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1
Salinas, Sara, and Yannick Simonin. "Les atteintes neurologiques liées au SARS-CoV-2 et autres coronavirus humains." médecine/sciences 36, no. 8-9 (August 2020): 775–82. http://dx.doi.org/10.1051/medsci/2020122.
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L’émergence récente d’un nouveau coronavirus, le SARS-CoV-2, responsable de la maladie appelée COVID-19, est un nouvel avertissement du risque pour la santé publique représenté par les zoonoses virales et notamment par les coronavirus. Principalement connus pour leur capacité à infecter les voies respiratoires supérieures et inférieures, les coronavirus peuvent également affecter le système nerveux central et périphérique, comme c’est le cas pour de nombreux virus respiratoires, tels que les virus influenza ou le virus respiratoire syncytial. Les infections du système nerveux sont un problème important de santé publique car elles peuvent provoquer des atteintes dévastatrices allant jusqu’au décès du patient, en particulier lorsqu’elles surviennent chez les personnes fragilisées ou âgées plus sensibles à ce type d’infection. Les connaissances de la physiopathologie des infections par les coronavirus émergents (MERS-CoV, SARS-CoV et SARS-CoV-2) et leurs moyens d’accéder au système nerveux central sont, pour l’heure, très sommaires. Les travaux en cours visent notamment à mieux appréhender les mécanismes associés aux atteintes neurologiques observées. Dans cette revue nous aborderons l’état des connaissances actuelles sur le neurotropisme des coronavirus humains et les mécanismes associés en développant tout particulièrement les dernières données concernant le SARS-CoV-2.
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POZZETTO, B., I. BECHRI, M. DELOLME, M. VOGRIG, J. RIGAILI, P. VERHOEVEN, T. BOURLET, and S. PILET. "État des lieux du diagnostic virologique de l’infection à SARS-CoV-2." EXERCER 31, no. 163 (May 1, 2020): 215–20. http://dx.doi.org/10.56746/exercer.2020.163.215.
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L’infection COVID-19 a émergé de façon soudaine en Chine, en décembre 2019 et est devenue rapidement pandémique. Le virus responsable a été identifié comme un nouveau coronavirus probablement issu d’un virus de chauve-souris, dénommé SARS-CoV-2, ce qui a permis de mettre au point des tests diagnostiques permettant l’identification de son ARN par techniques moléculaires. En plus du rappel de quelques données virologiques, l’objet de cette revue est de présenter les tests moléculaires de diagnostic direct et les tests sérologiques actuellement disponibles pour identifier cette infection. Le diagnostic repose principalement sur la détection du génome viral par RT-PCR en temps réel dans les sécrétions respiratoires (prélèvements nasopharyngés à la phase précoce et prélèvements respiratoires profonds au stade de pneumonie) ; les résultats sont disponibles dans un délai d’environ 4 heures. Le pic de l’infectiosité se situe entre le 3e jour avant et le 3e après le début des symptômes. Le virus peut également être détecté dans le sang et dans les selles, même si, à ce jour, l’infectiosité du virus dans ces prélèvements n’est pas avérée. A un stade plus tardif de l’infection, une réponse humorale anti-SARS-CoV-2 peut être mise en évidence, avec des anticorps de classes IgM et IgA à partir du 8 ou 9e jour après le début des symptômes, puis des anticorps de classe IgG qui signent un contact antérieur avec cet agent. L’apparition des anticorps peut se faire très tardivement dans les formes pauci- ou asymptomatiques. De nombreuses questions sont encore non résolues, notamment en ce qui concerne le caractère protecteur de cette réponse humorale et sa durée, ainsi que son rôle dans la physiopathologie des formes sévères.
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Meunier, Nicolas. "Odorat et virus respiratoires :une relation révélée par la Covid-19." médecine/sciences 39, no. 2 (February 2023): 119–28. http://dx.doi.org/10.1051/medsci/2023007.
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L’odorat, sens pendant longtemps sous-estimé chez l’homme, a été mis sur le devant de la scène par sa soudaine disparition, survenue pendant la pandémie de Covid-19, dont l’anosmie est un des symptômes majeurs. Pourtant, depuis longtemps, les virus respiratoires ont été associés aux troubles de l’odorat, dont 25 % seraient liés à une infection virale. L’olfaction débute dans le nez, au sein d’un épithélium olfactif qui a la particularité de contenir des neurones en contact direct avec l’environnement. Plusieurs virus respiratoires sont connus pour leur capacité réplicative au sein de cet épithélium. C’est notamment le cas du virus de la grippe (influenza) et du virus de la bronchiolite (VRS, pour virus respiratoire syncytial), mais leur tropisme pour ce tissu est bien moindre que celui du SARS-CoV-2. La physiopathologie de ce virus dans la cavité nasale a permis de commencer à comprendre les liens existant entre une infection virale et les troubles de l’olfaction.
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Kubiak, Jacek Z., and Małgorzata Kloc. "Coronavirus Disease Pathophysiology: Biomarkers, Potential New Remedies, Comorbidities, Long COVID-19, Post Pandemic Epidemiological Surveillance." International Journal of Molecular Sciences 24, no. 15 (July 31, 2023): 12236. http://dx.doi.org/10.3390/ijms241512236.
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Cespedes, Mateus da Silveira, and José Carlos Rosa Pires de Souza. "Sars-CoV-2: A clinical update - II." Revista da Associação Médica Brasileira 66, no. 4 (April 2020): 547–57. http://dx.doi.org/10.1590/1806-9282.66.4.547.
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SUMMARY INTRODUCTION A covid-19 pandemic decreed by WHO has raised greater awareness of it. EPIDEMIOLOGY The infection, reached the mark of 2,000,000 patients in 33 countries and caused the risk of the presence of comorbidities and advanced age. TRANSMISSIBILITY The transmissibility calculated so far is similar to the H1N1 epidemic, but with lower mortality rates. PHYSIOPATHOLOGY The SARS-CoV-2 virus, of the Coronaviridae family, has the capacity for cellular invasion through the angiotensin-converting enzyme 2 does not have a lower respiratory epithelium and in the cells of the small intestine mucosa. CLINICAL MANIFESTATIONS a presentation can be divided into mild (fever, fatigue, cough, myalgia, and sputum) and severe (cyanosis, dyspnoea, tachypnea, chest pain, hypoxemia and need for clinical measurement) and has an estimated estimate of 2%. DIAGNOSIS allows the detection of viral load in CRP-TR of patients with high clinical suspicion. TREATMENT based on supportive measures and infection control. In severe cases, the use of medications such as hydroxychloroquine and azithromycin or medication can be promising. Take care to avoid the use of corticosteroids. There are no restrictions on the use of resources and IECAs / BRAs.
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Enache, Alexandra, Veronica Ciocan, Camelia Oana Muresan, Talida Georgiana Cut, Dorin Novacescu, Corina Paul, Nicoleta Andreescu, Alexandra Mihailescu, Marius Raica, and Raluca Dumache. "Postmortem Documentation of SARS-CoV-2 in Utero and Postpartum Transmission, through Amniotic Fluid, Placental, and Pulmonary Tissue RT-PCR." Applied Sciences 11, no. 20 (October 13, 2021): 9505. http://dx.doi.org/10.3390/app11209505.
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The physiopathology of SARS-CoV-2 infection, during pregnancy and in early childhood, is poorly understood. Unfavorable maternal outcomes, the risk of vertical/postpartum transmission, and severe, multisystem involvement in infants and children highlight the importance of developing a cohesive treatment and nuanced prophylaxis strategy. In this study, we evaluate autopsy reports, pathological findings, and SARS-CoV-2 genome expression in three distinct clinical scenarios: maternal death due to severe COVID-19 with in utero fetal demise (27 weeks); mother with moderate COVID-19 and in utero fetal demise (29 weeks); and 2-month-old infant death with confirmed COVID-19 caregivers. We report the presence of the SARS-CoV-2 genome in amniotic fluid and placental tissue in the context of in utero transmission of SARS-CoV-2, but also in postmortem infant pulmonary tissue samples in a case of late postpartum SARS-CoV-2 transmission with asymptomatic, rapidly progressive disease, resulting in infant death. Key pathological findings offer a descriptive portrayal of maternal, in utero, and infantile COVID-19 pathogenesis. Further investigations are necessary to fully comprehend the clinical implications of SARS-CoV-2 infection during pregnancy, a prerequisite for adequate therapeutic management and harm reduction.
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Lansiaux, Edouard, Emmanuel Drouin, and Carsten Bolm. "Beta-Thalassemia Minor and SARS-CoV-2: Physiopathology, Prevalence, Severity, Morbidity, and Mortality." Thalassemia Reports 13, no. 1 (January 16, 2023): 21–32. http://dx.doi.org/10.3390/thalassrep13010003.
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Background: Since the first year of the COVID-19 global pandemic, a hypothesis concerning the possible protection/immunity of beta-thalassemia carriers has remained in abeyance. Methods: Three databases (Pubmed Central, Scopus, and Google Scholar) were screened and checked in order to extract all studies about the incidence of confirmed COVID-19 cases, mortality rate, severity assessment, or ICU admission among patients with beta-thalassemia minor, were included in this analysis. The language was limited to English. Studies such as case reports, review studies, and studies that did not have complete data for calculating incidences were excluded. Results and discussion: a total of 3 studies out of 2265 were selected. According to our systematic-review meta-analysis, beta-thalassemia carriers could be less affected by COVID-19 than the general population [IRR = 0.9250 (0.5752; 1.4877)], affected by COVID-19 with a worst severity [OR = 1.5933 (0.4884; 5.1981)], less admissible into the ICU [IRR = 0.3620 (0.0025; 51.6821)], and more susceptible to die from COVID-19 or one of its consequences [IRR = 1.8542 (0.7819; 4.3970)]. However, all of those results remain insignificant with a bad p-value (respectively 0.7479, 0.4400, 0.6881, and 0.1610). Other large case-control or registry studies are needed to confirm these trends.
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Sacramento, Carolina Q., Natalia Fintelman-Rodrigues, Suelen S. G. Dias, Jairo R. Temerozo, Aline de Paula D. Da Silva, Carine S. da Silva, Camilla Blanco, et al. "Unlike Chloroquine, Mefloquine Inhibits SARS-CoV-2 Infection in Physiologically Relevant Cells." Viruses 14, no. 2 (February 11, 2022): 374. http://dx.doi.org/10.3390/v14020374.
