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1
Meunier, Nicolas. "Odorat et virus respiratoires :une relation révélée par la Covid-19". médecine/sciences 39, n.º 2 (febrero de 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.
2
Darrault, Fanny, Mohamed Ibrahmen y Sophie Dupré-Crochet. "Anticorps et senseurs de l’ADN agissent de concert pour stimuler la réponse anti-virale des macrophages". médecine/sciences 38, n.º 3 (marzo de 2022): 321–24. http://dx.doi.org/10.1051/medsci/2022020.
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Pour la sixième année consécutive, dans le cadre du module d’enseignement « Physiopathologie de la signalisation » proposé par l’université Paris-sud, les étudiants du Master « Biologie Santé » de l’université Paris-Saclay se sont essayés à l’écriture scientifique. Ils ont sélectionné une quinzaine d’articles scientifiques récents dans le domaine de la signalisation cellulaire, présentant des résultats originaux, via des approches expérimentales variées, sur des thèmes allant des relations hôte-pathogène aux innovations thérapeutiques, en passant par la signalisation hépatique et le métabolisme. Après un travail préparatoire réalisé avec l’équipe pédagogique, les étudiants, organisés en binômes, ont ensuite rédigé, guidés par des chercheurs, une Nouvelle soulignant les résultats majeurs et l’originalité de l’article étudié. Ils ont beaucoup apprécié cette initiation à l’écriture d’articles scientifiques et, comme vous pourrez le lire, se sont investis dans ce travail avec enthousiasme ! Deux de ces Nouvelles sont publiées dans ce numéro, les autres le seront dans des prochains numéros.
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SARRADIN, P., P. BERTHON y F. LANTIER. "Le point sur l’épidémiologie et la physiopathologie des encéphalopathies spongiformes des ruminants". INRAE Productions Animales 10, n.º 2 (7 de abril de 1997): 123–32. http://dx.doi.org/10.20870/productions-animales.1997.10.2.3988.
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L’épidémie d’encéphalopathie spongiforme bovine (ESB) résulte de la consommation par les bovins de farines de viandes et d’os contaminées. En recyclant l’agent infectieux, ces farines ont permis d’amplifier la dissémination d’une maladie dont l’origine et l’agent responsable demeurent inconnus. Les hypothèses sur la nature protéique ou/et virale de l’agent sont évoquées, ainsi que l’éventualité d’une transmission à l’homme. Une grande partie de nos connaissances des encéphalopathies spongiformes résulte des études réalisées de longue date sur la tremblante des ovins. En particulier, l’idée que l’on peut se faire de la physiopathologie de l’infection des bovins est en grande partie extrapolée à partir du résultat d’infections expérimentales réalisées chez le mouton. Toutefois, la contamination des tissus lymphoïdes périphériques, qui est la règle au cours de la phase de dissémination dans l’organisme de l’agent de la tremblante, semble absente dans le cas de la maladie bovine. Il est donc possible que ce type de tissus, considéré comme infectieux en matière de tremblante, le soit peu au cours de la phase préclinique dans le cas de l’ESB. L’atteinte du système nerveux central des bovins pourrait alors résulter d’une dissémination empruntant les voies nerveuses.
Les mécanismes conduisant à la mort neuronale responsable des symptômes observés restent mal connus. La protéine PrP, protéine normale de la membrane de nombreux types cellulaires, et qui s’accumule sous sa forme pathologique PrPSC au niveau des lésions est indispensable au processus pathologique. Son polymorphisme influence considérablement le devenir de l’infection, mais elle ne peut être tenue pour seule responsable de la transmission de la maladie.
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Calvet, Charlotte, Ghizlene Lahlou y Saaid Safieddine. "Progrès de la thérapie génique". médecine/sciences 34, n.º 10 (octubre de 2018): 842–48. http://dx.doi.org/10.1051/medsci/2018210.
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La perte de l’audition et/ou de la fonction d’équilibration est un problème de santé publique majeur. La surdité touche des millions de personnes dans le monde. Leur prise en charge actuelle repose sur une réhabilitation prothétique sans réelle thérapie curative. Après deux décennies de recherches qui ont permis de progresser dans la physiopathologie de différentes formes génétiques de surdité, des avancées majeures ont été obtenues grâce à des études précliniques utilisant la thérapie génique virale chez l’animal. Ce succès, largement dû à l’amélioration des vecteurs de transfert, pourrait à terme révolutionner la prise en charge de certains malentendants. Nos progrès dans la compréhension des mécanismes cellulaires et moléculaires impliqués dans le fonctionnement de l’oreille interne ont contribué à ouvrir la voie à cette recherche à visée thérapeutique, qui consiste le plus souvent à remplacer localement les gènes endogènes altérés. Le but de cet article est de résumer les progrès récents de la thérapie génique dans la restauration des fonctions cochléaire et vestibulaire dans des modèles murins du syndrome d’Usher, principale cause génétique de surdité associée à une cécité. Nous nous concentrerons sur les approches thérapeutiques présentant le plus fort potentiel d’application clinique.
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Levasseur, Antoine. "L’hémophilie, une maladie royale : l’Histoire peut-elle changer le sang, et réciproquement ?" Revue de biologie médicale N° 377, n.º 2 (1 de febrero de 2024): 51–59. http://dx.doi.org/10.3917/rbm.377.0051.
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L’hémophilie est connue depuis l’Antiquité, sans être alors précisément comprise. C’est au cours des XIX e et XX e siècles que sa physiopathologie s’est éclaircie et que la terminologie actuelle est apparue. L’hémophilie était qualifiée de « maladie royale » ; en effet, la célèbre reine Victoria était « conductrice » d’hémophilie B sévère et l’a transmise aux familles royales prussienne, russe et espagnole par le jeu des alliances princières. Cette maladie héréditaire de la coagulation a affaibli l’image des monarchies et a pu participer à des événements politiques majeurs : d’une part, la révolution bolchévique orchestrée par Lénine et l’exécution du tsar Nicolas II et de sa famille et, d’autre part, l’abdication du trône espagnol par le roi Alphonse XIII, suivie de l’ascension au pouvoir du général Francisco Franco. Les incidents des dernières décennies, notamment le drame du sang contaminé, ont conduit à des modifications profondes dans la prise en charge des hémophiles devant l’urgence de la situation. La réaction immédiate de la communauté scientifique, des associations de patients et des laboratoires pharmaceutiques a abouti à des avancées : sécurisation des concentrés de facteurs de la coagulation dérivés du plasma par inactivation virale, ainsi que des dons du sang avec l’adoption de nouvelles méthodes de dépistage systématique des virus, production industrielle de facteurs VIII et IX recombinants, avènement de l’émicizumab rétablissant l’hémostase en l’absence de facteur VIIIa par sa liaison aux facteurs IXa et X.
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N’Guyen, Y. y L. Andreoletti. "Mise au point sur la physiopathologie des myocardites virales". Archives des Maladies du Coeur et des Vaisseaux - Pratique 2017, n.º 263 (diciembre de 2017): 16–20. http://dx.doi.org/10.1016/j.amcp.2017.10.005.
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Haque, Azizul y Anudeep B. Pant. "Long Covid: Untangling the Complex Syndrome and the Search for Therapeutics". Viruses 15, n.º 1 (22 de diciembre de 2022): 42. http://dx.doi.org/10.3390/v15010042.
