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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.
Full textAbstract:
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.
2
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.
3
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.
4
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.
5
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.
6
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.
7
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.
8
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.
9
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.
10
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.
11
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.
12
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.
13
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.
14
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.
15
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.
16
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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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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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.
19
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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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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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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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.
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Zhong, Han, Yang Zhou, Shu-Ya Mei, Ri Tang, Jin-Hua Feng, Zheng-Yu He, Qiao-Yi Xu, and Shun-Peng Xing. "Scars of COVID-19: A bibliometric analysis of post-COVID-19 fibrosis." Frontiers in Public Health 10 (September 20, 2022). http://dx.doi.org/10.3389/fpubh.2022.967829.
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BackgroundThe coronavirus disease 2019 (COVID-19) becomes a worldwide public health threat. Increasing evidence proves that COVID-19-induced acute injuries could be reversed by a couple of therapies. After that, post-COVID-19 fibrosis (PCF), a sequela of “Long COVID,” earns rapidly emerging concerns. PCF is associated with deteriorative lung function and worse quality of life. But the process of PCF remains speculative. Therefore, we aim to conduct a bibliometric analysis to explore the overall structure, hotspots, and trend topics of PCF.Materials and methodsA comprehensive search was performed in the Web of Science core database to collect literature on PCF. Search syntax included COVID-19 relevant terms: “COVID 19,” “COVID-19 Virus Disease,” “COVID-19 Virus Infection,” “Coronavirus Disease-19,” “2019 Novel Coronavirus Disease,” “2019 Novel Coronavirus Infection,” “SARS Coronavirus 2 Infection,” “COVID-19 Pandemic,” “Coronavirus,” “2019-nCoV,” and “SARS-CoV-2”; and fibrosis relevant terms: “Fibrosis,” “Fibroses,” and “Cirrhosis.” Articles in English were included. Totally 1,088 publications were enrolled. Searching results were subsequentially exported and collected for the bibliometric analysis. National, organizational, and individual level data were analyzed and visualized through biblioshiny package in the R, VOSviewer software, the CiteSpace software, and the Graphical Clustering Toolkit (gCLUTO) software, respectively.ResultsThe intrinsic structure and development in the field of PCF were investigated in the present bibliometric analysis. The topmost keywords were “COVID-19” (occurrences, 636) surrounded by “SARS-CoV-2” (occurrences, 242), “coronavirus” (occurrences, 123), “fibrosis” (occurrences, 120), and “pneumonia” (occurrences, 94). The epidemiology, physiopathology, diagnosis, and therapy of PCF were extensively studied. After this, based on dynamic analysis of keywords, hot topics sharply changed from “Wuhan,” “inflammation,” and “cytokine storm” to “quality of life” and “infection” through burst detection; from “acute respiratory syndrome,” “cystic-fibrosis” and “fibrosis” to “infection,” “COVID-19,” “quality-of-life” through thematic evolution; from “enzyme” to “post COVID.” Similarly, co-cited references analysis showed that topics of references with most citations shift from “pulmonary pathology” (cluster 0) to “COVID-19 vaccination” (cluster 6). Additionally, the overview of contributors, impact, and collaboration was revealed. Summarily, the USA stood out as the most prolific, influential, and collaborative country. The Udice French Research University, Imperial College London, Harvard University, and the University of Washington represented the largest volume of publications, citations, H-index, and co-authorships, respectively. Dana Albon was the most productive and cited author with the strongest co-authorship link strength. Journal of Cystic Fibrosis topped the list of prolific and influential journals.ConclusionOutcomes gained from this study assisted professionals in better realizing PCF and would guide future practices. Epidemiology, pathogenesis, and therapeutics were study hotspots in the early phase of PCF research. As the spread of the COVID-19 pandemic and progress in this field, recent attention shifted to the quality of life of patients and post-COVID comorbidities. Nevertheless, COVID-19 relevant infection and vaccination were speculated to be research trends with current and future interest. International cooperation as well as in-depth laboratory experiments were encouraged to promote further explorations in the field of PCF.
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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, and Maria Helena Mendonça de Araújo. "Séquelles de la COVID-19 : revue intégrative de la littérature." Revista Científica Multidisciplinar Núcleo do Conhecimento, August 8, 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.