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Despite the development of specific therapies against severe acute respiratory coronavirus 2 (SARS-CoV-2), the continuous investigation of the mechanism of action of clinically approved drugs could provide new information on the druggable steps of virus–host interaction. For example, chloroquine (CQ)/hydroxychloroquine (HCQ) lacks in vitro activity against SARS-CoV-2 in TMPRSS2-expressing cells, such as human pneumocyte cell line Calu-3, and likewise, failed to show clinical benefit in the Solidarity and Recovery clinical trials. Another antimalarial drug, mefloquine, which is not a 4-aminoquinoline like CQ/HCQ, has emerged as a potential anti-SARS-CoV-2 antiviral in vitro and has also been previously repurposed for respiratory diseases. Here, we investigated the anti-SARS-CoV-2 mechanism of action of mefloquine in cells relevant for the physiopathology of COVID-19, such as Calu-3 cells (that recapitulate type II pneumocytes) and monocytes. Molecular pathways modulated by mefloquine were assessed by differential expression analysis, and confirmed by biological assays. A PBPK model was developed to assess mefloquine’s optimal doses for achieving therapeutic concentrations. Mefloquine inhibited SARS-CoV-2 replication in Calu-3, with an EC50 of 1.2 µM and EC90 of 5.3 µM. It reduced SARS-CoV-2 RNA levels in monocytes and prevented virus-induced enhancement of IL-6 and TNF-α. Mefloquine reduced SARS-CoV-2 entry and synergized with Remdesivir. Mefloquine’s pharmacological parameters are consistent with its plasma exposure in humans and its tissue-to-plasma predicted coefficient points suggesting that mefloquine may accumulate in the lungs. Altogether, our data indicate that mefloquine’s chemical structure could represent an orally available host-acting agent to inhibit virus entry.
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Lazar, Mihai, Mihai Sandulescu, Ecaterina Constanta Barbu, Cristina Emilia Chitu-Tisu, Darie Ioan Andreescu, Andreea Nicoleta Anton, Teodora Maria Erculescu, et al. "The Role of Cytokines and Molecular Pathways in Lung Fibrosis Following SARS-CoV-2 Infection: A Physiopathologic (Re)view." Biomedicines 12, no. 3 (March 13, 2024): 639. http://dx.doi.org/10.3390/biomedicines12030639.
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SARS-CoV-2 infection is a significant health concern that needs to be addressed not only during the initial phase of infection but also after hospitalization. This is the consequence of the various pathologies associated with long COVID-19, which are still being studied and researched. Lung fibrosis is an important complication after COVID-19, found in up to 71% of patients after discharge. Our research is based on scientific articles indexed in PubMed; in the selection process, we used the following keywords: “lung fibrosis”, “fibrosis mediators”, “fibrosis predictors”, “COVID-19”, “SARS-CoV-2 infection”, and “long COVID-19”. In this narrative review, we aimed to discuss the current understanding of the mechanisms of initiation and progression of post-COVID-19 lung fibrosis (PC-19-LF) and the risk factors for its occurrence. The pathogenesis of pulmonary fibrosis involves various mediators such as TGF-β, legumain, osteopontin, IL-4, IL-6, IL-13, IL-17, TNF-α, Gal-1, Gal-3, PDGF, and FGFR-1. The key cellular effectors involved in COVID-19 lung fibrosis are macrophages, epithelial alveolar cells, neutrophils, and fibroblasts. The main fibrosis pathways in SARS-CoV-2 infection include hypoxemia-induced fibrosis, macrophage-induced fibrosis, and viral-fibroblast interaction-induced fibrosis.
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Sebastián-Martín, Alba, Belén G. Sánchez, José M. Mora-Rodríguez, Alicia Bort, and Inés Díaz-Laviada. "Role of Dipeptidyl Peptidase-4 (DPP4) on COVID-19 Physiopathology." Biomedicines 10, no. 8 (August 19, 2022): 2026. http://dx.doi.org/10.3390/biomedicines10082026.
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DPP4/CD26 is a single-pass transmembrane protein with multiple functions on glycemic control, cell migration and proliferation, and the immune system, among others. It has recently acquired an especial relevance due to the possibility to act as a receptor or co-receptor for SARS-CoV-2, as it has been already demonstrated for other coronaviruses. In this review, we analyze the evidence for the role of DPP4 on COVID-19 risk and clinical outcome, and its contribution to COVID-19 physiopathology. Due to the pathogenetic links between COVID-19 and diabetes mellitus and the hyperinflammatory response, with the hallmark cytokine storm developed very often during the disease, we dive deep into the functions of DPP4 on carbohydrate metabolism and immune system regulation. We show that the broad spectrum of functions regulated by DPP4 is performed both as a protease enzyme, as well as an interacting partner of other molecules on the cell surface. In addition, we provide an update of the DPP4 inhibitors approved by the EMA and/or the FDA, together with the newfangled approval of generic drugs (in 2021 and 2022). This review will also cover the effects of DPP4 inhibitors (i.e., gliptins) on the progression of SARS-CoV-2 infection, showing the role of DPP4 in this disturbing disease.
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Singh, Preeti, and Biplob Adhikari. "Journey of SARS-CoV-19 from Mucosa Towards Angiotensin-Converting Enzyme2 Pathway: A Review." Journal of Nepalese Society of Periodontology and Oral Implantology 5, no. 2 (December 31, 2021): 92–96. http://dx.doi.org/10.3126/jnspoi.v5i2.52980.
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The disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) or simply corona virus disease-2019 (COVID-19), has rapidly spread throughout the world. World Health Organization declared a global health emergency on January 30, 2020 announcing it as a Pandemic. The outbreak of the disease has posed serious health threat. A search was conducted for review which included various articles from 2019 to 2021 in PubMed/MEDLINE with keywords ACE2, 2019 NCOV, pandemic, physiopathology, SARS, Transmission. Both humoral and acquired immunity are targeted by the virus during progression of diseases. A cellular biology perceptive of pathogenesis is useful forframing clinical course of the diseases and its related complication. Knowledge of underlying pathophysiology regarding release of innate immune modulators such as CXCL10, beta and alpha interferons will facilitate the development of therapeutic modalities in future. Despite implementing all the preventive efforts SARS-CoV-2, exponential mode of infection rate is still existing with epidemic doubling time less than a week. In this review, an update on pathophysiology, cell biology of virus and immune modulation related to diseases are considered and has been described. Any of the mechanisms and assumptions discussed in the article and in our understanding of SARS-CoV-2 may be revised as further evidence emerges.
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Gaujac, Cristiano, and Regiane Cristina Amaral. "Neurological manifestations and pathophysiological mechanisms of Covid-19." ARCHIVES OF HEALTH INVESTIGATION 10, no. 7 (July 16, 2021): 1040–47. http://dx.doi.org/10.21270/archi.v10i7.5460.
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Background - Severe acute respiratory syndrome coronavirus-2 is a novel, highly infectious coronavirus and the etiologic agent of Covid-19. The course of Covid-19 can range from mild flu-like symptoms to severe, life-threatening symptoms, especially when comorbidities are present. Increasing studies have reinforced the association between SARS-CoV-2 and various neurological manifestations, although the pathophysiological mechanisms remain uncertain. Objective - The aim of this paper was to briefly describe current findings on the relationship between SARS-CoV-2 pathophysiology and major CNS and Peripheral Nervous System (PNS) manifestations. Methods and Material - This work consists of a literature review based on the study of academic papers. To this end, the Pubmed platform was used to search for scientific articles, using the keywords: covid-19, coronavirus, physiopathology, neuronal symptoms. Results - out of 114,660 articles found, 94 were selected for this review. Conclusions - Periodic reviews collaborate in the constant updating and summarization of findings. Understanding the pathophysiology of SARS-CoV-2 on the SN and the link between the systems may lead to earlier and earlier diagnoses of neurological involvement, guide therapeutic management, prevent sequelae, and preserve lives.
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Pacnejer, Aliteia-Maria, Anca Butuca, Carmen Maximiliana Dobrea, Anca Maria Arseniu, Adina Frum, Felicia Gabriela Gligor, Rares Arseniu, et al. "Neuropsychiatric Burden of SARS-CoV-2: A Review of Its Physiopathology, Underlying Mechanisms, and Management Strategies." Viruses 16, no. 12 (November 21, 2024): 1811. http://dx.doi.org/10.3390/v16121811.
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The COVID-19 outbreak, caused by the SARS-CoV-2 virus, was linked to significant neurological and psychiatric manifestations. This review examines the physiopathological mechanisms underlying these neuropsychiatric outcomes and discusses current management strategies. Primarily a respiratory disease, COVID-19 frequently leads to neurological issues, including cephalalgia and migraines, loss of sensory perception, cerebrovascular accidents, and neurological impairment such as encephalopathy. Lasting neuropsychological effects have also been recorded in individuals following SARS-CoV-2 infection. These include anxiety, depression, and cognitive dysfunction, suggesting a lasting impact on mental health. The neuroinvasive potential of the virus, inflammatory responses, and the role of angiotensin-converting enzyme 2 (ACE2) in neuroinflammation are critical factors in neuropsychiatric COVID-19 manifestations. In addition, the review highlights the importance of monitoring biomarkers to assess Central Nervous System (CNS) involvement. Management strategies for these neuropsychiatric conditions include supportive therapy, antiepileptic drugs, antithrombotic therapy, and psychotropic drugs, emphasizing the need for a multidisciplinary approach. Understanding the long-term neuropsychiatric implications of COVID-19 is essential for developing effective treatment protocols and improving patient outcomes.
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Zota, Ioana Mădălina, Cristian Stătescu, Radu Andy Sascău, Mihai Roca, Larisa Anghel, Alexandra Maștaleru, Maria Magdalena Leon-Constantin, et al. "Acute and Long-Term Consequences of COVID-19 on Arterial Stiffness—A Narrative Review." Life 12, no. 6 (May 25, 2022): 781. http://dx.doi.org/10.3390/life12060781.
