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Relevant bibliographies by topics / Cytopathic effect

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Academic literature on the topic 'Cytopathic effect'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 January 2023

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Journal articles on the topic "Cytopathic effect"

1

Rogers, Susan, and Dale W. Vance. "Unusual cytopathic effect in tissue culture." Clinical Microbiology Newsletter 7, no. 1 (January 1985): 7. http://dx.doi.org/10.1016/s0196-4399(85)80016-7.

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Saravanan, Chandrassegar, Zhiyi Cao, Janardan Kumar, Jiazhou Qiu, Andrew G. Plaut, David S. Newburg, and Noorjahan Panjwani. "Milk Components InhibitAcanthamoeba-Induced Cytopathic Effect." Investigative Opthalmology & Visual Science 49, no. 3 (March 1, 2008): 1010. http://dx.doi.org/10.1167/iovs.07-1130.

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Cao, Zhiyi. "Effect of Human Tears on Acanthamoeba-Induced Cytopathic Effect." Archives of Ophthalmology 126, no. 3 (March 1, 2008): 348. http://dx.doi.org/10.1001/archophthalmol.2007.74.

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Kavi, J., I. Chant, M. Maris, and P. E. Rose. "CYTOPATHIC EFFECT OF VEROTOXIN ON ENDOTHELIAL CELLS." Lancet 330, no. 8566 (October 1987): 1035. http://dx.doi.org/10.1016/s0140-6736(87)92609-2.

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Deshmukh, Dr Chanchal. "Study The Cytopathic Effect of BmNPV in The BOMBYX MORI Ovarian Cell Lines." Paripex - Indian Journal Of Research 3, no. 5 (January 15, 2012): 243–44. http://dx.doi.org/10.15373/22501991/may2014/76.

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Wales, Samantha Q., Diana Ngo, Kaoru Hida, and Michael Kulka. "Temperature and density dependent induction of a cytopathic effect following infection with non-cytopathic HAV strains." Virology 430, no. 1 (August 2012): 30–42. http://dx.doi.org/10.1016/j.virol.2012.04.010.

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Taylor, W. M., M. S. Pidherney, H. Alizadeh, and J. Y. Niederkorn. "In vitro Characterization of Acanthamoeba castellanii Cytopathic Effect." Journal of Parasitology 81, no. 4 (August 1995): 603. http://dx.doi.org/10.2307/3283860.

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Sam, Afshin, Felicia Goodrum, Robert Ricciotti, Kenneth Knox, and Richard Sobonya. "Medical image of the week: CMV cytopathic effect." Southwest Journal of Pulmonary and Critical Care 9, no. 6 (December 24, 2014): 341–42. http://dx.doi.org/10.13175/swjpcc161-14.

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HOLLYER, TARAS T., PAT A. DEGAGNE, and MICHELLE J. ALFA. "Characterization of the Cytopathic Effect of Haemophilus ducreyi." Sexually Transmitted Diseases 21, no. 5 (September 1994): 247–57. http://dx.doi.org/10.1097/00007435-199409000-00002.

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Croissant, Odile, Françoise Breitburd, and Gérard Orth. "Specificity of cytopathic effect of cutaneous human papillomaviruses." Clinics in Dermatology 3, no. 4 (October 1985): 43–55. http://dx.doi.org/10.1016/0738-081x(85)90048-3.

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Dissertations / Theses on the topic "Cytopathic effect"

1

Wong, Chun-nin Adam, and 黃春年. "Analyses of influenza viral cytopathic effect in human lower respiratory tract." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290860.

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Wong, Chun-nin Adam. "Analyses of influenza viral cytopathic effect in human lower respiratory tract." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290860.

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Iwatani, Yasumasa. "Human Immunodeficiency Virus Type 1 Vpu modifies Cytopathic Effect through Augmented Virus Release." Kyoto University, 1997. http://hdl.handle.net/2433/202156.

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Rai, Vijeta. "Screening of large collection of compounds for anti-human parainfluenza virus type-2 activity and evaluation of hit compounds." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-14385.