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Long Covid can affect anyone who has previously had acute COVID-19. The root causes of this syndrome are still unknown, and no effective therapeutics are available. This complex syndrome, with a wide array of symptoms, is still evolving. Given the dire situation, it is important to identify the causes of Long Covid and the changes occurring within the immune system of affected patients to figure out how to treat it. The immune system intersects with the persistent viral fragments and blood clots that are implicated in this syndrome; understanding how these complex systems interact may help in untangling the puzzling physiopathology of Long Covid and identifying mitigation measures to provide patients some relief. In this paper, we discuss evidence-based findings and formulate hypotheses on the mechanisms underlying Long Covid’s physiopathology and propose potential therapeutic options.
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Badita, Daniela Gabriela, Iulia Ioana Stanescu, Andra Balcangiu Stroescu, Dan Piperea Sianu, Daniela Miricescu, Bogdan Calenic y Maria Greabu. "Salivary and Serum Biochemical Alterations in Patients with Acute Viral Hepatitis". Revista de Chimie 69, n.º 3 (15 de abril de 2018): 747–51. http://dx.doi.org/10.37358/rc.18.3.6191.
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Viral hepatitis represents a major health problem worldwide. Approximately 1.4 million people are infected with hepatitis A virus every year, although given that most of the cases evolve asymptomatically the real number could be even higher. At the same time, hepatitis B virus affects up to 30% of the world population and represents one of the main causes of cirrhosis and hepatocellular carcinoma. Thus, it is very important to understand the physiopathology of viral hepatitis A and B not only for the diagnosis, but also for the therapeutic protocol. The present research aimed to determine if HAV and HBV can alter serum and salivary levels of total protein and of 2 important electrolytes: calcium and potassium.
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Genet, Philippe, Driss Chaoui, Virginie Masse, Ahmad Al Jijakli, Nina Arakelyan y Laurent Sutton. "Anaplastic Large Cell Lymphoma Occurring in an HIV-Positive Patient". Case Reports in Hematology 2012 (2012): 1–3. http://dx.doi.org/10.1155/2012/180204.
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Cases of anaplastic large-cell lymphoma (ALCL) of T phenotype are sparse in the setting of HIV patients. We report herein a case of T-ALCL, with an advanced stage, pulmonary involvement, high HIV viral load, and low CD4 level. Anaplastic lymphoma kinase (ALK) protein expression was negative. Anthracyclin-based chemotherapy was unsuccessful. The literature review was performed focusing on incidence, clinical characteristics, prognosis, and physiopathology of ALCL in HIV patients. More data are needed to improve the knowledge of such cases and to define a better treatment approach.
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De Conno, Franco, Carla Ripamonti, Alberto Sbanotto y Vittorio Ventafridda. "Oral Complications in Patients with Advanced Cancer". Journal of Palliative Care 5, n.º 1 (marzo de 1989): 7–15. http://dx.doi.org/10.1177/082585978900500102.
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Disturbances caused by lesions of the oral cavity play an important part in the alteration of the qualtity of life of cancer patients. The main complications affecting the oral cavity are infections (fungal, viral, bacterial), neutropenic ulcers, drug-induced stomatitis, dry mouth, and taste alteration. Most of the information available about these entities has been acquired in the cancer patient without advanced disease. The little known about the epidemiology and physiopathology of such lesions in the advanced phase of cancer is presented and approaches to management are suggested.
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Petat, Hortense, Vincent Gajdos, François Angoulvant, Pierre-Olivier Vidalain, Sandrine Corbet, Christophe Marguet, Jacques Brouard, Astrid Vabret y Meriadeg Ar Gouilh. "High Frequency of Viral Co-Detections in Acute Bronchiolitis". Viruses 13, n.º 6 (26 de mayo de 2021): 990. http://dx.doi.org/10.3390/v13060990.
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Over two years (2012–2014), 719 nasopharyngeal samples were collected from 6-week- to 12-month-old infants presenting at the emergency department with moderate to severe acute bronchiolitis. Viral testing was performed, and we found that 98% of samples were positive, including 90% for respiratory syncytial virus, 34% for human rhino virus, and 55% for viral co-detections, with a predominance of RSV/HRV co-infections (30%). Interestingly, we found that the risk of being infected by HRV is higher in the absence of RSV, suggesting interferences or exclusion mechanisms between these two viruses. Conversely, coronavirus infection had no impact on the likelihood of co-infection involving HRV and RSV. Bronchiolitis is the leading cause of hospitalizations in infants before 12 months of age, and many questions about its role in later chronic respiratory diseases (asthma and chronic obstructive pulmonary disease) exist. The role of virus detection and the burden of viral codetections need to be further explored, in order to understand the physiopathology of chronic respiratory diseases, a major public health issue.
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Ruiz-Real, José Luis, Bruno José Nievas-Soriano y Juan Uribe-Toril. "Has Covid-19 Gone Viral? An Overview of Research by Subject Area". Health Education & Behavior 47, n.º 6 (4 de septiembre de 2020): 861–69. http://dx.doi.org/10.1177/1090198120958368.
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When a pandemic outbreak occurs, it seems logical that related scientific production should increase substantially; however, it is important to recognize its interdisciplinary usefulness to find a solution to the problem. The main aim of this research is to analyse the main keywords of the scientific research about COVID-19, by subject area. To discover the influence of certain terms and their transferability, synergies, and future trends, a cluster analysis of the keywords was performed. The results show that Health Sciences dominate the publications with 88.23% of the total volume. As expected, the largest volume of research was dedicated to medical aspects of the disease, like experimental treatments, its physiopathology, or its respiratory syndrome. However, other fields, like Social Sciences (6.07%), Technology (2.68%), Physical Sciences (1.95%), and Arts and Humanities (1.08%), also played an important role in research on COVID-19.
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Scarcella, Melania, Danila d’Angelo, Mariangela Ciampa, Simona Tafuri, Luigi Avallone, Luigi Michele Pavone y Valeria De Pasquale. "The Key Role of Lysosomal Protease Cathepsins in Viral Infections". International Journal of Molecular Sciences 23, n.º 16 (13 de agosto de 2022): 9089. http://dx.doi.org/10.3390/ijms23169089.
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Cathepsins encompass a family of lysosomal proteases that mediate protein degradation and turnover. Although mainly localized in the endolysosomal compartment, cathepsins are also found in the cytoplasm, nucleus, and extracellular space, where they are involved in cell signaling, extracellular matrix assembly/disassembly, and protein processing and trafficking through the plasma and nuclear membrane and between intracellular organelles. Ubiquitously expressed in the body, cathepsins play regulatory roles in a wide range of physiological processes including coagulation, hormone secretion, immune responses, and others. A dysregulation of cathepsin expression and/or activity has been associated with many human diseases, including cancer, diabetes, obesity, cardiovascular and inflammatory diseases, kidney dysfunctions, and neurodegenerative disorders, as well as infectious diseases. In viral infections, cathepsins may promote (1) activation of the viral attachment glycoproteins and entry of the virus into target cells; (2) antigen processing and presentation, enabling the virus to replicate in infected cells; (3) up-regulation and processing of heparanase that facilitates the release of viral progeny and the spread of infection; and (4) activation of cell death that may either favor viral clearance or assist viral propagation. In this review, we report the most relevant findings on the molecular mechanisms underlying cathepsin involvement in viral infection physiopathology, and we discuss the potential of cathepsin inhibitors for therapeutical applications in viral infectious diseases.
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Pallotti, Federica, Claire Queffeulou, Mathieu Bellal, Bastien Jean-Jacques, Anne-Claire Gac, Valérie Chatelet, Annabel Boyer y Victor Gueutin. "Carfilzomib-Induced Thrombotic Microangiopathy Treated with Eculizumab: A Case Report and Rapid Literature Review". Kidney and Dialysis 2, n.º 4 (12 de diciembre de 2022): 625–37. http://dx.doi.org/10.3390/kidneydial2040056.
