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Journal articles on the topic 'Coxsakie viru'

Author: Grafiati

Published: 11 March 2023

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1

Begum, Nurun Nahar Fatema, Md Rabiul Hossain, and Md Ferdousur Rahman Sarker. "Dilated Cardiomyopathy due To Coxsackie-B Virus Myocarditis: A Case Report." Journal of Armed Forces Medical College, Bangladesh 13, no. 1 (April 23, 2017): 131–33. http://dx.doi.org/10.3329/jafmc.v13i1.41074.

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Dilated cardiomyopathy (DCM) is a rare disorder which may be caused by diverse reasons. Many of them are idiopathic also. The article reports a case of DCM resulting from acute Coxsackie virus myocarditis. Antibody to Coxsackie-B virus was positive from a lab of United States of America. This is first case report of Coxsackie-B virus myocarditis (proven) led to cardiomyopathy in Bangladesh. Journal of Armed Forces Medical College Bangladesh Vol.13(1) 2017: 131-133

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2

Zaheeruddin, Samad, Najeebah A. Bade, Sandeep Jani, and Monvadi B. Srichai. "A case of coxsackie B virus infection leading to multi-organ inflammation: Myopericarditis and acute liver failure." Case Reports in Internal Medicine 1, no. 2 (March 21, 2014): 45. http://dx.doi.org/10.5430/crim.v1n2p45.

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Myopericarditis refers to the development of acute pericarditis with myocardial involvement. Viral infections, including Coxsackie B virus, are amongst the most common causes of myopericarditis. The Coxsackie B viruses are known to have a role in the development of a number of clinical diseases including but not limited to cardiac disease, central nervous system infections, ocular infections, pleurodynia, gastrointestinal disease, and viral exanthems. In individual cases, Coxsackie B virus may also be associated with acute hepatitis. We describe a rare case of a 41 year-old female with multi-organ inflammation caused by Coxsackie B virus leading to myopericarditis, pleuritis, and acute liver failure. Laboratory and imaging data helped to make diagnosis of myopericarditis and appropriate management was initiated. Shortly after the patient developed acute liver failure with an INR greater than 13 and AST and ALT of 7946 u/L and 5684 u/L, respectively. Viral serology revealed Coxsackie B 1, 2, and 6 serum antibody positivity (> 1:32 titer) indicating acute or recent infection. A complete workup for other liver failure etiologies was negative. The case shows the significance of awareness and recognition of the possible complications of Coxsackie B virus infection including liver failure.

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3

Pulli, Timo, Pasi Koskimies, and Timo Hyypiä. "Molecular Comparison of Coxsackie A Virus Serotypes." Virology 212, no. 1 (September 1995): 30–38. http://dx.doi.org/10.1006/viro.1995.1450.

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4

Kümmerle-Deschner, J., R. Kandolf, G. Enders, F. Labay, D. Niethammer, and G. Dannecker. "Coxsackie-B-Virus-Infektion." Monatsschrift Kinderheilkunde 145, no. 1 (January 29, 1997): 23–25. http://dx.doi.org/10.1007/s001120050099.

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5

Joret, J. C., A. Hassen, P. Hartemann, and J. M. Foliguet. "Some Limits in Current Adsorption-Elution Methods for the Detection of Viruses in Large Volumes of Tap Water." Water Science and Technology 18, no. 10 (October 1, 1986): 133–40. http://dx.doi.org/10.2166/wst.1986.0121.

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Two types of electropositive filters (1 MDS double sheet - Cuno and AS - Seitz) were compared for Poliovirus 1, Coxsackie virus B3, Coxsackie virus A9 and E.C.H.O. virus 1 recovery from tap water with different pH levels. For small volumes of tap water sampled, both adsorbents gave equally satisfactory recoveries of Poliovirus 1 (46% to 82%) at pH 6.7, 7.9, or 9. However, elution percentages using 3% beef-extract solution pH 9.5 were generally better for 1 MDS than for AS filters. As the volume of tap water sampled increased, increasing amounts of Poliovirus were unadsorbed onto both types of filters at pH 7, 7.9, or 9. Lowering the pH to 6 gave better Poliovirus 1 and Coxsackie B3 recoveries with AS (respectively 61% and 95%) and 1 MDS filters (respectively 67% and 91%). E.C.H.O. virus 1 recovery was not affected by acidification and was lower with 1 MDS (6%) than with AS filters (37%). Coxsackie virus A9 recovery was very low for both filters (≤11%). As for electronegative adsorbents, currently available methods for concentrating viruses using electropositive filters have to be optimized to recover most enteric viruses occurring in waters.