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Human parainfluenza virus type-2 (HPIV-2) is a highly contagious respiratory pathogen that can cause severe respiratory disease known as laryngotracheobronchitis or croup-like disease in children. No specific vaccine or an antiviral drug is currently approved for treatment of HPIV-2 infections. In this project, a library of 14400 diverse compounds had been screened for anti-HPIV-2 activities in cultures of African green monkey kidney cells. All compounds that inhibited the virus induced syncytium-forming activity in these cells were considered as hit compounds. Three hit compounds showed moderate anti-HPIV-2 activity characterized by the IC50 values of 20 µM and selectivity indices of approximately 5. This suggests that the antiviral activity of these compounds was due to targeting activities of cellular rather than viral components. Another hit compound, referred to as compound 5, showed anti-HPIV-2 activity that was manifested as a reduction of area of the virus-induced plaques in cells at not cytotoxic concentrations. Interestingly, this compound did not inhibit initial infection nor the virus production in infected cells as revealed by the time-of-addition assay. Moreover, it showed no direct the virus-inactivating (virucidal activity) against HPIV-2 particles. However, relatively short pre-treatment (4 hours) of the cells with compound 5 prior to the virus infection was sufficient for its plaque size-reducing activity suggesting that anti-HPIV-2 activity of compound 5 was due to targeting activities of cellular rather than viral components. Further studies are needed to elucidate the anti-HPIV-2 mechanism of activity of hit compounds identified in the present study.

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McGuire, Kelly Lewis. "Governing Dynamics of Divalent Copper Binding by Influenza A Matrix Protein 2 His37 Imidazole." BYU ScholarsArchive, 2020. https://scholarsarchive.byu.edu/etd/8647.

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Influenza A is involved in hundreds of thousands of deaths globally every year resulting from viral infection-related complications. Previous efforts to subdue the virus by preventing proper function of wild-type (WT) neuraminidase (N), and M2 proteins using oseltamivir and amantadine (AMT) or rimantadine (RMT), respectively, exhibited success initially. Over time, these drugs began exhibiting mixed success as the virus developed drug resistance. M2 is a proton channel responsible for the acidification of the viral interior which facilitates release of the viral RNA into the host. M2 has a His37-tetrad that is the selective filter for protons. This protein has been demonstrated to be a feasible target for organic compounds. However, due to a mutation from serine to asparagine at residue 31 of M2, which is found in the majority of influenza strains circulating in humans, AMT and RMT block is insufficient. From simulations, it is unclear whether the insensitivity results from weak binding or incomplete block. The question of how the S31N mutation caused MT and RMT insensitivity in M2 is addressed here by analyzing the binding kinetics of AMT and RMT using the two-electrode voltage clamp electrophysiology method. The dissociation rate constant (k2) is dramatically increased compared to WT for both AMT and RMT, by 1500-fold and 17000-fold respectively. Testing of AMT at 10 mM demonstrates complete block, albeit weak, of the S31N M2 channel. At 10 mM, RMT does not reach complete block even though the binding site is saturated. When RMT is in the bound state, it is not blocking all the current, and is binding without block. These results motivated the development of novel M2 blockers using copper complexes focusing on the His37 complex in M2. I hypothesized that copper complexes would bind with the imidazole of a histidine in the His37 complex and prevent proton conductance. The His37 complex is highly conserved in the M2 channel and, therefore, would be important target for influenza therapeutics. By derivatizing the amines of known M2 blockers, AMT and cyclooctyalmine, to form the iminodiacetate or iminodiacetamide, we have synthesized Cu(II) containing complexes and characterized them by NMR, IR, MS, UVâ€“vis, and inductively coupled plasma mass spectroscopy (ICP-MS). The copper complexes, but not the copper-free ligands, demonstrated H37-specific blocking of M2 channel currents and low micromolar anti-viral efficacies in both Amt-sensitive and Amt-resistant IAV strains with, for the best case, nearly 10-fold less cytotoxicity than CuCl2. Isothermal titration calorimetry was used to obtain enthalpies that showed the copper complexes bind to one imidazole and curve fitting to the electrophysiology data provided rate constants for binding in the M2 channel. Computational chemistry was used to obtain binding geometries and energies of the copper complexes to the His37-tetrad. The results show that the copper complexes do bind with the His37 complex and prevent proton conductance and influenza infection.