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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the ongoing global coronavirus (COVID-19) pandemic. Although initially viewed as an acute respiratory illness, COVID-19 is clearly a complex multisystemic disease with extensive cardiovascular involvement. Emerging evidence shows that the endothelium plays multiple roles in COVID-19 physiopathology, as both a target organ that can be directly infected by SARS-CoV-2 and a mediator in the subsequent inflammatory and thrombotic cascades. Arterial stiffness is an established marker of cardiovascular disease. The scope of this review is to summarize available data on the acute and long-term consequences of COVID-19 on vascular function. COVID-19 causes early vascular aging and arterial stiffness. Fast, noninvasive bedside assessment of arterial stiffness could optimize risk stratification in acute COVID-19, allowing for early escalation of treatment. Vascular physiology remains impaired at least 12 months after infection with SARS-CoV-2, even in otherwise healthy adults. This raises concerns regarding the extent of arterial remodeling in patients with preexisting vascular disease and the potential development of a persistent, chronic COVID-19 vasculopathy. Long-term follow up on larger cohorts is required to investigate the reversibility of COVID-19-induced vascular changes and their associated prognostic implications.
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González-Villalva, Adriana, Aurora de la Peña-Díaz, Marcela Rojas-Lemus, Nelly López-Valdez, Martha Ustarroz-Cano, Isabel García-Peláez, Patricia Bizarro-Nevares, and Teresa I. Fortoul. "Fisiología de la hemostasia y su alteración por la coagulopatía en COVID-19." Revista de la Facultad de Medicina 63, no. 5 (September 10, 2020): 45–57. http://dx.doi.org/10.22201/fm.24484865e.2020.63.5.08.
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COVID-19 global pandemic caused by Sars-CoV-2 virus, has worried to health care providers due to the high mortality rate related to coagulopathy in many patients. COVID-19 coagulopathy is mainly thrombotic, first locally in lungs but later on it becomes micro and macrovascular systemic coagulopathy. It has been associated to endothelial damage, inflammation, neutrophil-extracellular traps, monocyte and macrophage activation, cytokines storm that induce a vicious cycle of thrombosis and inflammation. The increased levels of prothrombotic factors as tissue factor, Von Willebrand factor, fibrinogen, VIII factor and the decreased levels of antithrombotic factos, such as: antithrombin and Protein S have been reported in COVID-19 patients. Insufficiency of fibrinolysis because of the increased levels of PAI-1 (plasminogen activator inhibitor 1) have been reported also. During this disease there are intraalveolar fibrin deposits that needs to be degraded. Fibrinolysis of thrombus and fibrin intraalveolar degradation are responsible for the high increase of D-dimers levels that are an important predictor of severity of the disease. In this report, the physiology of hemostasis, thromboinflamation secondary to Sars-CoV-2 infection are reviewed, as well as the clinical evidence and the physiopathology of COVID-19 coagulopathy from the basic sciences point of view. Keywords:Hemostasis; coagulation; thrombosis; coagulopathy; Sars-CoV-2; COVID-19.
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Scarcella, Antonio, Maria Vincenza Mastrolia, Edoardo Marrani, Ilaria Maccora, Ilaria Pagnini, and Gabriele Simonini. "Neuro-PIMS-TS: a single case report and review of the literature." Therapeutic Advances in Musculoskeletal Disease 14 (January 2022): 1759720X2211396. http://dx.doi.org/10.1177/1759720x221139627.
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Neurological manifestations related to SARS-CoV-2 infection in adults have been largely reported since the beginning of the pandemic. Subsequent large-scale studies involving children confirmed the occurrence of neurological symptoms associated with SARS-CoV-2 infection also among paediatric patients, especially in the context of paediatric inflammatory multisystem syndrome temporally associated with COVID-19 (PIMS-TS). At this regard, we report the challenging case of a 10-month-old baby with PIMS-TS complicated by acute cerebral oedema successfully treated with intravenous immunoglobulins, corticosteroids and anakinra. Our results, combined with the evidence of larger case series suggest that higher inflammatory burden is more frequent in patients with neuro PIMS-TS. As regards neuroimaging, neuroimmune disorders are found to be more common during acute COVID-19, MERS is more frequent during PIMS-TS. Distinct immune mechanisms may underlie these different types of neurological involvement, which are yet to be understood. Further studies are required to better define the physiopathology of neuro PIMS-TS and its possible therapeutical implications.
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Méndez-García, Lucía Angélica, Helena Solleiro-Villavicencio, Sebastián Guartazaca-Guerrero, Jahir Rodríguez-Morales, and José Damián Carrillo-Ruiz. "Neurological Diseases Define the Cytokine Profile in CFS during SARS-CoV-2 Infection in Highly Ill Patients." Tropical Medicine and Infectious Disease 8, no. 6 (May 25, 2023): 290. http://dx.doi.org/10.3390/tropicalmed8060290.
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Neuroinflammation is critical in developing and progressing neurological diseases. The underlying pro-inflammatory cytokine expression combined with additional mechanisms in the neuropathology, such as oxidative stress, brain–blood barrier damage, and endothelial dysfunction, could contribute to the susceptibility to developing severe COVID-19. The physiopathology of SARS-CoV-2 and other human coronaviruses (H-CoVs) has not been completely understood; however, they have all been linked to a disproportionated response of the immune system, particularly an exacerbated cytokine production and the dysregulation of total cell counts. In this article, based on the compilation of studies reported by our working group regarding COVID-19 and neurological diseases, we propose that the inflammation observed in the central nervous system, through a CSF analysis, could be conditioned by neurological disease(s) and enhanced by COVID-19. Therefore, it is necessary to determine the cytokine profile in different neurological disorders to propose adequate treatments and avoid severe forms of the disease in these patients.
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Zarrilli, Giovanni, Valentina Angerilli, Gianluca Businello, Marta Sbaraglia, Giulia Traverso, Francesco Fortarezza, Stefania Rizzo, et al. "The Immunopathological and Histological Landscape of COVID-19-Mediated Lung Injury." International Journal of Molecular Sciences 22, no. 2 (January 19, 2021): 974. http://dx.doi.org/10.3390/ijms22020974.
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A complete understanding of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) physiopathology and related histopathologic lesions is necessary to improve treatment and outcome of coronavirus disease 2019 (COVID-19) patients. Many studies have focused on autopsy findings in COVID-19-related deaths to try and define any possible specific pattern. Histopathologic alterations are principally found within lungs and blood vessels, and these abnormalities also seem to have the highest clinical impact. Nevertheless, many of the morphological data collected so far are non-specific, fickle, and possibly associated with other co-existing factors. The aim of this minireview is to describe the main histopathological features related to COVID-19 and the mechanism known as “cytokine storm”.
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Evangelista, Heitor, César Amaral, Luís Cristóvão Porto, Sérgio J. Gonçalves Junior, Eduardo Delfino Sodré, Juliana Nogueira, Angela M. G. dos Santos, Marcio Cataldo, and Daniel Junger. "Modeling the initial phase of SARS-CoV-2 deposition in the respiratory tract mimicked by the 11C radionuclide." PLOS ONE 16, no. 1 (January 14, 2021): e0245019. http://dx.doi.org/10.1371/journal.pone.0245019.
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The knowledge on the deposition and retention of the viral particle of SARS-CoV-2 in the respiratory tract during the very initial intake from the ambient air is of prime importance to understand the infectious process and COVID-19 initial symptoms. We propose to use a modified version of a widely tested lung deposition model developed by the ICRP, in the context of the ICRP Publication 66, that provides deposition patterns of microparticles in different lung compartments. In the model, we mimicked the "environmental decay" of the virus, determined by controlled experiments related to normal speeches, by the radionuclide 11C that presents comparable decay rates. Our results confirm clinical observations on the high virus retentions observed in the extrathoracic region and the lesser fraction on the alveolar section (in the order of 5), which may shed light on physiopathology of clinical events as well on the minimal inoculum required to establish infection.
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Chaturvedi, Pragya, and Sudhanshu Singh. "Significance of Epigenetics in Sars-CoV-2 Infection and Proposed Epi-Drugs for Covid-19." SAMRIDDHI : A Journal of Physical Sciences, Engineering and Technology 13, SUP 1 (June 30, 2021): 21–26. http://dx.doi.org/10.18090/samriddhi.v13is1.6.
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We frequently come in contact with animal viruses through the food which we eat, the pets which we have, and our connections with nature. The enormous majority of viruses which enter our bodies pass inoffensively through our physiological systems or eradicate by our immune systems. However, on rare circumstances, a human-encounters by a virus which begins to replicate itself, accomplishing its entire lifecycle within human cells and intensifying themselves into a large number. Replication of an animal virus inside the human body is the key instant in the zoonotic process. SARS CoV-2 is one of these viruses which cause COVID-19 disease. To enter the target cell SARS-CoV-2 uses angiotensinconverting enzyme 2 (ACE2) and the cellular protease transmembrane protease serine 2 (TMPRSS2). Genome stability and maintenance of cellular equilibrium are the main parameters influenced by epigenetically regulated chromatin structure. Implication of regulation by epigenetic machinery has also been found in the physiopathology of the virus infection. By varying the function of gene locus. such regulation links genotype and phenotype without changing the original DNA sequences. However antiviral drugs have been used to treat various viral diseases since long, epi-drugs are now proposed to treat these diseases due to the epigenetic implications found in these infections. Epi-drugs are small agents that are able to reverse some epigenetic changes. This review is aimed to find implication of epigenetics in infection caused due SARS C0V-2 and if there is any epi-drugs approach possible to treat this infection.
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Moatar, Alexandra Ioana, Aimee Rodica Chis, Catalin Marian, and Ioan-Ovidiu Sirbu. "Gene Network Analysis of the Transcriptome Impact of SARS-CoV-2 Interacting MicroRNAs in COVID-19 Disease." International Journal of Molecular Sciences 23, no. 16 (August 17, 2022): 9239. http://dx.doi.org/10.3390/ijms23169239.
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According to the World Health Organization (WHO), as of June 2022, over 536 million confirmed COVID-19 disease cases and over 6.3 million deaths had been globally reported. COVID-19 is a multiorgan disease involving multiple intricated pathological mechanisms translated into clinical, biochemical, and molecular changes, including microRNAs. MicroRNAs are essential post-transcriptional regulators of gene expression, being involved in the modulation of most biological processes. In this study, we characterized the biological impact of SARS-CoV-2 interacting microRNAs differentially expressed in COVID-19 disease by analyzing their impact on five distinct tissue transcriptomes. To this end, we identified the microRNAs’ predicted targets within the list of differentially expressed genes (DEGs) in tissues affected by high loads of SARS-CoV-2 virus. Next, we submitted the tissue-specific lists of the predicted microRNA-targeted DEGs to gene network functional enrichment analysis. Our data show that the upregulated microRNAs control processes such as mitochondrial respiration and cytokine and cell surface receptor signaling pathways in the heart, lymph node, and kidneys. In contrast, downregulated microRNAs are primarily involved in processes related to the mitotic cell cycle in the heart, lung, and kidneys. Our study provides the first exploratory, systematic look into the biological impact of the microRNAs associated with COVID-19, providing a new perspective for understanding its multiorgan physiopathology.