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6

De Salins, C. A., S. Vallet, L. Misery, and C. Abasq-Thomas. "Présentations atypiques de syndrome pied-main-bouche à type d’« eczéma coxsakium » : rôle du Coxsackie virus A6." Annales de Dermatologie et de Vénéréologie 141, no. 12 (December 2014): S446—S447. http://dx.doi.org/10.1016/j.annder.2014.09.488.

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7

VAN KUPPEVELD, FRANK J. M., WILLEM J. G. MELCHERS, KARLA KIRKEGAARD, and JOHN R. DOEDENS. "Structure–Function Analysis of Coxsackie B3 Virus Protein 2B." Virology 227, no. 1 (January 1997): 111–18. http://dx.doi.org/10.1006/viro.1996.8320.

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8

Gubler, Borovicka, Diener, and Meyenberger. "Cholestatische Hepatitis." Praxis 92, no. 29 (July 1, 2003): 1269–72. http://dx.doi.org/10.1024/0369-8394.92.29.1269.

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Bei einem 27-jährigen Patienten mit einer cholestatischen Hepatitis werden ausgedehnte Abklärungen inklusive Leberbiopsie und Virusserologien durchgeführt. Die Histologie zeigt eine Cholestase mit Riesenzellen, im Verlauf kann ein Titeranstieg für eine Coxsackie-B5-Infektion dokumentiert werden. Aufgrund des Verlaufes wird dieses Virus für die Lebererkrankung verantwortlich gemacht. Die Riesenzellhepatitis ist ein Reaktionsmuster des Leberparenchyms auf verschiedene exogene Noxen, wie zum Beispiel das Coxsackie-B-Virus.

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9

Amin, Amina, Muhammad A. Rasheed, Rana A. Diwan, Muhammad Shahid, Saddia Bano, Adnan Riaz, Muhammad N. Iqbal, and Muhammad W. Sajid. "Inhibition of 2C Coxsackie B Virus Protein to Decrease Pathogenicity of Diabetes Mellitus Type 1." Current Computer-Aided Drug Design 16, no. 3 (June 2, 2020): 318–26. http://dx.doi.org/10.2174/1573409915666190820154422.

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Background: Insulin-dependent Diabetes Mellitus Type 1 (T1D) also referred to as autoimmune diabetes. T1D is a chronic disease which is characterized by way of insulin deficiency. The deficiency is due to the loss of pancreatic β cells and leads to hyperglycemia. There are many factors which play a significant role in T1D disease pathogenicity including genetic predisposition, the immune system, and environmental factors. The environmental factors may include Coxsackie B4 virus, a small RNA virus. Objective: The objective of current in silico study is to identify active lead compounds against Coxsackie B4 virus, a small RNA virus which has been reported in diabetic patients after PCR. There is a need to predict inhibitors against TID caused by Coxsackie B4 viral protein that may be used as a drug against TID in the future. Methods: For this purpose, different bioinformatics databases and tools were used. The protein structure generation and validation, retrieval of ligands and their properties analysis were performed by different databases, web servers, and software tools. Moreover, the docking tools were used to identify the target site of the protein and interaction of different inhibitors with the target protein molecule. Results: Based on the analysis, two lead compounds ZINC00034488 and ZINC00034585 were selected as potential drugs. These compounds are non-toxic and have best interaction energy and fulfill Lipinski rule, Veber rule, Ghose Rule, Weighted QED, Unweighted QED and BBB likeness parameters. Conclusion: Our work will help researchers to get an idea about the understanding of chemicals against Coxsackie B4 Viruses and helpful to design a drug and test these chemicals to overcome Diabetes Mellitus Type 1 caused by Coxsackie B4 virus.

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10

Watson, William J., Sami Awadallah, and Mary Jo Jaqua. "Intrauterine Infection With Coxsackievirus: Is it a Cause of Congenital Cardiac Malformations?" Infectious Diseases in Obstetrics and Gynecology 3, no. 2 (1995): 79–81. http://dx.doi.org/10.1155/s1064744995000366.

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Background: Although maternal infections with coxsackievirus during pregnancy are relatively common, fetal infections are quite rare. Coxsackievirus infection in utero has been associated with myocarditis, but has not been proven a teratogen.Case: A patient whose fetus had structural cardiac anomalies and hydrops was found to have an intrauterine infection with Coxsackie B-1 virus, proven by virus isolation from the amniotic fluid. This infection led to increasing intrauterine hydrops and subsequent neonatal death. Conclusion: This interesting association of intrauterine infection with Coxsackie B virus and structural cardiac anomalies in the fetus warrants further investigation.