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Background: Thrombotic microangiopathies (TMAs) can be induced by drugs. Recent works have indicated proteasome inhibitors, including carfilzomib, as a possible new causative agent. Although the physiopathology and management of carfilzomib-induced TMA are still unknown, eculizumab seems to be efficient. Results: We report a clinical case of TMA during carfilzomib treatment for multiple myeloma, possibly triggered by a concomitant influenza infection, suggesting a multi-hit process. Histologic analysis of the kidney biopsy proved renal TMA. Eculizumab allowed rapid and long-lasting renal and hematologic recovery. We enriched our work with a systemic review of published cases of carfilzomib-induced TMA treated by eculizumab. Twelve patients were included, all of whom presented acute renal failure and nine of them required hemodialysis. Eculizumab led to TMA resolution in eleven patients and complete renal recovery with hemodialysis withdrawal for seven of them within a month. One patient died from multiple myeloma progression. Two patients presented inter-current viral infection. Soluble complement fragment Bb and C5b9s were found in two patients and genetic benign variant of Factor H (CFH3–CFH1) in four. Conclusion: Our results suggest that eculizumab is effective in carfilzomib-induced TMA, which could support its inclusion as a treatment option. Further studies are required to clarify its physiopathology, complement role, and management.
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Lacombe, Karine y Juergen Rockstroh. "HIV and viral hepatitis coinfections: advances and challenges". Gut 61, Suppl 1 (12 de abril de 2012): i47—i58. http://dx.doi.org/10.1136/gutjnl-2012-302062.
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With a prevalence affecting over 30% of HIV infected patients, coinfection with hepatitis B (HBV) or C (HCV) virus remains one of the most frequent comorbidities in this population, with a significant impact in terms of morbidity and mortality associated with liver disease. Recent findings in the physiopathology of HIV in the liver have confirmed that it may contribute, along with hepatotoxicity of antiretrovirals and the burden of metabolic diseases, to a more rapid progression of liver fibrosis, especially when there is underlying chronic hepatitis coinfection. Both fields of research and clinical appraisal of HBV and HCV coinfection are rapidly evolving and prompt a change in the former paradigms of clinical care and management of chronic hepatic coinfection in the context of HIV. The advent of anti-HCV direct antiviral agents has indeed completely shaken up the treatment guidelines for HCV, and the tricky management of these new agents with antiretrovirals means referring patients to specialised centres. In HBV coinfection, therapeutic options have not changed recently but new challenges have emerged regarding the management of low replicating HBV-DNA in optimally treated patients and long term exposure to antivirals. Finally, the global increase in life expectancy in HIV infected patients has been accompanied in coinfected patients by a higher risk of emergence of end stage liver diseases for which access to orthotopic liver transplantation and innovative procedures such as targeted hepatocellular carcinoma therapies should be facilitated.
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Bellefroid, Maxime, Anthony Rodari, Mathilde Galais, Peter H. L. Krijger, Sjoerd J. D. Tjalsma, Lorena Nestola, Estelle Plant et al. "Role of the cellular factor CTCF in the regulation of bovine leukemia virus latency and three-dimensional chromatin organization". Nucleic Acids Research 50, n.º 6 (2 de marzo de 2022): 3190–202. http://dx.doi.org/10.1093/nar/gkac107.
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Abstract Bovine leukemia virus (BLV)-induced tumoral development is a multifactorial phenomenon that remains incompletely understood. Here, we highlight the critical role of the cellular CCCTC-binding factor (CTCF) both in the regulation of BLV transcriptional activities and in the deregulation of the three-dimensional (3D) chromatin architecture surrounding the BLV integration site. We demonstrated the in vivo recruitment of CTCF to three conserved CTCF binding motifs along the provirus. Next, we showed that CTCF localized to regions of transitions in the histone modifications profile along the BLV genome and that it is implicated in the repression of the 5′Long Terminal Repeat (LTR) promoter activity, thereby contributing to viral latency, while favoring the 3′LTR promoter activity. Finally, we demonstrated that BLV integration deregulated the host cellular 3D chromatin organization through the formation of viral/host chromatin loops. Altogether, our results highlight CTCF as a new critical effector of BLV transcriptional regulation and BLV-induced physiopathology.
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Turon-Lagot, Vincent, Antonio Saviano, Catherine Schuster, Thomas F. Baumert y Eloi R. Verrier. "Targeting the Host for New Therapeutic Perspectives in Hepatitis D". Journal of Clinical Medicine 9, n.º 1 (14 de enero de 2020): 222. http://dx.doi.org/10.3390/jcm9010222.
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Hepatitis D virus (HDV) is a small satellite virus of hepatitis B virus (HBV) requiring HBV infection to complete its life cycle. It has been recently estimated that 13% of chronic HBV infected patients (60 million) are co-infected with HDV. Chronic hepatitis D is the most severe form of viral hepatitis with the highest risk to develop cirrhosis and liver cancer. Current treatment is based on pegylated-interferon-alpha which rarely controls HDV infection and is complicated by serious side effects. The development of novel antiviral strategies based on host targeting agents has shown promising results in phase I/II clinical trials. This review summarizes HDV molecular virology and physiopathology as well as new therapeutic approaches targeting HDV host factors.
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Lebeau, Grégorie, Alisé Lagrave, Eva Ogire, Lauriane Grondin, Soundary Seriacaroupin, Cédric Moutoussamy, Patrick Mavingui et al. "Viral Toxin NS1 Implication in Dengue Pathogenesis Making It a Pivotal Target in Development of Efficient Vaccine". Vaccines 9, n.º 9 (25 de agosto de 2021): 946. http://dx.doi.org/10.3390/vaccines9090946.
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The mosquito-borne viral disease dengue is a global public health problem causing a wide spectrum of clinical manifestations ranging from mild dengue fever to severe dengue with plasma leakage and bleeding which are often fatal. To date, there are no specific medications to treat dengue and prevent the risk of hemorrhage. Dengue is caused by one of four genetically related but antigenically distinct serotypes DENV-1–DENV-4. The growing burden of the four DENV serotypes has intensified both basic and applied research to better understand dengue physiopathology. Research has shown that the secreted soluble hexameric form of DENV nonstructural protein-1 (sNS1) plays a significant role in the pathogenesis of severe dengue. Here, we provide an overview of the current knowledge about the role of sNS1 in the immunopathogenesis of dengue disease. We discuss the potential use of sNS1 in future vaccine development and its potential to improve dengue vaccine efficiency, particularly against severe dengue illness.
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Rotta, Indianara y Sérgio Monteiro de Almeida. "Genotypical diversity of HIV clades and central nervous system impairment". Arquivos de Neuro-Psiquiatria 69, n.º 6 (diciembre de 2011): 964–72. http://dx.doi.org/10.1590/s0004-282x2011000700023.
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The central nervous system (CNS) and the immune system are considered major target organs for HIV infection. The neurological manifestations directly related to HIV are acute viral meningitis, chronic meningitis, HIV associated dementia, vacuolar myelopathy and involvement of the peripheral nervous system. Changes in diagnosis and clinical management have changed the aspect of HIV infection so that it is no longer a fatal disease, and has become a chronic disease requiring sustained medical management. After HAART the incidence of most opportunistic infections, including those affecting the CNS, has dropped markedly. Some studies suggest that neurological involvement of infected patient occur with different frequency, depending on HIV subtype involved in the infection. Subtype C may have reduced neuroinvasive capacity, possibly due to its different primary conformation of HIV transactivating regulatory protein (Tat), involved in monocyte chemotaxis. This review focus on physiopathologic aspects of HIV infection in CNS and its correlation with HIV clades.