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Sanchez, Belén G., Jose M. Gasalla, Manuel Sánchez-Chapado, Alicia Bort, and Inés Diaz-Laviada. "Increase in Ischemia-Modified Albumin and Pregnancy-Associated Plasma Protein-A in COVID-19 Patients." Journal of Clinical Medicine 10, no. 23 (November 23, 2021): 5474. http://dx.doi.org/10.3390/jcm10235474.
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This study was undertaken due to the urgent need to explore reliable biomarkers for early SARS-CoV-2 infection. We performed a retrospective study analyzing the serum levels of the cardiovascular biomarkers IL-6, TNF-α, N-terminal pro-B natriuretic peptide, cardiac troponin T (cTnT), ischemia-modified albumin (IMA) and pregnancy-associated plasma protein-A (PAPP-A) in 84 patients with COVID-19.Patients were divided into three groups according to their RT-qPCR and IgG values: acute infection (n = 35), early infection (n = 25) or control subjects (n = 24). Levels of biomarkers were analyzed in patient serum samples using commercially available ELISA kits. Results showed a significant increase in IMA and PAPP-A levels in the early infected patients. Moreover, multivariate analysis and receiver operating characteristic (ROC) curve showed that IMA and PAPP-A had excellent discrimination value for the early stage of COVID-19. For IMA, the area under the ROC curve (AUC) had a value of 0.94 (95% confidence interval (CI): 0.881–0.999). Likewise, the serum level of PAPP-A was significantly higher in patients with early infection than in the control subjects (AUC = 0.801 (95% CI: 0.673–0.929)). The combined use of IMA and PAPP-A enhanced the sensitivity for total SARS-CoV-2-infected patients to 93%. These results suggest that the increased levels of PAPP-A and IMA shed light on underlying mechanisms of COVID-19 physiopathology and might be used as efficient biomarkers with high sensitivity and specificity for the early stage of COVID-19. Importantly, when monitoring pregnancy and cardiovascular diseases using PAPP-A or IMA levels, a SARS-CoV-2 infection should be discarded for proper interpretation of the results.
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Barbosa, Adriana Aparecida de Oliveira, Gabriel Cunha Beato, Pietra Antônia Filiol Belin, and Larissa Ramos Araújo. "ASPECTOS CLÍNICOS DA MÁ NUTRIÇÃO NA COVID-19." Simbio-Logias Revista Eletrônica de Educação Filosofia e Nutrição 12, no. 16 (2020): 01–19. http://dx.doi.org/10.32905/19833253.2020.12.16p01.
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The pandemic caused by the new coronavirus has sparked discussions among health professionals about the role of food and nutrition in the infectious condition caused by the SARS-CoV-2 virus in different population groups. Malnutrition, including obesity, may reflect more severe outcomes in the physiopathology of infection and systemic responses caused by COVID-19. The present work aims to make considerations directed to the nutritionist about the susceptibility of COVID-19 in individuals submitted to malnutrition, highlighting possible outcomes of the disease and the importance of nutritional care in maintaining the health of these patients. Therefore, maintaining a good nutritional status of these patients, combined with an adequate level of micronutrients will not guarantee protection against infection caused by COVID-19, however, it is essential to minimize the risks of worsening this disease.
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Franczuk, Monika, Tadeusz Przybyłowski, Małgorzata Czajkowska-Malinowska, Jakub Radliński, Grażyna Bochenek, Stefan Wesołowski, and Paweł Sliwiński. "Spirometry during the SARS-CoV-2 pandemic. Guidelines and practical advice from the expert panel of Respiratory Physiopathology Assembly of Polish Respiratory Society." Advances in Respiratory Medicine 88, no. 6 (December 30, 2020): 640–50. http://dx.doi.org/10.5603/arm.a2020.0186.
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Cespedes, Mateus da Silveira, and José Carlos Rosa Pires de Souza. "Coronavirus: a clinical update of Covid-19." Revista da Associação Médica Brasileira 66, no. 2 (February 2020): 116–23. http://dx.doi.org/10.1590/1806-9282.66.2.116.
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SUMMARY INTRODUCTION A covid-19 pandemic decreed by WHO has raised greater awareness of it. EPIDEMIOLOGY The infection reached the mark of 350,000 patients in 33 countries and affected as comorbidities the presence of comorbidities and advanced age. TRANSMISSIBILITY The transmissibility calculated so far is similar to the H1N1 epidemic, but with lower mortality rates. PHYSIOPATHOLOGY The SARS-CoV-2 virus, of the Coronaviridae family, has the capacity for cellular invasion through the angiotensin-converting enzyme 2 does not have a lower respiratory epithelium and in the cells of the small intestine mucosa. CLINICAL MANIFESTATIONS a presentation can be divided into mild (fever, fatigue, cough, myalgia, and sputum) and severe (cyanosis, dyspnoea, tachypnea, chest pain, hypoxemia and need for clinical measurement) and has an estimated estimate of 2%. DIAGNOSIS allows the detection of viral load in CRP-TR of patients with high clinical suspicion. TREATMENT based on supportive measures and infection control. In severe cases, the use of medications such as hydroxychloroquine and azithromycin or medication can be promising. Take care to avoid the use of corticosteroids. There are no restrictions on the use of resources and ACEIs / ARBs.
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Frías-De-León, María Guadalupe, Rodolfo Pinto-Almazán, Rigoberto Hernández-Castro, Eduardo García-Salazar, Patricia Meza-Meneses, Carmen Rodríguez-Cerdeira, Roberto Arenas, Esther Conde-Cuevas, Gustavo Acosta-Altamirano, and Erick Martínez-Herrera. "Epidemiology of Systemic Mycoses in the COVID-19 Pandemic." Journal of Fungi 7, no. 7 (July 13, 2021): 556. http://dx.doi.org/10.3390/jof7070556.
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The physiopathologic characteristics of COVID-19 (high levels of inflammatory cytokines and T-cell reduction) promote fungal colonization and infection, which can go unnoticed because the symptoms in both diseases are very similar. The objective of this work was to study the current epidemiology of systemic mycosis in COVID-19 times. A literature search on the subject (January 2020–February 2021) was performed in PubMed, Embase, Cochrane Library, and LILACS without language restrictions. Demographic data, etiological agent, risk factors, diagnostic methods, antifungal treatment, and fatality rate were considered. Eighty nine publications were found on co-infection by COVID-19 and pneumocystosis, candidiasis, aspergillosis, mucormycosis, coccidioidomycosis, or histoplasmosis. In general, the co-infections occurred in males over the age of 40 with immunosuppression caused by various conditions. Several species were identified in candidiasis and aspergillosis co-infections. For diagnosis, diverse methods were used, from microbiological to molecular. Most patients received antifungals; however, the fatality rates were 11–100%. The latter may result because the clinical picture is usually attributed exclusively to SARS-CoV-2, preventing a clinical suspicion for mycosis. Diagnostic tests also have limitations beginning with sampling. Therefore, in the remainder of the pandemic, these diagnostic limitations must be overcome to achieve a better patient prognosis.
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Laste, Gabriela, and Jorge de Oliveira Mateus. "Coronavirus in Pregnancy: The Role of Melatonin." Journal of Advances in Medicine and Medical Research 36, no. 2 (February 16, 2024): 97–112. http://dx.doi.org/10.9734/jammr/2024/v36i25371.
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The effects of COVID-19 on pregnant individuals are unclear due to a series of physiological changes and immune system adaptations that may affect the development of the fetus. There is evidence supporting the role of melatonin in human pregnancy, and it appears that melatonin is essential for a successful pregnancy. However, in pathological conditions, such as during SARS-CoV-2 infection, melatonin levels can be significantly inhibited. In addition, melatonin, a powerful endogen antioxidant, free radical scavenger, and anti-inflammatory molecule, has been reported to exert beneficial effects on viral diseases such as COVID-19. This review focuses on the current evidence regarding the physiopathology of COVID-19 in pregnancy conditions, the role of melatonin during pregnancy, and the use of melatonin as a promising treatment. Addressing these points should help us understand the knowledge currently available about COVID-19 during pregnancy and explore the possible beneficial effects of melatonin. Physiological and immunological adaptations during pregnancy may result in systemic effects that greatly contribute to the development of acute viral infectious diseases such as COVID-19. Melatonin as an adjuvant in COVID-19 treatment has anti-inflammatory, anti-oxidative, and immune response regulatory functions. The strategy that melatonin offers is to slow the cytokine storm observed and reduce oxidative damage to enhance the resistance of individuals and provide additional survival time. Although the direct evidence of melatonin application in COVID-19 is unclear, both its use in experimental animal models and studies on humans has consistently documented its efficacy and safety, and its use by COVID-19 patients would be highly beneficial.
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Ciorba, Andrea, Stavros Hatzopoulos, Cristina Cogliandolo, Chiara Bianchini, Martina Renna, Stefano Pelucchi, Piotr Henryk Skarżyński, et al. "Functional Magnetic Resonance Imaging in the Olfactory Perception of the Same Stimuli." Life 11, no. 1 (December 25, 2020): 11. http://dx.doi.org/10.3390/life11010011.
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Background. Data in the literature report that a number of studies have attempted to identify the exact location of the cortical olfaction representation, searching for evidence suggesting that sniffing odors can initiate a primary activation of the piriform cortex and the insula. Nowadays, due to the SARS-CoV-2 (COVID-19) outbreak, the functional study of the olfactory system could offer a better understanding of the physiopathology of olfactory perception, elucidating better the possible site(s) of damage induced by the COVID-19 infection. The aim of this paper was to evaluate brain maps generated from functional Magnetic Resonance Imaging (fMRI) data, collected from healthy individuals in response to the same olfactory stimulus. Methods. A total of 45 healthy volunteers, without history and/or no clinical signs of sinonasal disease and without history and/or presence of olfactory dysfunction underwent fMRI assessment. Subjects were presented with the same odorous stimuli at specific intervals. fMRI generated brain maps were used in the identification of different cortical areas, involved in the stimuli perception. Results. The fMRI brain maps showed that odorous stimuli activate primarily the left anterior insula (in 35/45 cases or 77.8%). Other activated areas include: the low temporal gyri, the middle and superior temporal gyri, the frontal and piriform cortex, the anterior cingulate gyrus, the parahippocampal gyrus, the temporopolar area, the para-insular area, the subcentral area, the supramarginal gyrus, the occipital cortex and the cerebellum. Conclusions. fMRI resulted as a safe and reliable means to study the perception of olfaction in the cortex. The data of this study suggest that the anterior insula is the main stimulated area when olfactory stimuli are present. This area is always activated, despite the hand and nostril dominance.