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11

Jones, David B., and Nigel W. Armstrong. "Coxsackie virus and diabetes revisited." Nature Medicine 1, no. 4 (April 1995): 284. http://dx.doi.org/10.1038/nm0495-284.

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12

Gauntt, C. J., W. C. Lutton, E. K. Godeny, S. M. Witherspoon, H. M. Arizpe, and R. E. Lanford. "Murine coxsackie virus B3 myocarditis." European Heart Journal 8, suppl J (November 2, 1987): 393–97. http://dx.doi.org/10.1093/eurheartj/8.suppl_j.393.

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13

Akram, Arifa, and Lubana Akram. "Hand Foot and Mouth Disease (HFMD) in a 3 Years Old Boy in Bangladesh: A Case Report." Bangladesh Journal of Infectious Diseases 6, no. 2 (March 20, 2020): 53–55. http://dx.doi.org/10.3329/bjid.v6i2.46106.

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Hand, foot & mouth disease (HFMD) is a contagious and emerging infectious disease caused by picorna viridae family. It was first reported in New Zealand in 1957 is caused by Coxsackie virus A16 (CVA16), human enterovirus 71 (HEV71) and occasionally by Coxsackie virus A6 and Coxsackie virus A10, are also associated with HFMD and herpangina. Though only small scale outbreaks have been reported from United States, Europe, Australia Japan and Brazil for the first few decades, since 1997 the disease has noticeably changed its character as noted in different Southeast Asian countries. In recent years Bangladesh also faces some cases of HFMD. Though HFMD is a mild disease but in rare cases may develop neurological complications. Early detection and good clinical assessment can prevent the fatal progression and also can reduce morbidity and mortality regarding HFMD. Bangladesh Journal of Infectious Diseases 2019;6(2):53-55

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14

Funke, Carsten, Martin Farr, Bianca Werner, Sven Dittmann, Klaus Überla, Cornelia Piper, Karsten Niehaus, and Dieter Horstkotte. "Antiviral effect of Bosentan and Valsartan during coxsackievirus B3 infection of human endothelial cells." Journal of General Virology 91, no. 8 (August 1, 2010): 1959–70. http://dx.doi.org/10.1099/vir.0.020065-0.

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In viral myocarditis, adeno- and enteroviruses have most commonly been implicated as causes of infection. Both viruses require the human coxsackie-adenovirus receptor (CAR) to infect the myocardium. Due to its crucial role for viral entry, CAR-downregulation may lead to novel approaches for treatment for viral myocarditis. In this study, we report on pharmaceutical drug influences on CAR levels in human umbilical vein endothelial cells (HUVEC) and cervical carcinoma cells (HeLa) detected by immunoblotting, quantitative real time-PCR and cellular susceptibility to the cardiotropic coxsackie-B3 virus strain Nancy (CVB3). Our results indicate, for the first time, a dose-dependent CAR mRNA and protein downregulation upon Valsartan and Bosentan treatment. Most interestingly, drug-induced CAR diminution significantly reduced the viral load in CVB3-infected HUVEC. In order to assess the regulatory effects of both drugs in detail, we knocked down their protein targets, the G-protein coupled receptors angiotensin-II type-1 receptor (AT1R) and endothelin-1 type-A and -B receptors (ETAR/ETBR) in HUVEC. Receptor-specific gene silencing indicates that CAR gene expression is regulated by agonistic and antagonistic binding to ETBR, but not ETAR. In addition, neither stimulation nor inhibition of AT1R seemed to be involved in CAR gene regulatory processes. Our study indicates that Valsartan and Bosentan protected human endothelial cells from CVB3-infection. Therefore, besides their well-known anti-hypertensive effects these drugs may also protect the myocardium and other tissues from coxsackie- and adenoviral infection.

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15

Yongping, Han. "A Case of Laryngitis without Hoarseness Caused by Coxsackie virus In Group B." Otolaryngology Open Access Journal 7, no. 2 (2022): 1–2. http://dx.doi.org/10.23880/ooaj-16000247.

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A rare laryngitis patient who had no obvious inducement to severe laryngeal pain but had silent hoarseness, laryngoscopy showed only herpes, congestion and edema in the laryngeal cavity mucosa. After intravenous administration of acyclovir and methylprednisolone, the symptoms of laryngeal pain were significantly alleviated on the same day and recovered in 5 days. Through the diagnosis and treatment of this patient, it is suggested that Coxsackie virus B can only invade the laryngeal cavity mucosa and sensory nerve endings without invading the vocal cords.