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Salinas, Sara y Yannick Simonin. "Les atteintes neurologiques liées au SARS-CoV-2 et autres coronavirus humains". médecine/sciences 36, n.º 8-9 (agosto de 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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Agut, Henri. "Une histoire de la virologie". médecine/sciences 38, n.º 12 (diciembre de 2022): 979–89. http://dx.doi.org/10.1051/medsci/2022162.
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La virologie est née à la fin du XIXe siècle de la reconnaissance d’agents infectieux, dits filtrables, qui franchissaient les filtres destinés à retenir les bactéries. L’étude de ces agents, en particulier celle du virus de la mosaïque du tabac et les bactériophages, a conduit à montrer l’originalité de leurs propriétés structurales et physico-chimiques, tout en stimulant le développement de la biologie moléculaire. Les virus des animaux, en plus de leur caractérisation, ont servi de sondes pour explorer le fonctionnement moléculaire des cellules eucaryotes, notamment l’organisation du génome, la régulation transcriptionnelle et les mécanismes d’oncogenèse. Au début des années 1960, une définition précise des virions et du mode de réplication des virus, ainsi qu’une classification internationalement reconnue fondée sur les propriétés moléculaires de ces agents, ont été publiées. Au cours des dernières décennies, la compréhension de la physiopathologie des infections virales a conduit à identifier de nombreux nouveaux virus et à développer des procédures standardisées de diagnostic virologique, une chimiothérapie antivirale spécifique et des vaccinations efficaces. Associées au succès des études plus fondamentales, ces avancées ont contribué au bilan exceptionnellement positif de la virologie au cours des cent dernières années.
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FIGUEIREDO, Luiz Tadeu M., Marcos L. MORELI, Vanessa S. O. ALMEIDA, Paulo R. FÉLIX, Júlio C. BRUNO, Ivani B. FERREIRA y Francisco D. MANÇANO. "HANTAVIRUS PULMONARY SYNDROME (HPS) IN GUARIBA, SP, BRAZIL: REPORT OF 2 CASES". Revista do Instituto de Medicina Tropical de São Paulo 41, n.º 2 (marzo de 1999): 131–37. http://dx.doi.org/10.1590/s0036-46651999000200012.
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Human infections caused by a hantavirus were reported in different regions of the State of São Paulo (SP), Brazil during the first six months of 1998. Two cases of fatal pulmonary syndrome occurred in May of 1998 in the City of Guariba, located in the Northeastern Region of SP. Both patients worked in a corn storage barn infested by rodents. These patients, after 2 or 3 days of non-specific febrile illness, developed a severe interstitial pneumonia spreading widely in both lungs, causing respiratory failure and death. At autopsy both patients showed lung interstitial edema with immunoblast-like mononuclear cell infiltrates, consistent with a viral etiology. Hantavirus infection was diagnosed by ELISA in both cases and by RT-PCR in one of the patients. Aspects of the clinical presentation, physiopathology and differential diagnosis of Hantavirus Pulmonary Syndrome are discussed.
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Carvalho, Ana Araújo, Cláudia B. Silva, Maria Luísa Martins y Gonçalo Cassiano Santos. "Congenital cytomegalovirus infection in twin pregnancy". BMJ Case Reports 14, n.º 7 (julio de 2021): e242712. http://dx.doi.org/10.1136/bcr-2021-242712.
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Cytomegalovirus (CMV) infection is one of the preeminent congenital viral infections, and despite its potential morbidity, uncertainty about its physiopathology, prevention and treatment remains until now. We report a case of a dichorionic and diamniotic twin pregnancy in which only one of the fetus had signs of being affected. The first twin had prenatal diagnosis of intrauterine growth restriction and hyperechogenic bowel, attributable to CMV infection, while there was no evidence of infection of the second one. Prenatal treatment was done with maternal administration of valacyclovir and postnatal treatment of the infected newborn with oral valganciclovir with normal neurodevelopment assessment at 12 months corrected age. In this case, maternal CMV infection was not equally transmitted to both fetuses, suggesting that there may be intrinsic fetal and placental factors influencing both transmission and the clinical features of the infection.
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Palich, Romain, Alain Makinson, Marianne Veyri, Amélie Guihot, Marc-Antoine Valantin, Sylvie Brégigeon-Ronot, Isabelle Poizot-Martin et al. "Kaposi’s Sarcoma in Virally Suppressed People Living with HIV: An Emerging Condition". Cancers 13, n.º 22 (15 de noviembre de 2021): 5702. http://dx.doi.org/10.3390/cancers13225702.
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Since the advent of highly effective combined antiretroviral treatment (cART), and with the implementation of large HIV testing programs and universal access to cART, the burden of AIDS-related comorbidities has dramatically decreased over time. The incidence of Kaposi’s sarcoma (SK), strongly associated with HIV replication and CD4 immunosuppression, was greatly reduced. However, KS remains the most common cancer in patients living with HIV (PLHIV). HIV physicians are increasingly faced with KS in virally suppressed HIV-patients, as reflected by increasing description of case series. Though SK seem less aggressive than those in PLHIV with uncontrolled HIV-disease, some may require systemic chemotherapy. Persistent lack of specific anti-HHV-8 cellular immunity could be involved in the physiopathology of these KS. These clinical forms are a real therapeutic challenge without possible short-term improvement of anti-HHV-8 immunity, and no active replication of HIV to control. The cumulative toxicity of chemotherapies repeatedly leads to a therapeutic dead end. The introduction or maintenance of protease inhibitors in cART does not seem to have an impact on the evolution of these KS. Research programs in this emerging condition are important to consider new strategies.
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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, n.º 3 (13 de marzo de 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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Evangelista, Heitor, César Amaral, Luís Cristóvão Porto, Sérgio J. Gonçalves Junior, Eduardo Delfino Sodré, Juliana Nogueira, Angela M. G. dos Santos, Marcio Cataldo y Daniel Junger. "Modeling the initial phase of SARS-CoV-2 deposition in the respiratory tract mimicked by the 11C radionuclide". PLOS ONE 16, n.º 1 (14 de enero de 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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Teles, Carolina, Rui Santos, Carlos Dias Silva y Teresa Vaio. "Postinfantile giant cell hepatitis in the setting of autoimmune hepatitis: exclusively a histological pattern or a prognosis predictor?" BMJ Case Reports 14, n.º 7 (julio de 2021): e243660. http://dx.doi.org/10.1136/bcr-2021-243660.
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Autoimmune hepatitis (AIH) is a rare chronic liver disease with a non-specific clinical presentation. Its physiopathology is not fully understood and, if untreated, can progress to cirrhosis and even fulminant liver failure. Here, we describe a case of a 73-year-old patient with an 11-month history suggestive of liver disease, who was concomitantly diagnosed with AIH and the extremely rare postinfantile giant cell hepatitis (PIGCH). Despite standard immunosuppressive therapy, the patient presented a severe clinical course, culminating in acute-on-chronic liver failure and death. This case reminds physicians of the importance of an early diagnosis, close monitoring and timely treatment of AIH. It also highlights the significant role in prognosis of the specific histological pattern of PIGCH, which has been mainly associated with a serious clinical outcome and unpredictable response to immunosuppressive therapy. Triggers of both AIH and PIGCH, such as viral infections, must be excluded, given their treatment implications.
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Núñez-Troconis, José. "Papel del virus del papiloma humano en el desarrollo del cáncer del cuello uterino." Investigación Clínica 64, n.º 2 (1 de junio de 2023): 233–54. http://dx.doi.org/10.54817/ic.v64n2a09.