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Humphries, Matthew Phillip, Victoria Bingham, Fatima Abdullah Sidi, Stephanie Craig, Beatrize Lara, Hesham El-daly, Nicole O'Doherty, et al. "Technical note on the exploration of COVID-19 in autopsy material." Journal of Clinical Pathology, January 30, 2023, jcp—2022–208525. http://dx.doi.org/10.1136/jcp-2022-208525.
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Interrogation of immune response in autopsy material from patients with SARS-CoV-2 is potentially significant. We aim to describe a validated protocol for the exploration of the molecular physiopathology of SARS-CoV-2 pulmonary disease using multiplex immunofluorescence (mIF).The application of validated assays for the detection of SARS-CoV-2 in tissues, originally developed in our laboratory in the context of oncology, was used to map the topography and complexity of the adaptive immune response at protein and mRNA levels.SARS-CoV-2 is detectable in situ by protein or mRNA, with a sensitivity that could be in part related to disease stage. In formalin-fixed, paraffin-embedded pneumonia material, multiplex immunofluorescent panels are robust, reliable and quantifiable and can detect topographic variations in inflammation related to pathological processes.Clinical autopsies have relevance in understanding diseases of unknown/complex pathophysiology. In particular, autopsy materials are suitable for the detection of SARS-CoV-2 and for the topographic description of the complex tissue-based immune response using mIF.
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Devaux, Christian A., Jean-Christophe Lagier, and Didier Raoult. "New Insights Into the Physiopathology of COVID-19: SARS-CoV-2-Associated Gastrointestinal Illness." Frontiers in Medicine 8 (February 18, 2021). http://dx.doi.org/10.3389/fmed.2021.640073.
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Although SARS-CoV-2 is considered a lung-tropic virus that infects the respiratory tract through binding to the ACE2 cell-surface molecules present on alveolar lungs epithelial cells, gastrointestinal symptoms have been frequently reported in COVID-19 patients. What can be considered an apparent paradox is that these symptoms (e.g., diarrhea), sometimes precede the development of respiratory tract illness as if the breathing apparatus was not its first target during viral dissemination. Recently, evidence was reported that the gut is an active site of replication for SARS-CoV-2. This replication mainly occurs in mature enterocytes expressing the ACE2 viral receptor and TMPRSS4 protease. In this review we question how SARS-CoV-2 can cause intestinal disturbances, whether there are pneumocyte-tropic, enterocyte-tropic and/or dual tropic strains of SARS-CoV-2. We examine two major models: first, that of a virus directly causing damage locally (e.g., by inducing apoptosis of infected enterocytes); secondly, that of indirect effect of the virus (e.g., by inducing changes in the composition of the gut microbiota followed by the induction of an inflammatory process), and suggest that both situations probably occur simultaneously in COVID-19 patients. We eventually discuss the consequences of the virus replication in brush border of intestine on long-distance damages affecting other tissues/organs, particularly lungs.
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Teixeira, Lívia, Jairo R. Temerozo, Filipe S. Pereira-Dutra, André Costa Ferreira, Mayara Mattos, Barbara Simonson Gonçalves, Carolina Q. Sacramento, et al. "Simvastatin Downregulates the SARS-CoV-2-Induced Inflammatory Response and Impairs Viral Infection Through Disruption of Lipid Rafts." Frontiers in Immunology 13 (February 18, 2022). http://dx.doi.org/10.3389/fimmu.2022.820131.
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Coronavirus disease 2019 (COVID-19) is currently a worldwide emergency caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). In observational clinical studies, statins have been identified as beneficial to hospitalized patients with COVID-19. However, experimental evidence of underlying statins protection against SARS-CoV-2 remains elusive. Here we reported for the first-time experimental evidence of the protective effects of simvastatin treatment both in vitro and in vivo. We found that treatment with simvastatin significantly reduced the viral replication and lung damage in vivo, delaying SARS-CoV-2-associated physiopathology and mortality in the K18-hACE2-transgenic mice model. Moreover, simvastatin also downregulated the inflammation triggered by SARS-CoV-2 infection in pulmonary tissue and in human neutrophils, peripheral blood monocytes, and lung epithelial Calu-3 cells in vitro, showing its potential to modulate the inflammatory response both at the site of infection and systemically. Additionally, we also observed that simvastatin affected the course of SARS-CoV-2 infection through displacing ACE2 on cell membrane lipid rafts. In conclusion, our results show that simvastatin exhibits early protective effects on SARS-CoV-2 infection by inhibiting virus cell entry and inflammatory cytokine production, through mechanisms at least in part dependent on lipid rafts disruption.
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Piotrowicz, Karolina, Jerzy Gąsowski, Jean-Pierre Michel, and Nicola Veronese. "Post-COVID-19 acute sarcopenia: physiopathology and management." Aging Clinical and Experimental Research, July 30, 2021. http://dx.doi.org/10.1007/s40520-021-01942-8.
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AbstractIn this review, we discuss the pathophysiologic and management aspects of acute sarcopenia in relation to SARS-CoV-2 infection. COVID-19 is as a multi-organ infectious disease characterized by a severe inflammatory and highly catabolic status, influencing the deep changes in the body build, especially the amount, structure, and function of skeletal muscles which would amount to acutely developed sarcopenia. Acute sarcopenia may largely impact patients’ in-hospital prognosis as well as the vulnerability to the post-COVID-19 functional and physical deterioration. The individual outcome of the COVID-19 and the degree of muscle mass and functional loss may be influenced by multiple factors, including the patient’s general pre-infection medical and functional condition, especially in older adults. This paper gathers the information about how the SARS-CoV-2 hyper-inflammatory involvement exacerbates the immunosenescence process, enhances the endothelial damage, and due to mitochondrial dysfunction and autophagy, induces myofibrillar breakdown and muscle degradation. The aftermath of these acute and complex immunological SARS-CoV-2-related phenomena, augmented by anosmia, ageusia and altered microbiota may lead to decreased food intake and exacerbated catabolism. Moreover, the imposed physical inactivity, lock-down, quarantine or acute hospitalization with bedrest would intensify the acute sarcopenia process. All these deleterious mechanisms must be swiftly put to a check by a multidisciplinary approach including nutritional support, early physical as well cardio-pulmonary rehabilitation, and psychological support and cognitive training. The proposed holistic and early management of COVID-19 patients appears essential to minimize the disastrous functional outcomes of this disease and allow avoiding the long COVID-19 syndrome.
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Martin-Cardona, Albert, Josep Lloreta Trull, Raquel Albero-González, Marta Paraira Beser, Xavier Andújar, Pablo Ruiz-Ramirez, Jaume Tur-Martínez, et al. "SARS-CoV-2 identified by transmission electron microscopy in lymphoproliferative and ischaemic intestinal lesions of COVID-19 patients with acute abdominal pain: two case reports." BMC Gastroenterology 21, no. 1 (August 26, 2021). http://dx.doi.org/10.1186/s12876-021-01905-3.
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Abstract Background SARS-CoV-2 may produce intestinal symptoms that are generally mild, with a small percentage of patients developing more severe symptoms. The involvement of SARS-CoV-2 in the physiopathology of bowel damage is poorly known. Transmission electron microscopy (TEM) is a useful tool that provides an understanding of SARS-CoV-2 invasiveness, replication and dissemination in body cells but information outside the respiratory tract is very limited. We report two cases of severe intestinal complications (intestinal lymphoma and ischaemic colitis) in which the presence of SARS-CoV-2 in intestinal tissue was confirmed by TEM. These are the first two cases reported in the literature of persistence of SARS-CoV-2 demonstrated by TEM in intestinal tissue after COVID 19 recovery and SARS-CoV-2 nasopharyngeal clearance. Case presentation During the first pandemic peak (1st March–30th April 2020) 932 patients were admitted in Hospital Universitari Mútua Terrassa due to COVID-19, 41 (4.4%) required cross-sectional imaging techniques to assess severe abdominal pain and six of them (0.64%) required surgical resection. SARS-CoV-2 in bowel tissue was demonstrated by TEM in two of these patients. The first case presented as an ileocaecal inflammatory mass which turned to be a B-cell lymphoma. Viral particles were found in the cytoplasm of endothelial cells of damaged mucosa. In situ hybridization was negative in tumour cells, thus ruling out an oncogenic role for the virus. SARS-CoV-2 remained in intestinal tissue 6 months after nasopharyngeal clearance, suggesting latent infection. The second patient had a severe ischaemic colitis with perforation and SARS-CoV-2 was also identified in endothelial cells. Conclusions Severe intestinal complications associated with COVID-19 are uncommon. SARS-CoV-2 was identified by TEM in two cases, suggesting a causal role in bowel damage.
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Monchatre-Leroy, Elodie, Sandrine Lesellier, Marine Wasniewski, Evelyne Picard-Meyer, Céline Richomme, Franck Boué, Sandra Lacôte, et al. "Hamster and ferret experimental infection with intranasal low dose of a single strain of SARS-CoV-2." Journal of General Virology 102, no. 3 (March 1, 2021). http://dx.doi.org/10.1099/jgv.0.001567.
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Understanding the pathogenesis of the SARS-CoV-2 infection is key to developing preventive and therapeutic strategies against COVID-19, in the case of severe illness but also when the disease is mild. The use of appropriate experimental animal models remains central in the in vivo exploration of the physiopathology of infection and antiviral strategies. This study describes SARS-CoV-2 intranasal infection in ferrets and hamsters with low doses of low-passage SARS-CoV-2 clinical French isolate UCN19, describing infection levels, excretion, immune responses and pathological patterns in both animal species. Individual infection with 103 p.f.u. SARS-CoV-2 induced a more severe disease in hamsters than in ferrets. Viral RNA was detected in the lungs of hamsters but not of ferrets and in the brain (olfactory bulb and/or medulla oblongata) of both species. Overall, the clinical disease remained mild, with serological responses detected from 7 days and 10 days post-inoculation in hamsters and ferrets respectively. The virus became undetectable and pathology resolved within 14 days. The kinetics and levels of infection can be used in ferrets and hamsters as experimental models for understanding the pathogenicity of SARS-CoV-2, and testing the protective effect of drugs.