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16

Szopa, T. M., D. R. Gamble, and K. W. Taylor. "Biochemical changes induced by Coxsackie B4 virus in short-term culture of mouse pancreatic islets." Bioscience Reports 5, no. 1 (January 1, 1985): 63–69. http://dx.doi.org/10.1007/bf01117442.

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Isolated mouse pancreatic islets were infected in vitro with two strains of Coxsackie B4 virus – a tissue culture – adapted strain and a mouse pancreas-adapted strain. Within 48 h of infection changes had occurred in the biochemical activities of islets infected with the mouse pancreas-adapted strain of virus. Basal insulin release was increased two-fold in these islets, while glucose-induced insulin secretion remained unchanged. Insulin biosynthesis was greatly reduced at a sti, mulatory concentration of glucose (20 raM), thus leading to a reduced insulin content in these islets. These effects are of importance because they demonstrate that certain strains of Coxsackie B4 virus, like encephalo-myocarditis virus, may selectively alter B-cell function in vitro.

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17

Bhambhani, Vikas, Jacob Abraham, Mohit Sahni, A. K. Harit, Shashi Khare, and Jacob M. Puliyel. "Outbreak of Coxsackie B4 arthritis among newborns and staff of a neonatal unit." Tropical Doctor 37, no. 3 (July 1, 2007): 188–89. http://dx.doi.org/10.1258/004947507781524728.

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We investigated an outbreak of Coxsackie B4 arthritis in a neonatal unit involving 20 neonates and 12 staff members, over an eight-month period. Laboratory investigations, serology tests, indicate that the outbreak was caused by Coxsackie B4 virus. Contamination of one of the overhead water reservoirs, supplying the nursery, was responsible. After the water tanks were cleaned out, no new cases were reported over five years.

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18

Wang, Ru-Bing, Shuang-Gang Ma, Cooper S. Jamieson, Rong-Mei Gao, Yun-Bao Liu, Yong Li, Xiao-Jing Wang, et al. "Library construction of stereochemically diverse isomers of spirooliganin: their total synthesis and antiviral activity." Chemical Science 12, no. 20 (2021): 7003–11. http://dx.doi.org/10.1039/d1sc01277k.

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19

Cioroba, Teodora, Corina Gica, Radu Botezatu, Mihaela Demetrian, Nicolae Gica, Gheorghe Peltecu, Anca Marina Ciobanu, Brindusa Ana Cimpoca-Raptis, and Anca Maria Panaitescu. "Coxsackie virus B infection and pregnancy." Romanian Journal of Infectious Diseases 24, S (November 30, 2021): 66–69. http://dx.doi.org/10.37897/rjid.2021.s.14.

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Frequently, enteroviral infection with Coxsackie virus B (CV-B) goes unnoticed, without or only with mild symptoms. The infection is well known for the gastro-intestinal transmission, but recently, the severe forms of neonate’s infection, suggested that vertical transmission should not be neglected and moreover the fetal consequences should be studied. This review relates the most important findings regarding infection with CV-B during pregnancy, most of the information being based on murine studies. It seems that CV-B infection is associated with high rate of abortion and could also impair fertility. Regarding long term effects, CV-B might cause autoimmune diseases, congenital heart defects and neurologic disorders. Severe acute disease in new-born is generally acquired from a symptomatic mother that develop a febrile illness during the last week of pregnancy.

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20

Trayer, James, and Claudia Gore. "Severe eczema flare and Coxsackie virus." BMJ Case Reports 15, no. 2 (February 2022): e247656. http://dx.doi.org/10.1136/bcr-2021-247656.

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21

Tate, J., M. Smyth, T. Hyypiä, and D. Stuart. "Crystal structure of coxsackie virus A9." Acta Crystallographica Section A Foundations of Crystallography 52, a1 (August 8, 1996): C183. http://dx.doi.org/10.1107/s0108767396091970.

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22

Foster, Harold D. "Coxsackie B virus and myocardial infarction." Lancet 359, no. 9308 (March 2002): 804. http://dx.doi.org/10.1016/s0140-6736(02)07871-6.

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23

Zaher, S. R., A. S. Kassem, and J. J. Hughes. "Coxsackie virus infections in rheumatic fever." Indian Journal of Pediatrics 60, no. 2 (March 1993): 289–98. http://dx.doi.org/10.1007/bf02822194.