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Abstract. The present narrative review was conducted to investigate and to compile information about the physiopathology of the Human Papilloma Virus (HPV) and the viral mechanisms of infection of the host’s cells, as well as how the virus survives the host’s innate immunological mechanisms and the mechanisms to produce cervical benign and malignant lesions. Literature searches were performed electronically in PubMed, Medline, ISI, DOAJ, Spring-er, Embase. Web of Knowledge, DOAJ, y Google Scholar, Hinari, JAMA Network, Oxford Academic and Research Life for original articles written in English and Scielo, Lantidex, Imbiomed-L, Redalyc, and Google Scholar for original articles written in Spanish. The searches included the keywords (MESH): physiopathol-ogy of HPV, HPV viral cycle, Carcinogenesis of HPV, HPV genomic structure, infection mechanism, and HPV taxonomy. Publications from January 1985 to August 2021 were reviewed. This narrative review allows us to understand how HPV produces productive and non-productive infection in the cells of the strati-fied squamous epithelium of the human being, especially that of the cervix, ex-plains how infection by the virus can produce benign lesions and malignant le-sions and explains why they are classified as HPV-HR and HPV-LR, according to their oncogenic capacity. These processes have made it possible to understand the behavior of the virus and establish primary treatment for the prevention of cervical cancer.
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Cespedes, Mateus da Silveira y José Carlos Rosa Pires de Souza. "Coronavirus: a clinical update of Covid-19". Revista da Associação Médica Brasileira 66, n.º 2 (febrero de 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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Cespedes, Mateus da Silveira y José Carlos Rosa Pires de Souza. "Sars-CoV-2: A clinical update - II". Revista da Associação Médica Brasileira 66, n.º 4 (abril de 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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Laste, Gabriela y Jorge de Oliveira Mateus. "Coronavirus in Pregnancy: The Role of Melatonin". Journal of Advances in Medicine and Medical Research 36, n.º 2 (16 de febrero de 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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Yakovenko, O. K., M. I. Lynnyk, I. V. Liskina, V. I. Ignatieva, G. L. Gumeniuk y M. G. Palivoda. "Radiological and morphological features of vanishing lung syndrome development in patients with COVID-19 community-acquired viral pneumonia". Infusion & Chemotherapy, n.º 1 (27 de marzo de 2024): 24–30. http://dx.doi.org/10.32902/2663-0338-2024-1-24-30.
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BACKGROUND. Presently actively new direction develops in digital treatment of CТ images – radiomics, that presents the result of co-operation on verge of different sciences (radiology, computer sciences and mathematical statistics). Inaccessible for the unarmed eye additional information of CT images can be got by means of their mathematical treatment and creation of the segmented histograms. Last it is possible to compare and analyse both isolated and with regard to the dynamics of physiopathology descriptions of organs and fabrics at the different human diseases.
OBJECTIVE. To define the roentgenologic and morphological features of development of vanishing lung syndrome for patients with non-hospital viral pneumonia.
MATERIALS AND METHODS. Data of CТ are analysed in a dynamics for patients with non-hospital viral pneumonia of COVID-19, that were on treatment in SI “National institute of phthisiology and pulmonology named after F.G. Yanovsky of the NAMS of Ukraine” or were directed from other medical establishments. The Dragonfly program from Object Research Systems (Montreal, Canada), which performs micro-X-ray structural analysis of the examined tissues, was used to analyze CT images of chest. Pathomorphological examination was performed in the laboratory of pathomorphology of the institute.
RESULTS. Monitoring of CT is conducted in the group, that consisted of 90 patients with non-hospital viral pneumonia of COVID-19. 27 (30,0 %) patients (18 men and 9 women in age from 23 to 68) are educed with the roentgenologic signs of vanishing lung syndrome. 12 from them (9 men and 3 women in age from 23 to 56) were on treatment in the institute in an acute period of disease. Other 15 patients (9 men and 6 women in age from 26 to 68) directed from other curative establishments, where they treated oneself 3-4 months ago.
CONCLUSIONS. Micro-X-ray structural analysis of data of CT allows to educe the features of changes of parenchima at development of vanishing lung syndrome. These changes are confirmed by the educed changes at pathomorphological research of postoperative preparations of lungs.
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Biver, Emmanuel, Alexandra Calmy y René Rizzoli. "Bone health in HIV and hepatitis B or C infections". Therapeutic Advances in Musculoskeletal Disease 9, n.º 1 (8 de octubre de 2016): 22–34. http://dx.doi.org/10.1177/1759720x16671927.
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Chronic infections with human immunodeficiency virus (HIV), hepatitis B virus (HBV) or hepatitis C virus (HCV) add to age-dependent bone loss and may contribute to lower bone strength in the elderly. In this review, we report recent highlights on the epidemiology of bone fragility in chronic viral infections with HIV, HCV and HBV, its physiopathology and discuss the interference of antiviral therapies with bone metabolism. Chronic infections influence bone through the interactions between risk factors for bone fragility and falls (which are highly prevalent in infected patients), virus activity and antiviral drugs. HIV-infected patients are at increased risk of fracture and the risk is higher in cases of co-infection with HIV and untreated chronic viral hepatitis. In HIV patients, the majority of bone loss occurs during virus activity and at initiation of antiretroviral therapy (ART). However, long-term elderly HIV-infected patients on successful ART display bone microstructure alterations only partially captured by dual energy X-ray absorptiometry (DXA). Bone loss is associated with an increase of bone resorption, reflecting the upregulation of the receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) pathways via a crosstalk between virus activity, inflammation and the immune system. The use of some antiviral drugs, such as tenofovir (controlling both HBV and HIV infections) or protease inhibitors, may be associated with higher bone toxicity. The reduction of tenofovir plasma concentrations with the implementation of tenofovir alafenamide (TAF) attenuates bone mineral density (BMD) loss but it remains unknown whether it will contribute to reducing fracture risk in long-term HIV-treated patients. Moreover, to what extent the new direct-acting agents for treatment of HCV, including nucleotide inhibitors and protease inhibitors, may affect bone health similarly as ART in HIV should be investigated.
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POZZETTO, B., I. BECHRI, M. DELOLME, M. VOGRIG, J. RIGAILI, P. VERHOEVEN, T. BOURLET y S. PILET. "État des lieux du diagnostic virologique de l’infection à SARS-CoV-2". EXERCER 31, n.º 163 (1 de mayo de 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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Gizzi, Giulia, Claudia Mazzeschi, Elisa Delvecchio, Tommaso Beccari y Elisabetta Albi. "Possible Stress–Neuroendocrine System–Psychological Symptoms Relationship in Pregnant Women during the COVID-19 Pandemic". International Journal of Environmental Research and Public Health 19, n.º 18 (13 de septiembre de 2022): 11497. http://dx.doi.org/10.3390/ijerph191811497.
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The COVID-19 pandemic induced long-term damages that weigh on the national health systems of various countries in terms of support and care. This review aimed to highlight the mental health impact of the COVID-19 pandemic in pregnant women. We first report data on the immune system physiopathology and the main viral infections in pregnancy, including COVID-19. Then, the attention is focused on the main factors that affect the mental health of pregnant women during the COVID-19 pandemic, such as (1) the fear of being infected and transmitting the infection to the fetus, (2) the cancellation of checkups and pre-child courses, and (3) confinement and the inability to have close friends or a partner at the time of delivery or in the first days after delivery, as well as family tensions. Because of all this, pregnant women find themselves in a stressful condition independent of the pregnancy, and thus experience anxiety, depression, insomnia, hostility, delirium, and an alteration of the mother–baby relationship. Several studies have shown an involvement of the hypothalamic–pituitary–adrenal axis and the hypothalamic–pituitary–thyroid axis in response to the pandemic. We propose a possible involvement of the neuroendocrine system as a mediator of the psychological symptoms of pregnant women induced by COVID-19-related stress.