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Zazzara, Maria Beatrice, Anna Modoni, Alessandra Bizzarro, Alessandra Lauria, Francesca Ciciarello, Cristina Pais, Vincenzo Galluzzo, et al. "COVID-19 atypical Parsonage-Turner syndrome: a case report." BMC Neurology 22, no. 1 (March 16, 2022). http://dx.doi.org/10.1186/s12883-022-02622-4.
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Abstract Background Neurological manifestations of Sars-CoV-2 infection have been described since March 2020 and include both central and peripheral nervous system manifestations. Neurological symptoms, such as headache or persistent loss of smell and taste, have also been documented in COVID-19 long-haulers. Moreover, long lasting fatigue, mild cognitive impairment and sleep disorders appear to be frequent long term neurological manifestations after hospitalization due to COVID-19. Less is known in relation to peripheral nerve injury related to Sars-CoV-2 infection. Case presentation We report the case of a 47-year-old female presenting with a unilateral chest pain radiating to the left arm lasting for more than two months after recovery from Sars-CoV-2 infection. After referral to our post-acute outpatient service for COVID-19 long haulers, she was diagnosed with a unilateral, atypical, pure sensory brachial plexus neuritis potentially related to COVID-19, which occurred during the acute phase of a mild Sars-CoV-2 infection and persisted for months after resolution of the infection. Conclusions We presented a case of atypical Parsonage-Turner syndrome potentially triggered by Sars-CoV-2 infection, with symptoms and repercussion lasting after viral clearance. A direct involvement of the virus remains uncertain, and the physiopathology is unclear. The treatment of COVID-19 and its long-term consequences represents a relatively new challenge for clinicians and health care providers. A multidisciplinary approach to following-up COVID-19 survivors is strongly advised.
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Valdez-Cruz, Norma A., Enrique García-Hernández, Clara Espitia, Laura Cobos-Marín, Claudia Altamirano, Carlos G. Bando-Campos, Luis F. Cofas-Vargas, et al. "Integrative overview of antibodies against SARS-CoV-2 and their possible applications in COVID-19 prophylaxis and treatment." Microbial Cell Factories 20, no. 1 (April 22, 2021). http://dx.doi.org/10.1186/s12934-021-01576-5.
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AbstractSARS-CoV-2 is a novel β-coronavirus that caused the COVID-19 pandemic disease, which spread rapidly, infecting more than 134 million people, and killing almost 2.9 million thus far. Based on the urgent need for therapeutic and prophylactic strategies, the identification and characterization of antibodies has been accelerated, since they have been fundamental in treating other viral diseases. Here, we summarized in an integrative manner the present understanding of the immune response and physiopathology caused by SARS-CoV-2, including the activation of the humoral immune response in SARS-CoV-2 infection and therefore, the synthesis of antibodies. Furthermore, we also discussed about the antibodies that can be generated in COVID-19 convalescent sera and their associated clinical studies, including a detailed characterization of a variety of human antibodies and identification of antibodies from other sources, which have powerful neutralizing capacities. Accordingly, the development of effective treatments to mitigate COVID-19 is expected. Finally, we reviewed the challenges faced in producing potential therapeutic antibodies and nanobodies by cell factories at an industrial level while ensuring their quality, efficacy, and safety.
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Cezar, Renaud, Lucy Kundura, Sonia André, Claire Lozano, Thierry Vincent, Laurent Muller, Jean-Yves Lefrant, et al. "T4 apoptosis in the acute phase of SARS-CoV-2 infection predicts long COVID." Frontiers in Immunology 14 (January 3, 2024). http://dx.doi.org/10.3389/fimmu.2023.1335352.
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BackgroundAs about 10% of patients with COVID-19 present sequelae, it is important to better understand the physiopathology of so-called long COVID.MethodTo this aim, we recruited 29 patients hospitalized for SARS-CoV-2 infection and, by Luminex®, quantified 19 soluble factors in their plasma and in the supernatant of their peripheral blood mononuclear cells, including inflammatory and anti-inflammatory cytokines and chemokines, Th1/Th2/Th17 cytokines, and endothelium activation markers. We also measured their T4, T8 and NK differentiation, activation, exhaustion and senescence, T cell apoptosis, and monocyte subpopulations by flow cytometry. We compared these markers between participants who developed long COVID or not one year later.ResultsNone of these markers was predictive for sequelae, except programmed T4 cell death. T4 lymphocytes from participants who later presented long COVID were more apoptotic in culture than those of sequelae-free participants at Month 12 (36.9 ± 14.7 vs. 24.2 ± 9.0%, p = 0.016).ConclusionsOur observation raises the hypothesis that T4 cell death during the acute phase of SARS-CoV-2 infection might pave the way for long COVID. Mechanistically, T4 lymphopenia might favor phenomena that could cause sequelae, including SARS-CoV-2 persistence, reactivation of other viruses, autoimmunity and immune dysregulation. In this scenario, inhibiting T cell apoptosis, for instance, by caspase inhibitors, could prevent long COVID.
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Pagano, S., S. Yerly, N. Suh, C. Le Terrier, L. Farrera-Soler, G. Piumatti, C. S. Eberhardt, et al. "Sars-CoV2- infection as a trigger of humoral response against apolipoprotein A-1." European Heart Journal 42, Supplement_1 (October 1, 2021). http://dx.doi.org/10.1093/eurheartj/ehab724.2757.
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Abstract Background Unravelling autoimmune targets triggered by SARS-CoV-2 infection may provide crucial insights in the physiopathology of the disease and foster the development of potential therapeutic candidate targets and prognostic tools. SARS-CoV-2 autoimmune-mediated inflammation have been reported, but the existence of autoantibodies against apolipoprotein A-1 (anti-apoA-1 IgG) in COVID-19 remains unexplored. Anti-apoA-1 IgGs have emerged as an independent biomarker for cardiovascular disease and mortality in humans with proinflammatory and proatherogenic functions in vivo and in vitro. Purpose We want to determine i) the degree of homology between SARS-CoV-2, apoA-1, and Toll-like receptor-2 (TLR2) epitopes, ii) the association between anti-SARSCoV2 and anti-apoA-1 IgGs, and iii) their relationship to prognosis. Methods We performed bioinformatics modelling coupled with mimetic peptides engineering, as well as functional and competition assays with antibodies to identify molecular mimicry between SARS-CoV-2, apoA-1 and TLR2 epitopes. Anti-Spike domain 1 (SD1) IgGs, anti-apoA-1 IgGs and against mimic peptides, as well as cytokines were assessed by immunoassays on a case-control (n=101), an intensive care unit (ICU; n=126) with a 28-days follow-up for overall mortality, and a general population cohort (n=663) with available samples in the pre and post-pandemic period. Results Linear sequence homologies and antibodies cross-reactivity between apoA-1, TLR2, and Spike epitopes were identified. Overall, anti-apoA-1 IgG levels were higher in COVID-19 patients or anti-SARS-CoV-2 seropositive individuals than in healthy donors or anti-SARS-CoV-2 seronegative individuals (p<0.0001). Significant and similar associations were noted between anti-apoA-1, anti-SARS-CoV-2 IgG, cytokines, and lipid profile. In ICU patients, anti-SARS-CoV-2 and anti-apoA-1 seroconversion rates displayed similar 7-days kinetics, reaching 82% for anti-apoA-1 seropositivity. C-statistics (CS) indicated that baseline anti-Spike/TLR2 mimic-peptide IgGs displayed a significant prognostic accuracy for overall mortality at 28 days (CS: 0.64; p=0.02). In the general population, SARS-CoV-2 exposure increased baseline anti-apoA-1 IgG levels. Conclusions COVID-19 induces a marked humoral response against the major protein of high-density lipoproteins. As a correlate of poorer prognosis in other clinical settings, such autoimmunity signatures may relate to long-term COVID-19 prognosis assessment and warrant further scrutiny in the current COVID-19 pandemic. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): This study was funded by the Swiss Federal Office of Public Health, Swiss School of Public Health (Corona Immunitas research program), the Fondation de Bienfaisance du Groupe Pictet, the Fondation Ancrage, the Fondation Privée des HUG, and the Center for Emerging Viral Diseases. The De Reuter (grant Nr 657) and the Schmidheiny Foundation.
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Valdés, José, Fernando Vivanco, Marianella Hernández, and Lorna Galleguillos. "COVID-19 Related Encephalopathy." Medical Research Archives 10, no. 12 (2022). http://dx.doi.org/10.18103/mra.v10i12.3462.
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SARS-CoV-2 infection can present with neurological symptoms due to direct or indirect invasion of the central nervous system. There are many hypotheses of why this happens, focusing on systemic inflammation, cytokines and cells, but none of them are completely understood. We present a case of a 66-year-old female that presented with a severe encephalopathy during her COVID-19 infection. We discuss physiopathology, risk factors, work up, possible treatments according to the physiopathological damage and prognosis according to the treatment response.
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Devaux, Christian A., and Laurence Camoin-Jau. "An update on angiotensin-converting enzyme 2 structure/functions, polymorphism, and duplicitous nature in the pathophysiology of coronavirus disease 2019: Implications for vascular and coagulation disease associated with severe acute respiratory syndrome coronavirus infection." Frontiers in Microbiology 13 (November 28, 2022). http://dx.doi.org/10.3389/fmicb.2022.1042200.