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Gamlen, Toby Philip Edward. "Non-structural proteins derived from non-cytopathic or cytopathic biotypes of bovine viral diarrhoea virus have distinct effects on cell survival and antiviral signalling pathways." Thesis, University of Leeds, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435778.

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Rossignol, Rodrigue. "Expression métabolique de défauts dans le fonctionnement des oxydations phosphorylantes mitochondriales : effet de seuil et théorie du contrôle du métabolisme appliqués à l'étude de la spécificité tissulaire des cytopathies." Bordeaux 2, 2000. http://www.theses.fr/2000BOR28781.

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Combes, Maud. "Rôle du peptide amyloïde dans les maladies neurodégénératives Operational Dissection of b-Amyloid Cytopathic Effects on Cultured Neurons Glutamate Protects Neuromuscular Junctions from Deleterious Effects of b-Amyloid Peptide and Conversely: an In Vitro Study in a Nerve–Muscle Coculture." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS311.

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Les maladies neurodégénératives touchent plus de 33 millions de personnes dans le monde. Elles sont caractérisées par la dégénérescence progressive des neurones et un dysfonctionnement dans le cerveau et/ou la moëlle épinière. Leurs mécanismes (perte des cellules neuronales, axonopathie, perte synaptique, inflammation, dysfonction immunitaire...) ont une incidence sur les fonctions moteurs et cognitives et peuvent générer une dépendance croissante des malades. Le traitement de la plupart des maladies neurodégénératives reste à l'heure actuelle essentiellement symptomatique ; s'il permet d'améliorer la qualité de vie des patients, il est le plus souvent sans effet sur l'évolution de la maladie. L’ensemble de nos résultats a permis de mettre en évidence des mécanismes physiopathologiques inédits de la maladie d’Alzheimer et la sclérose latérale amyotrophique, et d’imaginer de nouvelles pistes thérapeutiques. Nous avons étudié les effets toxiques des AβO, sur un modèle in vitro de neurones primaires ainsi que sur un modèle de coculture nerf muscle reproduisant des jonctions neuromusculaires, en nous concentrant sur leur cinétique de développement, puis sur leur mécanismes moléculaires et cellulaires. Nous avons pu avancer l’hypothèse d’un lien de causalité étroit entre le glutamate et les AβO aussi bien dans la maladie d’Alzheimer que dans la sclérose latérale amyotrophique. Il a été mis en évidence que des modèles de culture cellulaire permettaient de répondre à des questions ciblées, dans la mesure où ils reproduisent certains phénomènes neuropathologiques observés chez les malades
Neurodegenerative diseases affect more than 33 million people in the world. They are characterized by the progressive degeneration of neurons and a dysfunction in of the brain and/or the spinal cord. Their mechanisms (loss of the neuronal cells, axonopathy, synaptic loss, inflammation, immunizing dysfunction...) have an impact on the motor and cognitive functions and can generate an increasing dependence of the patient. The treatment of most of the neurodegenerative diseases remains at the moment essentially symptomatic. Many treatments improve the quality of life of the patients, but most of them remain ineffective on the evolution of the disease. The results allowed us to reveal some unprecedented facts about physiopathological mechanisms of Alzheimer's disease and amyotrophic lateral sclerosis, and to imagine new therapeutic targets. We studied the toxic effects of the AβO on an in vitro model of primary neurons as well as on a model of coculture nerve muscle reproducing neuromuscular junctions, by concentrating on their kinetics development, then on their molecular and cellular mechanisms. We were able to move forward the hypothesis of a link of causality between the glutamate and the AβO in the Alzheimer's disease as well as in amyotrophic lateral sclerosis. Using the models of cell cultures and observing how they reproduce, we were able to answer some of the targeted questions concerning some of the neuropathological phenomena observed in the patients

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9

Hollyer, Taras. "Characterization of the cytopathic effect of Haemophilus ducreyi on human foreskin fibroblast (HFF) cells in vitro." 1994. http://hdl.handle.net/1993/18123.