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Bentata, Yassamine. "BK Virus-Associated Nephropathy in Adult Patients Post Kidney Transplantation: What Progress in 30 Years of History?" OBM Transplantation 08, n.º 03 (25 de julio de 2024): 1–26. http://dx.doi.org/10.21926/obm.transplant.2403221.
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Completely unknown before the 90s and exceptional up to the 2000s, BK virus nephropathy (BKvN), usually known as polyomavirus-associated nephropathy, has emerged as a significant and severe viral complication in kidney transplantation (KT). More than twenty years after Gardner's discovery of BKv in 1971, Purighalla described, in 1995, the first case of BKvN. Four years later in 1999, Nickeleit et al. published a first series of five cases of BKvN and made very precious and pertinent contributions to understanding this new entity. It has been well established that in post-KT, 30 to 50% of kidney transplant recipients are positive for BK viruria, of whom approximately one-third will develop BK viremia and, without intervention, could progress in 1 to 10% of cases to BKvN, leading to kidney graft failure in more than half of the cases. For now, there is no preventive antiviral treatment for BKvN; only a strategy of rapid, efficient screening allows for the preservation of renal graft function. The only effective and sure treatment measure is to reduce the intensity of total immunosuppression, including immunosuppressive drugs and corticosteroids. Based on the current data, this review describes the physiopathology, diagnosis, and management of BKvN in adult KTRs. It presents the results of the fifty most important studies published during the last two decades.
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Chaturvedi, Pragya y 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 (30 de junio de 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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He, Liyu, Xiaofei Peng, Jiayi Wang, Chengyuan Tang, Xun Zhou, Hong Liu, Fuyou Liu, Lin Sun y Youming Peng. "Synthetic Double-Stranded RNA Poly(I:C) Aggravates IgA Nephropathy by Triggering IgA Class Switching Recombination through the TLR3-BAFF Axis". American Journal of Nephrology 42, n.º 3 (2015): 185–97. http://dx.doi.org/10.1159/000440819.
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Background: Immunoglobulin class-switch recombination (CSR) is crucial for the expression of IgA, and it plays a vital role in the physiopathology of IgA nephropathy (IgAN). The aim of the study is to investigate the effect of polyriboinosinic:polyribocytidylic acid (poly(I:C)) in modulating toll-like receptor (TLR) 3-B-cell-activating factor belonging to the TNF family (BAFF) axis activation, which in turn promotes IgA CSR of IgAN patients and the IgAN rat model. Methods: Blood samples and tonsillar tissue specimens were obtained from 24 patients with IgAN and 26 patients with chronic tonsillitis as control. We also used the IgAN rat model to investigate the relationship between viral infection and IgA CSR. Results: Immunohistochemical and ELISA western blotting examination revealed that the TLR3/BAFF axis is activated in IgAN patients when compared to controls. Synthetic double-stranded RNA poly(I:C) stimulation upregulates the TACI/TLR3/TRIF/TRAF6 expression and promotes IgA CSR and BAFF productions in tonsil mononuclear cells. TLR3 or BAFF siRNA decreases IgA expression. In IgAN rat models, TLR3/BAFF signaling was highly activated. With 200 μg poly(I:C) sodium salt into the left naris for 8 weeks, IgA was highly deposited on glomeruli. It also revealed that poly(I:C) activated TLR3/BAFF axis and IgA CSR in vivo. Conclusion: These data points toward the role of TLR3/BAFF axis in IgA CSR of IgAN, and the data also support the notion that mucosal immunization with virus infection results in impaired mucosal and systemic IgA responses.
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Martinez, R., A. Gonzáles Godínez, I. Vasquez Tercero, C. Elizondo Solis, A. Montoya Rosales, M. Salinas Carmona y N. Macias-Segura. "AB0626 DIFFERENTIALLY EXPRESSED GENES (DEGS) OVERLAP AMONG BLOOD SAMPLES DATASETS FROM PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) THROUGH INTEGRATIVE BIOINFORMATICS METANALYSIS". Annals of the Rheumatic Diseases 82, Suppl 1 (30 de mayo de 2023): 1515.1–1516. http://dx.doi.org/10.1136/annrheumdis-2023-eular.207.
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BackgroundSystemic Lupus Erythematosus is an autoimmune chronic disease mainly characterized by the presence of auto-autoantibodies, and periods of flares and remission [1]. Understanding the mechanisms of physiopathology is still being the aim for several researchers. In the last 20 years multiple studies tried to look for molecular mechanisms associated to the disease using biomolecular techniques [2]. Specifically, the gene expression patterns play an important role in the pathophysiology of this disease, in which the interferon signature has been widely found in SLE patients, but also in other autoimmune diseases like rheumatoid arthritis and Sjögren’s syndrome [3]. However, there is a discordance in which genes from the interferon signature are specific biomarkers for SLE, since there are multiple studies that describe the interferon signature but with different differentially expressed genes.ObjectivesWe aimed to identify differentially expressed genes that overlap across different datasets of gene expression from blood samples of SLE patients using an integrative bioinformatics metanalysis.MethodsWe design a search strategy in the Gene Expression Omnibus platform to identify data sets of gene expression profile by array from blood samples of patients with SLA. The inclusion criteria were: 1) assays performed in humans, 2) the dataset include SLE patients and healthy controls, 3) expression profiling by array, 4) data analysis using GEO2R, 5) samples from blood. The exclusion criteria was: 1) incomplete information of the genes, 2) gene expression by RNAseq. Differentially expressed genes were selected when logfold change was >2 withp<0.05. Integrative bioinformatics strategy was applied. Using the platforms GeneMania and DAVID we identify overlapped genes among datasets and functional enrichment analysis of the differentially expressed genes.ResultsWe selected 3 datasets that fulfill the inclusion criteria: GSE110174, GSE10325, and GSE154851. A total of 29 up-regulated genes were identified among datasets. Venn diagram shows 3 genes overlapped among all the datasets, and 1 or 2 genes overlapped between different pairs of datasets (Figure 1).Figure 1.Venn diagram of the 3 datasets.A prediction analysis yielded 20 co-expressed genes, that interact with the overlapped genes. A functional enrichment analysis yielded the 3 principal biological processes involving those genes: 17 genes participate in defense response to virus; 13 genes associated to response to virus; and 8 genes involved in negative regulation of viral genome replication (Table 1). Most of the genes identified belong to the interferon signature.Table 1.Functional enrichment Analysis of the Co-Expressed genes.Functional Enrichment AnalysisProcessGene CountpValueDefense Response to Virus178,1E-26Response to Virus131,8E-21Negative Regulation of Viral Genome Replication89,1E-14ConclusionWe aimed to obtain upregulated genes and their co-expressed pairs through transcriptomic and functional enrichment analysis. 6 genes appeared upregulated across the 3 datasets, and 20 genes were listed as their co-expressed pairs. Those genes were involved in the processes of Defense Response to Virus, Response to virus, and Negative Regulation of Viral Genome Replication. These genes can serve as possible biomarkers for early diagnosis, and maybe even possible therapeutic targets.References[1]Yu, C., M.E. Gershwin, and C. Chang,Diagnostic criteria for systemic lupus erythematosus: a critical review.Journal of autoimmunity, 2014.48: p. 10-13.[2]Fujio, K., et al.,transcriptome and trans-omics analysis of systemic lupus erythematosus.Inflammation and regeneration, 2020.40(1): p. 1-6.[3]Rönnblom, L. and M.-L. Eloranta,The interferon signature in autoimmune diseases.Current opinion in rheumatology, 2013.25(2): p. 248-253.Acknowledgements:NIL.Disclosure of InterestsNone Declared.