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It has been known for many years that the angiotensin-converting enzyme 2 (ACE2) is a cell surface enzyme involved in the regulation of blood pressure. More recently, it was proven that the severe acute respiratory syndrome coronavirus (SARS-CoV-2) interacts with ACE2 to enter susceptible human cells. This functional duality of ACE2 tends to explain why this molecule plays such an important role in the clinical manifestations of coronavirus disease 2019 (COVID-19). At the very start of the pandemic, a publication from our Institute (entitled “ACE2 receptor polymorphism: susceptibility to SARS-CoV-2, hypertension, multi-organ failure, and COVID-19 disease outcome”), was one of the first reviews linking COVID-19 to the duplicitous nature of ACE2. However, even given that COVID-19 pathophysiology may be driven by an imbalance in the renin-angiotensin system (RAS), we were still far from understanding the complexity of the mechanisms which are controlled by ACE2 in different cell types. To gain insight into the physiopathology of SARS-CoV-2 infection, it is essential to consider the polymorphism and expression levels of the ACE2 gene (including its alternative isoforms). Over the past 2 years, an impressive amount of new results have come to shed light on the role of ACE2 in the pathophysiology of COVID-19, requiring us to update our analysis. Genetic linkage studies have been reported that highlight a relationship between ACE2 genetic variants and the risk of developing hypertension. Currently, many research efforts are being undertaken to understand the links between ACE2 polymorphism and the severity of COVID-19. In this review, we update the state of knowledge on the polymorphism of ACE2 and its consequences on the susceptibility of individuals to SARS-CoV-2. We also discuss the link between the increase of angiotensin II levels among SARS-CoV-2-infected patients and the development of a cytokine storm associated microvascular injury and obstructive thrombo-inflammatory syndrome, which represent the primary causes of severe forms of COVID-19 and lethality. Finally, we summarize the therapeutic strategies aimed at preventing the severe forms of COVID-19 that target ACE2. Changing paradigms may help improve patients’ therapy.
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Bracaccia, Maria Elena, Nicolò De Cicco, Alessandra Moioli, Simona Barberi, Claudia Fofi, and Paolo Mene'. "MO240A FATAL CASE OF VASCULITIS AFTER SARS-COV-2 NEGATIVIZATION." Nephrology Dialysis Transplantation 36, Supplement_1 (May 1, 2021). http://dx.doi.org/10.1093/ndt/gfab092.00118.
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Abstract Background and Aims Spectrum of acute severe respiratory syndrome Coronavirus 2 (SARS-CoV-2) ranges from mild to critical and probably mortality rate is largely underestimated. Complications may represent different manifestation of a profound endothelial dysfunction and injury. Biopsies reveal macro and microvascular thrombosis involving larger and smaller vessels. Different Authors described accumulation of inflammatory cells across vascular bed, viral inclusions and apoptotic bodies across vascular bed. Endotheliitis leads to loss of vessel integrity with bleedings and lumen restriction with tissue ischemia and necrosis. SARS-CoV-2 also can cause vasculitis and a systemic inflammatory vascular disease with COVID-19-associated coagulopathy. Several cases of vasculitis have been described during COVID-19 pandemy but in literature, to our knowledge, there are few cases of patients developing vasculitis after SARS-CoV-2 infection. Method A 59-year-old male patient in chronic haemodialysis with hypertension, chronic thrombocytopenia, uncertain history of type 2 diabetes mellitus and recent COVID-19 pneumonia (1 month before) was admitted to our E.R. with psycho-motor slowdown, dyspnoea, profound hypotension, diffuse and extensive purpura especially on extremities and nose with petechiae and ecchymoses, thrombocytopenia, widespread arthritis and myalgia and atrial fibrillation with high ventricular response. Laboratory tests revealed leucocytosis with elevation of inflammatory markers (GB 15.6 x 103/µL CRP 6.61 mg/dl, procalcitonin 2.64 ng/ml), thrombocytopenia (PLTs 55 x 103/µL), Hb 11.2 g/dl, increased amylase (444 UI/L) and lipase (608 UI/L), hyperkaliaemic metabolic acidosis, mild impaired blood clotting with normal fibrinogen and severe D-Dimer elevation (3453 mcg/ml), normal haptoglobin and bilirubin. SARS-CoV-2 rapid antigen test and three molecular swab tests (at admission and during recovery) were negative. Contrast-enhanced chest-abdomen CT did not demonstrate relevant findings. Results We suspected thrombotic thrombocytopenic purpura, COVID-19 related vasculitis or an autoimmune disease reactivation after SARS-CoV-2 or other concurrent viral infections. A peripheral blood smear excluded presence of schistocytes, HBV, HCV, HIV, c-ANCA, p-ANCA, LAC anti-mitochondrial and ENA antibodies were negative, such as complement factor C4 (C3 at low limits). IgA immunoglobulins resulted increased (952 mg/dl). We administered intravenous (IV) hydration, analgesic therapy, broad spectrum antibiotics and Methylprednisolone 40 mg IV without benefit. Three days after clinical conditions were critical with further neurological deterioration and haemodynamic instability, consequently we started methylprednisolone 1 g/day IV for three days, followed by oral prednisone 25 mg/die with rapid improvement of clinical conditions and laboratory findings. A skin biopsy revealed a variable and discontinuous presence of C4d and IgM along capillary walls and traces of IgG, supporting the hypothesis of an immune-mediated vasculitic process. Patient was discharged in stable condition with Prednisone 25 mg/die per os. Later we learned that patient had been hospitalized again for severe anaemia, thrombocytopenia and septic shock with fatal outcome. Conclusion SARS-CoV-2 clinical spectrum appears to be extremely varied; the direct cytolysis and the immune-mediated damage are among the most accredited hypotheses on disease physiopathology, but molecular mimicry mechanisms may also be involved. Vascular endothelium can be considered among the first targets. Vasculitis are frequently described in literature during COVID, this case, instead, is an anecdotal report of severe angiitis arising after swab negativization, underlying the possibility that hyperinflammation can either cause an autoimmune syndrome de novo or trigger a flare-up of a pre-existing condition.
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Olivier, Thibaut, Joël Blomet, and Daniel Desmecht. "Central role of lung macrophages in SARS-CoV-2 physiopathology: a cross-model single-cell RNA-seq perspective." Frontiers in Immunology 14 (June 7, 2023). http://dx.doi.org/10.3389/fimmu.2023.1197588.
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Cytokine storms are considered a driving factor in coronavirus disease 2019 (COVID-19) severity. However, the triggering and resolution of this cytokine production, as well as the link between this phenomenon and infected cells, are still poorly understood. In this study, a cross-species scRNA-seq analysis showed that cytokine-producing macrophages together with pneumocytes were found to be the main contributors of viral transcripts in both Syrian hamsters and African green monkeys. Whatever the cell type, viral read-bearing cells show an apoptotic phenotype. A comparison of SARS-CoV-2 entry receptor candidates showed that Fc receptors are better correlated with infected cells than ACE2, NRP1, or AXL. Although both species show similar interferon responses, differences in adaptive immunity were highlighted. Lastly, Fc receptor and cytokine upregulation in M1 macrophages was found to correlate with a comprehensive interferon response. Based on these results, we propose a model in which lung macrophages play a central role in COVID-19 severity through antibody-dependent enhancement.
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Oliviero, Antonio, Fernando de Castro, Francesca Coperchini, Luca Chiovato, and Mario Rotondi. "COVID-19 Pulmonary and Olfactory Dysfunctions: Is the Chemokine CXCL10 the Common Denominator?" Neuroscientist, July 13, 2020, 107385842093903. http://dx.doi.org/10.1177/1073858420939033.
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COVID-19 is an ongoing viral pandemic that emerged from East Asia and quickly spread to the rest of the world. SARS-CoV-2 is the virus causing COVID-19. Acute respiratory distress syndrome (ARDS) is definitely one of the main clinically relevant consequences in patients with COVID-19. Starting from the earliest reports of the COVID-19 pandemic, two peculiar neurological manifestations (namely, hyposmia/anosmia and dysgeusia) were reported in a relevant proportion of patients infected by SARS-CoV-2. At present, the physiopathologic mechanisms accounting for the onset of these symptoms are not yet clarified. CXCL10 is a pro-inflammatory chemokine with a well-established role in the COVID-19-related cytokine storm and in subsequent development of ARDS. CXCL10 is also known to be involved in coronavirus-induced demyelination. On these bases, a role for CXCL10 as the common denominator between pulmonary and olfactory dysfunctions could be envisaged. The aim of the present report will be to hypothesize a role for CXCL10 in COVID-19 olfactory dysfunctions. Previous evidences supporting our hypothesis, with special emphasis to the role of CXCL10 in coronavirus-induced demyelination, the anatomical and physiological peculiarity of the olfactory system, and the available data supporting their link during COVID-19 infections, will be overviewed.
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Errasfa, Mourad. "Milk Oligosaccharides and Lectins as Candidates for Clinical Trials Against Covid-19." Current Nutrition & Food Science 16 (August 19, 2020). http://dx.doi.org/10.2174/1573401316999200819125355.
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Background: Covid-19 pandemia is causing a very high death toll around the world and a serious fall in the global economy. Many clinical trials are currently underway to check the effectiveness of some known drugs. The physiopathology associated with the virus infection is currently better understood and good prophylactic drug therapies are implemented, such as antibiotics and blood thinners, though, no specific drugs against SARS-Cov-2 were developed yet. Objective: In the present research work, it is aimed to carry out a bibliographic investigation on some active molecular species that could be used against Covid-19, based on their chemical properties to bind to glycoproteins. In the case of SARS-Cov-2, the targeted glycoprotein is the surface virus spike S glycoprotein, that the virus uses to attach to and invade human cells. It is of high pharmacological value to investigate possible active natural substances endowed with a property to bind glycoproteins. In this line of research, oligosaccharides and lectins are two molecular species that have glycoprotein binding properties. Methods: A bibliographic research was carried out on oligosaccharides and lectins in various sources of scientific publications. Relevant chemical and pharmacological properties of oligosaccharides and lectins were searched and their main natural sources were identified. Results: In the present paper, I summarize some scientific evidence to support the therapeutic potential of camel milk as a source of oligosaccharides and its possible use as a functional diet in parallel to drug therapies of Covid-19. On the other hand, sugar- and glycoprotein binding properties of some lectins of plant and seaweed origin are reported, and their pharmaceutical use is underlined. Conclusion: In the present study, scientific evidence was documented that encouraged further clinical investigations on camel milk oligosaccharides and lectins of plant and seaweed origin in the management of Covid-19 physiopathology.
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Mendonça Filho, Valder Cavalcante Maia, Amanda Gomes de Oliveira, Isabelle de Fátima Vieira Camelo Maia, Ananda Carolina Moraes de Falcone, Beatriz Gioppo Betini, Lucas Bruno Rezende, and Fernando Henrique Magri Alves. "COVID-19 in the nervous system: physiopathology and neurological manifestations." Arquivos de Neuro-Psiquiatria, July 4, 2023. http://dx.doi.org/10.1055/s-0043-1769123.