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24

Zarubaev, V. V., A. V. Slita, E. O. Sinegubova, A. A. Muryleva, and I. N. Lavrentieva. "Anti-viral activity of enisamium iodide against viruses of influenza and ARVI’s on different cell lines." Terapevticheskii arkhiv 92, no. 11 (December 26, 2020): 45–50. http://dx.doi.org/10.26442/00403660.2020.11.000872.

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Influenza and ARVI represent the most numerous and dangerous group of causative agents of respiratory infections human. Aim. Characterization of the antiviral properties of enisamium iodide against human respiratory viruses in in vitro experiments. Materials and methods. In the course of experiments, the cytotoxic properties of enisamium iodide were studied against the cell lines Vero, MA-104, A549, L-41 and HEp-2. The antiviral activity of enisamium iodide was studied using virus yield reduction assay against influenza viruses, parainfluenza virus, respiratory syncytial virus, Coxsackie B3 and Coxsackie B4 viruses, as well as adenoviruses types 5 and 6. Results. The most sensitive to the action of enisamium iodide was the human parainfluenza virus, whose activity decreased by 2.3 orders of magnitude under the action of the drug in A549 cells. Of the cell cultures used, enisamium iodide exhibited the maximum antiviral effect in human lung carcinoma cells A549, where, in its presence, the level of reproduction of adenoviruses of types 5 and 6, Coxsackie viruses B3 and B4, and human parainfluenza virus decreased by an order of magnitude or more. The antiviral activity of enisamium iodide was least manifested in Vero cells. Conclusion. According to the results of in vitro experiments, enisamium iodide can be considered as an antiviral drug with a wide spectrum of activity against human respiratory viruses.

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25

Tang, DO, MPH, Wesley, Sulagna Das, MD, and Zoltán Krudy, MD. "Coxsackie Virus Induced Graves’ Disease in an Immunocompetent Patient." International Journal of Innovative Research in Medical Science 6, no. 10 (October 10, 2021): 731–34. http://dx.doi.org/10.23958/ijirms/vol06-i10/1231.

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Enteroviruses, such as Coxsackie virus, have been implicated in the past as a pathogen associated with subacute thyroiditis, also known as de Quervain’s thyroiditis. Less commonly are viruses associated with autoimmune thyroid diseases such as Hashimoto’s thyroiditis and Graves’ disease. We present a case of a healthy 43 year old female who presented to the emergency department complaining of several months of weakness, nausea, loose bowel movements, anxiousness, and shortness of breath. Physical exam revealed tachycardia, tremors, and a non-tender thyroid gland to palpation. Skin exam showed a rash on the palms of her hands and soles of her feet bilaterally with dark papules, suggestive of Hand, foot, and mouth disease. Laboratory workup would reveal an undetectable thyroid stimulating hormone (TSH), and levels of T3 & T4 too high to quantify. Thyroid receptor antibodies would return as positive, diagnostic of Graves’ disease. Coxsackie virus (the causative agent of Hand, foot, and mouth disease) IgM titers also returned positive suggesting recent infection. Although the etiology of Graves’ disease is still not clear, this case report provides evidence that environmental triggers such as Coxsackie viral infection may be involved in its pathogenesis.

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26

Mehta, Alaap, Kali Larson, Bindu Sarika Ganapathineedi, Esteffania Villegas, Susmitha Dande, Wahaj Ahmed, and Nadew Sebro. "An Out-of-Season Case of Coxsackie B Myocarditis with Severe Rhabdomyolysis." Case Reports in Infectious Diseases 2018 (October 30, 2018): 1–4. http://dx.doi.org/10.1155/2018/4258296.

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A 21-year-old woman was found to have fulminant myocarditis as a result of Coxsackie B infection (a virus shown to exhibit summer-fall seasonality) in mid-December. In this case report, seasonality of enteroviruses is examined, as well as additional factors which may contribute to sporadic cases during winter months. The case report also discusses clinical criteria for endomyocardial biopsy, utility of PCR vs. antibody serological tests, coinfection with multiple serotypes, and rhabdomyolysis in Coxsackie B.

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27

Dorta-Contreras, Alberto J., Piotr Lewczuk, Bárbara Padilla-Docal, Elena Noris-García, Raisa Bu Coifiu-Fanego, Consuelo Sánchez-Martínez, Alexis Rodríguez-Rey, and Marlén González-Hernández. "sICAM-1 intrathecal synthesis and release during the acute phase in children suffering from Coxsackie A9 and S. pneumoniae meningoencephalitis." Arquivos de Neuro-Psiquiatria 66, no. 3a (September 2008): 504–8. http://dx.doi.org/10.1590/s0004-282x2008000400013.