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Besson, Caroline, Danielle Canioni, Catherine Settegrana, Henda Driss, Laurent Alric, Patrice Cacoub, Cyrille Feray et al. "Clinico-Pathological Characteristics of B-Cell Non Hodgkins Lymphomas Associated with Hepatitis C Virus ANRS HC13 LYMPHO-C Observational Study." Blood 114, n.º 22 (20 de noviembre de 2009): 1927. http://dx.doi.org/10.1182/blood.v114.22.1927.1927.
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Abstract Abstract 1927 Poster Board I-950 Introduction: Hepatitis C virus (HCV) associated B-cell non-Hodgkin's lymphoma (B-NHL) is a rare entity that constitutes a model to study chronic immune stimulation related lymphomas. They are known to be preferentially Marginal Zone Lymphomas (MZL) and Diffuse Large B Cell Lymphoma (DLBCL) subtypes. Conflicting results are reported on the association between Follicular Lymphoma (FL) and HCV. In order to study the physiopathology of HCV-related B-NHL, we pursue a multicentric observational study in France. We present here the clinicopathological characteristics of the patients included. Patients and methods: Adult patients with a history of HCV associated B-NHL are included in the study. HCV infection is defined by a positive viral load at diagnosis of NHL. Patients with HIV infection are excluded from the study. Each patient is followed every 6 months during 5 years. At each follow-up, a blood sample is withdrawn allowing ancillary studies. Data collection concerns clinical presentation, treatment and evolution of NHL and HCV infection. Pathological and cytological materials are centralized in order to allow their review and a concerted analysis by a group of expert hematopathologists, haematologists and immunologists. Results: The data of the 54 consecutive patients included between november 2006 and april 2009 in 20 french centers are presented. Median age is 63 years (ranging from 39 to 87 years). There is a predominance of men: sex ratio (m/f) is 1.45 (32/22). Included women are older than men (p<0.01), median age being 71 among women and 60 years among men. HCV genotypic distribution does not differ from expected in a HCV infected population in France: 1: 51% (25/49), 2: 29% (14/49), 3: 8% (4/49), 4: 12% (6/49), 5 missing data. Transmission risk groups, known in 50% (27/54) of cases, are transfusion (18), drug abuse (5), endemic origin (2), and tattoo/acupuncture (2). Two patients are co-infected with HBV. Twenty-four patients out of 42 tested (57%) had positive cryoglobulinemia at diagnosis of NHL. This proportion did not differ with gender nor with genotype. Fifteen cases were included at diagnosis of B-NHL. The 39 other cases were included during follow-up of NHL. The median interval between NHL diagnosis and last follow-up is 15 months (range 0-13y). The histological subtype distribution is DLBCL 39% (21), MZL 35% (19), FL 13% (7), CLL 6% (3). Remarkably, there is a continuum between MZL and DLBCL, 6 cases with ongoing transformation. Four cases could not be classified due to small disease infiltration or lack of material. We confirm the link between cryoglobulinemia and MZL, 12+ out of 17 tested, 6+/12 in DLBCL versus 2+/5 in FL and 1+/2 in CLL. Nodal involvement is infrequent (5 out of 21 cases of DLBCL, 2/19 MZL, 4/7 FL). Extranodal involvements predominated in spleen (15 including 8 MZL), lung (6), digestive tract (4), liver (3), heart (1), skin (6) and bone marrow (4). The efficiency of antiviral treatment is confirmed in 5 cases with MZL, and remarkably, was followed by a good response in one case with FL. However, most patients in this observational study received treatment with Rituximab (R) either alone (5 cases with MZL), or combined with chemotherapy (including 15 cases with DLBCL and 4 with FL) or with antiviral treatment. This was associated with good clinical responses in most cases and low toxicity. Indeed, only 5 patients died during follow-up – two from disease progression - a 85 y man and a 40 y woman with liver DLBCL who was resistant to 3 lines of R-chemotherapy. The other patients died of sepsis (2), and cardiac ischemia (1). Conclusions: This study strengthens the heterogeneity of HCV-related lymphomas. The observation of cases with MZL and, remarkably, of one case with FL responding to antiviral treatment suggests that they are both linked to chronic immune stimulation. Therefore, the concept of antigen-driven lymphomagenesis seems more heterogeneous than initially anticipated: it could involve a T independent response in MZL, and a T dependent response in FL. The ongoing pathophysiological study will improve further understanding of the mechanisms by which antigen-driven lymphoproliferation arise. Disclosures: No relevant conflicts of interest to declare.
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Lopes, Luiz Thiago Oliveira, Marcelus de Andrade Oliveira, Willian Guilherme Lobato Gonçalves, Donizete Vago Daher, Irma da Silva Brito, Carla Viana Dendasck, Cláudio Alberto Gellis de Mattos Dias, Amanda Alves Fecury y Maria Helena Mendonça de Araújo. "Séquelles de la COVID-19 : revue intégrative de la littérature". Revista Científica Multidisciplinar Núcleo do Conhecimento, 8 de agosto de 2023, 68–87. http://dx.doi.org/10.32749/nucleodoconhecimento.com.br/sante/sequelles-de-la-covid.
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La grande affinité entre la protéine Spike du virus SARS-CoV-2 et le récepteur de l’enzyme de conversion de l’angiotensine 2 est postulée comme l’une des principales raisons de la forte taux de transmission virale, ce qui a conduit l’OMS à déclarer la COVID-19 comme une Urgence de Santé Publique d’Intérêt International, ainsi qu’à adopter des mesures de contenances de la propagation virale. De plus, grâce au mécanisme physiopathologique du virus, on observe généralement des symptômes non spécifiques, une évolution atypique, principalement chez les personnes âgées et immunodéprimées, ainsi qu’une progression plus rapide et létale. De même, avec l’avancement des connaissances sur l’histoire naturelle de l’infection virale, des symptômes persistants et/ou des séquelles ont été constatés, entraînant des dysfonctionnements organiques et ayant un impact négatif sur la qualité de vie des patients. Ainsi, l’objectif de l’article était de présenter une revue intégrative sur les principales séquelles de la COVID-19 pour les années 2021 et 2022. À cette fin, des articles complets ont été recherchés dans les bases de données de recherche Scientific Electronic Library Online, Biblioteca Virtual em Saúde et PubMed, en portugais et en anglais, et la méthodologie PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) a été utilisée, avec la sélection de 14 articles. Parmi les résultats, on peut noter : la physiopathogénèse de la COVID-19 persistante repose sur la théorie des phénomènes immunitaires secondaires à l’infection, une réponse immunitaire anormale et la présence du virus dans des endroits immunologiquement privilégiés ; la fatigue, la dyspnée, les altérations cognitives subjectives, les séquelles neurologiques, les maladies inflammatoires du système nerveux central et les dysfonctions olfactives post-virales sont des complications courantes ; des preuves d’une relation causale entre la COVID-19 et la thyroïdite subaiguë ont été présentées ; un plus grand nombre de complications et d’hospitalisations a été démontré chez les patients présentant une carence en vitamine D ; ainsi que la présence de symptômes neuropsychiatriques dans la population des professionnels de la santé. En conclusion, la rareté des travaux portant directement sur les séquelles de la COVID-19 a été constatée, rendant nécessaire un approfondissement de ces recherches en vue de la création de protocoles plus spécifiques pour le diagnostic.