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Abstract Background Coronavirus disease 2019 (COVID-19) is a viral infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although respiratory manifestations have received greater visibility during the pandemic caused by this virus, numerous neurological complaints related to coronavirus 2 infection have been documented in several countries. These records suggest that this pathogen presents neurotropism, and it can cause different neurological conditions of varying intensity. Objective To investigate the ability of coronavirus 2 to invade the central nervous system (CNS) and its neurological clinical outcomes. Methods The present study consists in a comprehensive literature review of the records available in the PubMed, SciELO, and Google Scholar databases. The descriptors COVID-19, brain and physiopathology, associated with the Boolean operator AND, were used in the search. Regarding the inclusion and exclusion criteria, we selected the papers published since 2020 with the highest number of citations. Results We selected 41 articles, most of them in English. The main clinical manifestation associated with COVID-19 patients was headache, but cases of anosmia, hyposmia, Guillain-Barré syndrome, and encephalopathies were also described with considerable frequency. Conclusion Coronavirus-2 presents neurotropism, and it can reach the CNS by hematogenous dissemination and by direct infection of the nerve endings. It causes brain injuries through several mechanisms, such as cytokine storm, microglial activation, and an increase in thrombotic factors.
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Lamoth, Frederic, Russell E. Lewis, Thomas J. Walsh, and Dimitrios P. Kontoyiannis. "Navigating the uncertainties of COVID-19 associated aspergillosis (CAPA): A comparison with influenza associated aspergillosis (IAPA)." Journal of Infectious Diseases, March 26, 2021. http://dx.doi.org/10.1093/infdis/jiab163.
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Abstract Invasive pulmonary aspergillosis (IPA) is increasingly recognized as a life-threatening superinfection of severe respiratory viral infections, such as influenza. The pandemic of Coronavirus Disease 2019 (COVID-19) due to emerging SARS-CoV-2 rose concern about the eventuality of IPA complicating COVID-19 in intensive care unit mechanically-ventilated patients. While the association between severe influenza and IPA has been demonstrated, it remains unclear whether SARS-CoV-2 infection represents a specific risk factor for IPA. A variable incidence of such complication has been previously reported, which can be partly attributed to differences in diagnostic strategy and IPA definitions, and possibly local environmental/epidemiological factors. In this article, we discuss the similarities and differences between influenza-associated pulmonary aspergillosis (IAPA) and COVID-19-associated pulmonary aspergillosis (CAPA). Compared to IAPA, the majority of CAPA cases have been classified as putative rather than proven/probable IPA, in the absence of positive serum galactomannan or histopathologic evidence of angio-invasion. Discrimination between Aspergillus airways colonization and CAPA is difficult. Distinct physiopathology and cytokine profiles of influenza and COVID-19 may explain these discrepancies. Whether CAPA represents a distinct entity is still debatable and many questions remain unanswered, such as its actual incidence, the predisposing role of corticosteroids or immunomodulatory drugs, and the indications for antifungal therapy.
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Colosio, Marta, Lorenza Brocca, Marco Gatti, Marianna Neri, Emanuela Crea, Francesca Cadile, Monica Canepari, et al. "Structural and functional impairments of skeletal muscle in patients with post-acute sequelae of SARS-CoV-2 infection." Journal of Applied Physiology, September 7, 2023. http://dx.doi.org/10.1152/japplphysiol.00158.2023.
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Background: Following acute COVID-19, a substantial proportion of patients showed symptoms and sequelae for several months, namely the post-acute sequelae of COVID-19 (PASC) syndrome. Major phenomena are exercise intolerance, muscle weakness and fatigue. We aimed to investigate the physiopathology of exercise intolerance in patients with PASC syndrome by structural and functional analyses of skeletal muscle.Methods: At least 3 months after infection, non-hospitalized patients with PASC (n=11,ys:54±11; PASC) and patients without long-term symptoms (n=12,ys:49±9; CTRL) visited the laboratory on four non-consecutive days. Spirometry, lung diffusion capacity and quality of life were assessed at rest. Cardiopulmonary incremental exercise test was performed. Oxygen consumption (VO2) kinetics were determined by moderate-intensity exercises. Muscle oxidative capacity (k) was assessed by near-infrared spectroscopy. Histochemical analysis, O2 flux (JO2) by high-resolution respirometry, and quantification of key molecular markers of mitochondrial biogenesis and dynamics were performed in vastus lateralis biopsies.Results: Pulmonary and cardiac functions were within normal range in all patients. VO2peak was lower in PASC than CTRL (24.7±5.0vs32.9±7.4mL*min-1*kg-1, respectively, P<.05). VO2 kinetics was slower in PASC than CTRL (41±12vs30±9s-1, P<.05). k was lower in PASC than CTRL (1.54±0.49vs2.07±0.51min-1, P<.05). Citrate synthase, PGC1alfa and JO2 for mitochondrial complex II were significantly lower in PASC vs CTRL (all P<.05).Conclusion: In our cohort of patients with PASC, we showed limited exercise tolerance mainly due to "peripheral" determinants. Substantial reductions were observed for biomarkers of mitochondrial function, content, and biogenesis. PASC syndrome appears to negatively impact skeletal muscle function, although the disease is an heterogenous condition.
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Arruda, Renato, and Carlos Alberto Bordini. "Trends in physiopathology research of primary headaches over the last 50 years." Headache Medicine, October 27, 2022, 27. http://dx.doi.org/10.48208/headachemed.2022.supplement.27.
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Introduction The headache field, mainly migraine, is passing through a transformative era of new treatments. These breakthroughs would not be possible without the evolving knowledge on mechanisms of headaches. However, there are still unmet needs for headaches' understanding and treatments. Objectives Assess whether there is a trend in the number of publications regarding physiopathology of each primary headache disorders (PHD) in the past 50 years. Secondarily, we aimed to evaluate how the SARS-CoV-2 pandemics impacted on physiopathology research of PHD. Methods PHD were divided hierarchically in first- and second-digit, according to ICHD-3 criteria. PubMed database was searched using both the name of the PHD and MeSH terms related to physiopathology. Each search yielded the number of publications for a determined PHD along the period selected (1971-2021). Data were retrieved and separated in two groups: a) per decades (1971-2020); and b) per year (2011-2021). Ratios between every two timepoints in each group were calculated, as well as a total ratio for the whole interval. Results Either divided per decades, or divided annually for the last 10 years, migraine had the highest absolute number of pathophysiology publications, significantly above the other PHD. Divided per decades, with exception of tension-type headache (TTH), all the other PHD groups have increased their number of publications over time. Meanwhile, TTH in the last decade decreased the total number of mechanisms research. The number of papers published in 2020 was lower than in 2019 for TTH, trigeminal autonomic cephalalgias (TACs) and group 4 "other PHD" (4.OPHD), migraine kept practically the same number. Conclusion There is a clear disparity in the number of publications on mechanisms of each PHD, being migraine well above TTH, TACs and 4.OPHD. As expected, the recent COVID pandemics has clearly impaired pathophysiologic research in the headache field. Keywords: Headache, Migraine, Mechanisms, Physiopathology, Research.
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Prosperi, Sara, and Francesco Chiarelli. "Early and precocious puberty during the COVID-19 pandemic." Frontiers in Endocrinology 13 (January 9, 2023). http://dx.doi.org/10.3389/fendo.2022.1107911.
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During the year 2020, the COVID-19 pandemic rapidly became a severe health emergency worldwide. In order to contrast the spread of the novel SARS-CoV-2, many countries implemented extraordinary restrictive measures, such as a strict lockdown and school closures. The pandemic had a great impact on children and adolescents’ daily life, leading to a much more sedentary lifestyle, to larger use of electronic devices and to an increase in stress-related symptoms. These conspicuous changes acted as disruptors of children’s normal development. Since the beginning of the pandemic, many studies reported an increase in the number of precocious puberty cases as well as a faster progression rate of puberty itself, if compared to the pre-pandemic years. In this review, our aim was to evaluate the incidence of new cases of early and precocious puberty during the COVID-19 pandemic, analyzing variations in the timing of puberty and in pubertal progression rate, and to investigate the role of environmental and lifestyle factors during the pandemic in modulating the physiopathology of pubertal development. While a direct effect of SARS-CoV-2 infection remains, at the moment, a remote hypothesis, both physical and psychological factors related to the pandemic seem to have a role in triggering GnRH pulsatile secretion leading to earlier pubertal onset. It is indeed important to stress the need to clarify the exact role of COVID-19 in early pubertal onset comparing data from all over the world; long-term comprehensive studies are also pivotal to explain whether this phenomenon will continue while we resume pre-pandemic habits.
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Eslami, Majid, Anna Abdolshahi, Alireza Emadi, and Bahman Yousefi. "IMPORTANCE OF PROBIOTICS IN THE PREVENTION AND TREATMENT OF COVID-19." Journal of microbiology, biotechnology and food sciences, October 20, 2022, e4594. http://dx.doi.org/10.55251/jmbfs.4594.
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The novel severe acute respiratory syndrome COVID-19 outbreak is brought on by the SARS-CoV-2 coronavirus. Taking into account the criticism that SARS-CoV-2 has received on a global scale, efficient preventive actions and treatment for COVID-19 would be an urgent need. New strategies were developed based on immune responses. The immunomodulating properties of a few bioactive substances, minerals, and micronutrients have led to recommendations. Probiotics' therapeutic uses in COVID-19 patients were looked into in this review. A decline in the amount of various probiotic species, including Bifidobacterium and Lactobacillus, was observed in some COVID-19 patients, which may be indicative of a compromised immune system. The use of probiotics has been predominantly explored for the inhibition and management handling of gastrointestinal disorders, but other potential properties of these microorganisms have been considered for nutritional effects, inflammatory diseases, Helicobacter pylori infections, allergic diseases, and anti-tumor properties. Some investigations have revealed that these probiotics stimulate and modify innate immune responses through multiple membrane molecules that transfer signaling massages with the epithelial cells of the gut. In addition to the gut microbiota, which has been widely studied, the physiopathology of numerous respiratory illnesses is known to depend on the lung microbiota. Through microaspiration and inhalation, which bacteria, molds, and viruses can create, the healthy lung acquired its unique microbiota. Probiotic strains might be used to influence these microbiotas, contributing novel views in the managing of respiratory diseases. Returning gut microbiota has been revealed to recover resistance to virus or pathogenic invades moreover at the respiratory mucosal stages.