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Pinilla, Vicente. "In vitro and in vivo effects of deoxynivalenol (DON) mycotoxin on porcine reproductive and respiratory syndrome virus (PRRSV) in piglets." Thèse, 2015. http://hdl.handle.net/1866/13368.

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Les récoltes de céréales sont souvent contaminées par des moisissures qui se développent pendant la récolte et l’entreposage et produisent des métabolites secondaires appelés mycotoxines. Le porc est reconnu pour être sensible au déoxynivalénol (DON). L’infection virale la plus importante chez le porc est causée par le virus du syndrome reproducteur et respiratoire porcin (VSRRP). Celui-ci provoque un syndrome grippal et des troubles de reproduction. L’objectif du présent projet était de déterminer l'effet in vitro de DON sur la réplication du VSRRP dans de lignées cellulaires permissives, MARC-145 et PAM, et déterminer in vivo l'impact de DON dans des aliments naturellement contaminés sur l’infection au VSRRP chez le porcelet. Tout d’abord, les cellules ont été incubées avec des doses croissantes de DON et ont été infectées avec du VSRRP pour évaluer la viabilité et la mortalité cellulaire, la réplication virale et l’expression de cytokines. Les résultats ont montré que les concentrations de DON de 560ng/ml et plus affectaient significativement la survie des cellules MARC-145 et PAM infectées par le VSRRP. En revanche, il y avait une augmentation significative de la viabilité et une réduction de la mortalité cellulaire à des concentrations de DON de 140 à 280 ng/ml pour les cellules PAM et de 70 à 280 ng/ml pour les cellules MARC-145 avec une réduction de l'effet cytopathique provoqué parle VSRRP. Au niveau in vivo, 30 porcelets divisés en 3 groupes de 10 porcelets et nourris pendant 2 semaines avec 3 différentes diètes naturellement ont été contaminées avec DON (0; 2,5 et 3,5 mg/kg). Les porcelets ont été subdivisés en 6 groupes, 3 groupes de 6 porcelets et ont été exposés au DON pendant 2 semaines et infectés par voie intratrachéale et intramusculaire avec le virus. Les 3 autres groupes de 4 porcelets servaient de contrôle non infectés. Les signes cliniques ont été enregistrés pendant 21 jours. La virémie a été évaluée par PCR. À la fin de l’expérimentation, les porcelets ont été euthanasiés et les lésions pulmonaires ont été évaluées. Les résultats ont montré que l’ingestion de DON à 3,5 mg/kg a augmenté l’effet du VSRRP sur la sévérité des signes cliniques, les lésions pulmonaires et la mortalité. L’ingestion de DON à 2,5 mg/kg a entrainé une augmentation de la virémie au jour 3 après l’infection mais sans impact sur les signes cliniques et les lésions pulmonaires. Mot clés: DON, VSRRP, MARC-145, PAM, effet cytopathique, cytokines, PCR
Cereal crops are often contaminated with moulds that grow during harvest and storage and produce secondary metabolites called mycotoxins. Pig is known to be sensitive to deoxynivalenol (DON). On the other hand, infection by porcine reproductive and respiratory syndrome virus (PRRSV) causes a flu-like syndrome and reproductive disorders. The objectives of this project were to determine the in vitro effect of DON on the replication of PRRSV in permissive cell lines, MARC-145 and PAM and the in vivo impact of DON-naturally contaminated feed on PRRSV infection in piglets. Firstly, cells were incubated with gradually increasing doses of DON and were infected with PRRSV to evaluate cytopathic effect and to assess cell viability, virus replication and cytokine mRNA expression on infected and uninfected cells. Results showed that DON concentrations of 560 ng/ml and higher were significantly detrimental to the survival of MARC-145 cells infected with PRRSV. In contrast, there was a significant increase of cell viability and decreased of cell mortality at DON concentrations within 140 to 280 ng/ml for PAM cells and 70 to 280 ng/ml ranges for MARC-145 showing a reduced cytopathic effect (CPE) caused by PRRSV. In vivo study was carried out on 30 piglets divided into 3 groups of 10 piglets fed naturally contaminated diets with different levels of DON; 0, 2.5 and 3.5 mg/kg. After 2 weeks, pigs were further divided into 6 subgroups, 3 subgroups of 6 piglets were infected intra tracheally and intramuscularly with PRRSV. The other 3 subgroups of 4 piglets were used as uninfected controls. Clinical signs were recorded for 21 days post-infection (p.i.). Sera were evaluated for viremia by PCR. At the end of the experiment, piglets were euthanized and pulmonary lesions were evaluated. Results showed that ingestion of diet highly contaminated with DON at 3.5 mg/kg increased the effect of PRRSV infection on the severity of clinical signs, weight loss, lung lesions and mortality. Diet with DON at 2.5 mg/kg showed an increase of viremia at day 3 but had not significant impact on clinical signs and lung lesions. Keywords: DON, PRRSV, MARC-145, PAM, cytopathic effect, cytokines, PCR

