the Mercatus Center at George Mason University. The funding bodies did not have roles in the design of the study or data collection, analysis, and interpretation and played no role in writing the manuscript.