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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 y Fernando Henrique Magri Alves. "COVID-19 in the nervous system: physiopathology and neurological manifestations". Arquivos de Neuro-Psiquiatria, 4 de julio de 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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Devaux, Christian A., Jean-Christophe Lagier y Didier Raoult. "New Insights Into the Physiopathology of COVID-19: SARS-CoV-2-Associated Gastrointestinal Illness". Frontiers in Medicine 8 (18 de febrero de 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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Olivier, Thibaut, Joël Blomet y Daniel Desmecht. "Central role of lung macrophages in SARS-CoV-2 physiopathology: a cross-model single-cell RNA-seq perspective". Frontiers in Immunology 14 (7 de junio de 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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Yuan, Shun, Qi Wu, Zhiwei Wang, Yanjia Che, Sihao Zheng, Yuanyang Chen, Xiaohan Zhong y Feng Shi. "miR-223: An Immune Regulator in Infectious Disorders". Frontiers in Immunology 12 (10 de diciembre de 2021). http://dx.doi.org/10.3389/fimmu.2021.781815.
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MicroRNAs (miRNAs) are diminutive noncoding RNAs that can influence disease development and progression by post-transcriptionally regulating gene expression. The anti-inflammatory miRNA, miR-223, was first identified as a regulator of myelopoietic differentiation in 2003. This miR-223 exhibits multiple regulatory functions in the immune response, and abnormal expression of miR-223 is shown to be associated with multiple infectious diseases, including viral hepatitis, human immunodeficiency virus type 1 (HIV-1), and tuberculosis (TB) by influencing neutrophil infiltration, macrophage function, dendritic cell (DC) maturation and inflammasome activation. This review summarizes the current understanding of miR-223 physiopathology and highlights the molecular mechanism by which miR-223 regulates immune responses to infectious diseases and how it may be targeted for diagnosis and treatment.
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Prada-Arismendy, Jeanette y Jaime E. Castellanos. "Real time PCR. Application in dengue studies". Colombia Medica, 1 de junio de 2011, 243–58. http://dx.doi.org/10.25100/cm.v42i2.778.
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PCR (polymerase chain reaction) is a routinely used tool in every diagnostic and research laboratory. This technique has been used in detection of mutations and pathogens, forensic investigation, and even is the base tool for human genome sequencing. A modification of PCR technique, real time PCR, allows the quantification of nucleic acids with higher sensibility, specificity and reproducibility. This article is intended to clarify the foundations of real-time PCR, using an application model for virology. In the actual work, it was quantified the viral load of dengue virus serotype 2 produced from infected murine macrophages; the obtained results in this work established that murine strain BALB/c presents a greater susceptibility to dengue virus infection, which establishes BALB/c murine strain as a best model of study for investigation of dengue virus infection physiopathology.
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Rodrigues, Renato Barradas, Marco Orsini, Sofia Vieira Neves, Wladimir Bocca Vieira de Rezende Pinto, Antônio Marcos da Silva Catarino, Daniel Antunes Pereira y Acary Souza Bulle Oliveira. "Differential Diagnosis or Etiology: A Case Report on Amyotrophic Lateral Sclerosis-like Neuropathy Associated with HIV Infection". Current HIV Research 21 (14 de septiembre de 2023). http://dx.doi.org/10.2174/1570162x21666230914104220.
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Background: Retroviruses are described as a risk factor for chronic neuropathy. However, it is still unknown if they can work as amyotrophic lateral sclerosis triggers. Over the years, some cases of this association have been described with heterogenous disclosures. Case Representation: This study aimed to report a case of HIV and ALS-like neuropathy and briefly discuss peculiarities of clinical aspects, such as physiopathology and treatment options. The patient underwent neurological examination associated with blood tests, electromyography, analysis of cerebrospinal fluid, and imaging studies. Discussion: A non-systematic review was performed in major databases regarding the topic. The case presented mixed upper and lower motor neuron signs and was framed as a probable case of ALS following the present criteria. Conclusion: After a short follow-up and viral load cleansing, neurological stabilization was achieved.
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Wee, Jee Hye, Young-Kyung Ko, Roza Khalmuratova, Hyun-Woo Shin, Dae Woo Kim y Chae-Seo Rhee. "Effect of lipopolysaccharide and polyinosinic:polycytidylic acid in a murine model of nasal polyp". Scientific Reports 11, n.º 1 (13 de enero de 2021). http://dx.doi.org/10.1038/s41598-020-80483-y.
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AbstractSeveral factors, including bacterial and viral infections, have been associated with rhinosinusitis and nasal tissue remodelling that may result in nasal polyp formation. However, the potential role of bacterial or viral stimuli triggering polyp development is unclear. Here, we used lipopolysaccharide (LPS) and polyinosinic:polycytidylic acid [poly(I:C)] in a murine model of allergic rhinosinusitis to compare different effects of bacterial- and virus-derived stimuli in the pathogenesis of nasal polyp formation. Briefly, BALB/c mice were sensitised and challenged with ovalbumin and staphylococcal enterotoxin, with or without LPS or poly(I:C), and the consequent histopathological profiles, cytokines, and systemic humoral responses were studied. While no significant differences in polyp formations and epithelial disruptions were observed among the experimental groups, the local cell recruitment patterns slightly differed in animals that received either LPS or poly(I:C). Additionally, the local immune environments generated by LPS or poly(I:C) stimulation varied. LPS stimulation induced a marked Th1/Th17 response and predominantly neutrophilic nasal polyp formations, whereas poly(I:C) induced a Th2-skewed environment in neutrophilic nasal polyp development. Overall, our findings show that both cell recruitment patterns and local immune environments induced by these two stimuli differ, which may have implications in the physiopathology of rhinosinusitis with nasal polyp.
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de Castro, Fabíola Attié, Parinaz Mehdipour, Ankur Chakravarthy, Ilias Ettayebi, Helen Loo Yau, Tiago Silva Medina, Sajid A. Marhon et al. "Ratio of stemness to interferon signalling as a biomarker and therapeutic target of myeloproliferative neoplasm progression to acute myeloid leukaemia". British Journal of Haematology, 19 de septiembre de 2023. http://dx.doi.org/10.1111/bjh.19107.
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SummaryProgression to aggressive secondary acute myeloid leukaemia (sAML) poses a significant challenge in the management of myeloproliferative neoplasms (MPNs). Since the physiopathology of MPN is closely linked to the activation of interferon (IFN) signalling and that AML initiation and aggressiveness is driven by leukaemia stem cells (LSCs), we investigated these pathways in MPN to sAML progression. We found that high IFN signalling correlated with low LSC signalling in MPN and AML samples, while MPN progression and AML transformation were characterized by decreased IFN signalling and increased LSC signature. A high LSC to IFN expression ratio in MPN patients was associated with adverse clinical prognosis and higher colony forming potential. Moreover, treatment with hypomethylating agents (HMAs) activates the IFN signalling pathway in MPN cells by inducing a viral mimicry response. This response is characterized by double‐stranded RNA (dsRNA) formation and MDA5/RIG‐I activation. The HMA‐induced IFN response leads to a reduction in LSC signature, resulting in decreased stemness. These findings reveal the frequent evasion of viral mimicry during MPN‐to‐sAML progression, establish the LSC‐to‐IFN expression ratio as a progression biomarker, and suggests that HMAs treatment can lead to haematological response in murine models by re‐activating dsRNA‐associated IFN signalling.
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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 (18 de febrero de 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.