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Books on the topic "Cytopathic effect"

1

Filippo, Anna Beatriz De. Cytopathic effects of Treponema denticola on KB epithelial cells. [Toronto: s.n.], 1993.

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2

Elliott, Perry, and Giuseppe Limongelli. Cardiac Aspects of INHERITED METABOLIC DISEASES. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0070.

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More than 40 inherited metabolic disorders cause heart disease, including fatty acid oxidation defects, glycogen storage disorders, lysosomal storage disorders, peroxisomal diseases, mitochondrial cytopathies, organic acidemias, aminoacidopathies, and congenital disorders of glycosylation. The pattern and severity of cardiac involvement varies between disorders but includes congenital heart diseases, heart muscle diseases, arrhythmias and sudden death, and heart failure. The majority of IMDs are multisystem diseases, but in a few cases cardiac disease is the predominant clinical feature and the main determinant of prognosis. For an increasing number of IEMs there are specific therapies designed to treat or ameliorate the effects of the underlying metabolic defect. In some cases, these therapies have an important effect on the progression of cardiac disease.

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S, Weislow Owen, and National Cancer Institute (U.S.), eds. New soluble-formazan assay for HIV-1 cytopathic effects: Application to high-flux screening of synthetic and natural products for AIDS-antiviral activity. [Bethesda, Md.?: National Cancer Institute, 1989.

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S, Weislow Owen, and National Cancer Institute (U.S.), eds. New soluble-formazan assay for HIV-1 cytopathic effects: Application to high-flux screening of synthetic and natural products for AIDS-antiviral activity. [Bethesda, Md.?: National Cancer Institute, 1989.

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S, Weislow Owen, and National Cancer Institute (U.S.), eds. New soluble-formazan assay for HIV-1 cytopathic effects: Application to high-flux screening of synthetic and natural products for AIDS-antiviral activity. [Bethesda, Md.?: National Cancer Institute, 1989.

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Vinod, Nikhra. COVID-19 and Long Covid: Organs Damage and Dysfunctions, and Implications for Clinical Course. Heighten Science Publications Inc., 2021. http://dx.doi.org/10.29328/ebook1005.

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Like any other infectious disease, the prognosis of COVID-19 is influenced by infecting agent, the SARS-CoV-2 virus load and the extent of organs affliction and damage. COVID-19 having a propensity for multiorgan involvement carries an adverse prognosis during the clinical course as well as later during the post-recovery period persisting as Long Covid. The direct cytopathic effects of SARS-CoV-2 virus and the erratic and hyper-inflammatory response lead to tissue injury in various organs coupled with physiological dysfunctions and complications. In fact, the multi-system manifestations of COVID-19 are caused by a combination of specific host defence responses with associated inflammatory activity and vascular involvement with coagulopathy and a distinct propensity to develop thromboembolic complications. Simultaneously, comorbidities such as diabetes, hypertension and cardiovascular diseases influence the disease severity and mortality.

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McShane, Tony, Peter Clayton, Michael Donaghy, and Robert Surtees. Neurometabolic disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0213.

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Various disorders result from genetically determined abnormalities of enzymes, the metabolic consequences of which affect the development or functioning of the nervous system. The range of metabolic disturbances is wide, as is the resultant range of clinical syndromes. Although most occur in children, some can present in adult life, and increasing numbers of affected children survive into adult life. In some, specific treatments are possible or are being developed. The last 20 years has seen a considerable expansion in our understanding of the genetic and metabolic basis for many neurological conditions. Particular clinical presentations of neurometabolic disorders include ataxias, movement disorders, childhood epilepsies, or peripheral neuropathy. Detailed coverage of the entire range of inherited metabolic diseases of the nervous system is available in other texts (Brett 1997; Scriver et al. 2001; Menkes et al. 2005).Treatment is possible for some metabolic diseases. For instance, the devastating neurological effects of phenylketonuria have been recognized for many years. Neonatal screening for this disorder and dietary modification in the developed world has removed phenylketonuria from the list of important causes of serious neurological disability in children. This success has led to new challenges in the management of the adult with phenylketonuria and unexpected and devastating effect of the disorder on the unborn child of an untreated Phenylketonuria mother. More recently Biotinidase deficiency has been recognized as an important and easily treatable cause of serious neurological disease usually presenting with early onset drug resistant seizures. This and some other neurometabolic diseases can be identified on neonatal blood screening although a full range of screening is not yet routine in the United Kingdom. More disorders are likely to be picked up at an earlier asymptomatic stage as the sophistication of screening tests increases (Wilcken et al. 2003; Bodamer et al. 2007).Although individual metabolic disorders are rare, collectively such disorders are relatively common. In reality most clinicians will see an individual condition only rarely in a career. Furthermore, patients with certain rare conditions are often concentrated in specialist referral centres, further reducing the exposure of general and paediatric neurologists to these disorders. A recent study into progressive intellectual and neurological deterioration, PIND, gives some information about the relative frequency and distribution of some childhood neurodegenerative diseases in the United Kingdom (Verity et al. 2000; Devereux et al. 2004). Although primarily designed to identify any childhood cases of variant Creutzfeldt- Jakob disease, the study also provided much information about the distribution of neurometabolic disease in children in the United Kingdom. The commonest five causes of progressive intellectual and neurological deterioration over 5 years were Sanfilippo syndrome, 41 cases, adrenoleukodystrophy, 32 cases, late infantile neuronal ceroid lipofuschinosis, 32 cases, mitochondrial cytopathy, 30 cases, and Rett syndrome, 29 cases. Notably, geographical foci of these disorders were also found and correlate with high rate of consanguinity in some local populations.

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Book chapters on the topic "Cytopathic effect"

1

Gooch, Jan W. "Cytopathic Effect (CPE)." In Encyclopedic Dictionary of Polymers, 885. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13509.

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Sodroski, Joseph, William Haseltine, and Mark Kowalski. "Role of the Human Immunodeficiency Virus Type I Envelope Glycoprotein in Cytopathic Effect." In Mechanisms and Specificity of HIV Entry into Host Cells, 193–201. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5976-0_12.

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Chalareng, C., F. Pillien, M. Boury, C. Tasca, J. De Rycke, and A. Milon. "AF/R2 Adhesin and Cytopathic Effect as Virulence Traits of Diarrhea-Inducing Escherichia coli O103 in European Rabbit." In Advances in Experimental Medicine and Biology, 269–71. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1828-4_44.

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Oberhaus, S. M., T. S. Dermody, and K. L. Tyler. "Apoptosis and the Cytopathic Effects of Reovirus." In Current Topics in Microbiology and Immunology, 23–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72095-6_2.

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Greiser-Wilke, I., B. Liess, J. Schepers, C. Stahl-Hennig, and V. Moennig. "Correlation of bovine viral diarrhoea virus induced cytopathic effects with expression of a biotype-specific marker." In Ruminant Pestivirus Infections, 55–66. Vienna: Springer Vienna, 1991. http://dx.doi.org/10.1007/978-3-7091-9153-8_7.

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Stephens, D. S., Z. A. McGee, and M. D. Cooper. "Cytopathic effects of the pathogenic Neisseria. Studies using human fallopian tube organ cultures and human nasopharyngeal organ cultures." In Gonococci and Meningococci, 827–36. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1383-7_128.

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BURLESON, FLORENCE G., THOMAS M. CHAMBERS, and DANNY L. WIEDBRAUK. "CYTOPATHIC EFFECT INHIBITION BIOASSAY." In Virology, 157–60. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-12-144730-4.50037-0.

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"The Turning Point: Cytopathic Effect in Tissue Culture." In To Catch a Virus, 113–56. American Society of Microbiology, 2013. http://dx.doi.org/10.1128/9781555818586.ch5.

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Martinez-Palomo, Adolfo, Arturo González-Robles, and Bibiana Chavez. "Cell Biology of the Cytopathic Effect of Entamoeba Histolytica." In Amebiasis: Infection and Disease by Entamoeba histolytica, 43–58. CRC Press, 2020. http://dx.doi.org/10.1201/9780429282539-4.

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Muñoz, A., and L. Carrasco. "Effects Of Interferon On Viral Replication And On The Cytopathic Effects Induced By Animal Viruses." In Mechanisms of Viral Toxicity in Animal Cells, 147–88. CRC Press, 2018. http://dx.doi.org/10.1201/9781351074353-7.

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Conference papers on the topic "Cytopathic effect"

1

Singhera, Gurpreet K., Ruth MacRedmond, Samuel J. Wadsworth, and Delbert Dorscheid. "CLA Inhibits RSV Entry And Cytopathic Effect In Isolated Airway Epithelial Cells." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5650.

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Elbashir, Israa, Aisha Aisha Nasser J. M. Al-Saei, Paul Thornalley, and Naila Rabbani. "Evaluation of antiviral activity of Manuka honey against SARS-CoV-2." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0113.

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Background and aims: In 2020 a global pandemic was declared caused by the severe acute respiratory syndrome coronavirus (SARS-CoV-2). The pandemic is still ongoing and continues to cause considerable mortality and morbidity world-wide and new variants of the virus are emerging. Rapid development and rollout of vaccines for SARS-CoV-2 is in progress to counter the pandemic but has been tempered by the emergence of new SARS-CoV-2 variants, many of which exhibit reduced vaccine effectiveness. To date there is no approved antiviral treatment for coronavirus disease 2019 (COVID-19). Several studies have shown that Manuka honey has virucidal/antiviral effect. Methylglyoxal (MG), a bioactive component in Manuka honey, has antiviral activity in vitro. MG may modify arginine residues in the functional domains of viral spike and nucleocapsid proteins, resulting in loss of charge, protein misfolding and inactivation. The aim of this study was to characterize the antiviral activity of Manuka honey against SARS-CoV-2 in vitro Materials and methods: Wild-type SARS-CoV-2 with titers of multiplicities of infection (MOI) 0.1 and 0.05 were incubated with 2-fold serial dilutions of 250+ Manuka honey (equivalent to 250 to 31 µM) in infection medium (Dulbecco's Modified Eagle Medium + 2% fetal bovine serum + 100 units/ml penicillin + 100 µg/ml streptomycin) for 3 h. Manuka honey treated and untreated control SARS-CoV-2 was incubated with confluent cultures of Vero cells in vitro for 1 h, cultures washed with phosphate-buffered saline and incubated in fresh infection medium at 37°C for 4 - 5 days until 70% of virus control cells displayed cytopathic effect. We also studied the effect of scavenging MG in Manuka Honey with aminoguanidine (AG; 500 µM) on virucidal activity. The antiviral activity of MG was judged by median tissue culture infectious dose (TCID50) assays. Data analysis was by logistic regression. TCID50 (mean ± SD) was deduced by interpolation. Results: Diluted Manuka honey inhibited SARS-CoV-2 replication in Vero cells. SARS-CoV-2 was incubated in diluted Manuka honey in medium at 37°C for 3 h before adding to Vero cells. Manuka honey dilutions down to 125 µM MG equivalents completely inhibited cytopathic effect of SARS-CoV-2 whereas 31.25 µM and 62.5 µM MG equivalents had limited effect. Logistic regression and interpolation of the cytopathic effect indicated that the TCID50 = 72 ± 2 µM MG equivalents for MOI of 0.1. Prior scavenging of MG by addition of AG resulted in virus replication levels equivalent to those seen in the virus control without AG. Conclusion: Manuka honey has antiviral activity against SARS-CoV-2 when incubated with the virus in cell-free media at no greater than ca. 40-fold dilutions of 250+ grade. Anti-viral activity was inhibited by AG, consistent with the anti-viral effect being mediated by MG. Manuka honey dilutions in MG equivalents had similar antiviral effect compared to authentic MG, also consistent with MG content of Manuka honey mediating the antiviral effect. Whilst Manuka honey may inactivate SARS-CoV-2 in cell-free culture medium, its antiviral activity in vivo for other than topical application may be limited because of the rapid metabolism of MG by the glyoxalase system and limited bioavailability of oral MG.

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Lewis, R. M., P. B. Jahrling, B. P. Griffin, and T. M. Cosgriff. "THE EFFECTS OF HEMORRHAGIC FEVER VIRUS INFECTION OF ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643352.

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Pichindé viral infection of strain 13 guinea pigs is a model for Lassa fever virus in humans. Infected animals show impaired platelet function and altered coagulation parameters. Human endothelial cells and the human endothe1ia1-1 ike cell line, EA926, were infected with Pichinde virus. Following infection, cultures were monitored by phase contract microscopy for cytopathic effect (CPE). Assays of supernatant were used to document viral growth and to measure those endothelial-produced components that might affect hemostasis. In addition, the cells were stimulated with phorbol ester (PMA), which stimulates the production of prostacyclin. Infection showed no noticeable effect on the endothelial cells or EA926 cells which were untreated with PMA. PHA-treated EA926 cells were subject to CPE. Factor VIII antigen was not significantly affected by viral infection, PMA treatment, or endotoxin exposure. The production of PGFl, measured as an estimate of prostacyclin synthesis, was dependent on the concentration of stimulating PMA. Infected cultures showed decreased responsiveness to PMA stimulation when infected by increasing concentrations of Pichindé. The most noticeable effect was noted when cultures were infected with a multiplicity of infection of 0.1 and 100 ng/ml PMA. Thromboxane B2 an estimate of thromboxane A2, showed no significant change. No detectable leukotriene C4 was produced and no significant change in leukotriene B4 was measured. The decreased prostacyclin production by the infected endothelial cells may indicate a role for the endothelium in the hemorrhagic syndrome that accompanies some viral diseases.

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Wernet, P., E. M. Scheider, P. Sarin, P. Chandra, H. H. Brackmann, M. Kessler, and H. Egli. "Demonstration of HIV-encoded Proteins in Cultured and in Uncultured CD 4 Positive Mononuclear Cells from Hemophilia Patients Employing Monoclonal Antibodies against p 15, p 24, GP 41, GP 120, and Reverse Transcriptase." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644683.

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In the light of the large percentage of hemophilia patients with antibodies to HIV the identification of a specific virus infection in comparison to HIV antibody negative hemophilia patients has reached crucial importance. The low success rates of direct virus culture techniques together with the as yet low AIDS-di-sease rate observed in these patients separate these patients from the other main risk groups. Within this context, we studied the expression of CD3, CD4, CD8, and HLA class II antigens on fixed cells after PHA stimulation and Interleukin 2 propagation as well as on untreated blood mononuclear cells from healthy individuals and from hemophilia patients by fluorescence activated flow cytometry. Monoclonal antibodies thought to be specific for p 15, p 24, GP 41, GP 120, and for reverse transcriptase revealed a certain number of positive cells on all defined subpopulations analysed. From cell specimen of HIV antibody positive hemophilia patients cells with specific HIV antigens could be enriched by in vitro cultivation. Importantly the expression of virus-encoded antigens preceedes a cytopathic effect for several daVs. Current analyses aim at the prognostic relevance of low amounts of such viral HIV proteins selectively detectable by moAbs.directed to either p 24, GP 41, GP 120, and RT. The reliability, high sensitivity and monoclonal antibody dependent specificity of this newly developed method for the demonstration of HIV specific proteins make it applicable also for longitudinal surveys of hemophilia patients to assess a potential state of viremia or virus antigen processing in their mononuclear cells.

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Reports on the topic "Cytopathic effect"

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Cytopathic SARS-Cov2 screening on VERO-E6 cells in a large repurposing effort. EMBL-EBI, December 2020. http://dx.doi.org/10.6019/chembl4495565.

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