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The intercellular adhesion molecule is a transmembrane glycoprotein belonging to the immunoglobulin superfamily. Serum and cerebrospinal fluid (CSF) soluble intercellular adhesion molecule 1 (sICAM-1) from normal control children as well as from children with Guillain-Barré syndrome (GBS), with Coxsackie A9 virus meningoencephalitis and with Streptococcus pneumoniae meningoencephalitis were studied. sICAM-1 was quantified using an immunoenzimatic assay and albumin using the immunodiffusion technique in both biological fluids. Increased sICAM-1 values in CSF in patients with GBS correspond to an increase of the albumin CSF/serum quotient. In contrast, in inflammatory diseases like S. pneumoniae and Coxsackie A9 virus meningoencephalitis an increased brain-derived fraction was observed. In particular cases these values are 60-65% and 70-75% respectively. The results indicate an additional synthesis of sICAM-1 in subarachnoidal space during central nervous system (CNS) inflammatory process. An important role of sICAM-1 in the transmigration of different cell types into CSF during CNS inflammation in children with S. pneumoniae and Coxsackie A9 meningoencephalitis may be suggested.

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Andriushkova, Natalia G., Volodymyr P. Shyrobokov, Nataliia S. Turchyna, Valentyna V. Melnyk, Olena V. Kuzminska, and Ludmyla V. Dolinchuk. "RESEARCH OF BIOLOGICAL PROPERTIES OF ENTEROVIRUS STRAINS ASSOCIATED WITH ISCHEMIC STROKE." Wiadomości Lekarskie 73, no. 3 (2020): 423–27. http://dx.doi.org/10.36740/wlek202003102.

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Introduction: The research of biological properties of enteroviruses associated with ischemic stroke (IS) allows us to identify their intratypic differences. The aim: to identify genetic markers of strains of enteroviruses associated with IS. Materials and methods: 11 strains of enteroviruses isolated from the serum of patients with IS were identified in the virus neutralization test. Genetic markers of isolated strains (Abent, marker S, marker rct40) were determined. Results: Eleven strains of enteroviruses were isolated from the serum of patients with IS. Eight viruses: Coxsackie B viruses (serotypes 2, 3, 4) and ECHO viruses (serotypes 6, 9, 27 (two strains), 29) were identified in these strains. Other three strains of enteroviruses were unidentified. Different combinations of genetic markers were found. Seven strains of enteroviruses (Coxsackie B2, B3, ECHO 6, ECHO 9, ECHO 27 (two strains) and one unidentified virus) had virulence markers: Abent–, rct40+ and S−. Three strains (Coxsackie B4, ECHO 29, one unidentified virus) had markers: Abent–, rct40+, S+. Another one unidentified virus had markers: Abent+, rct40+, S –. Conclusions: All 11 isolates of enteroviruses associated with IS had rct40+ marker, 10 of the 11 isolates had marker Abent– and 8 of 11 isolates had marker S–. The research of genetic markers allows to perform typic and intratypic differentiation of strains of enteroviruses associated with the IS.

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29

Gil, Pedro, João Gil, Catarina Paiva, Guilherme Castela, and Rui Castela. "Medical and Surgical Treatment in Pediatric Orbital Myositis Associated with Coxsackie Virus." Case Reports in Ophthalmological Medicine 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/917275.

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Purpose.To report a case of orbital myositis associated with Coxsackie virus and its medical and surgical approach.Methods.Complete ophthalmological examination and imaging and analytical investigation were performed.Results. A 6-year-old male presented with subacute painless binocular horizontal diplopia. Examination revealed bilateral best-corrected visual acuity (BCVA) of 20/20 and right eye 45-prism-dioptre (PD) esotropia in near and distance fixations, with no motility restrictions. Serologic screening was positive for Coxsackie virus acute infection and computerized tomography (CT) suggested right eye medial rectus orbital myositis. An oral corticosteroid 1.0 mg/kg/day regimen was started. A new CT after two months showed symmetrical lesions in both medial rectus muscles. Corticosteroids were increased to 1.5 mg/kg/day. After imagiological resolution on the 4th month, alternating 45 PD esotropia persisted. Bilateral 7 mm medial rectus recession was performed after 1 year without spontaneous recovery. At 1-year follow-up, the patient is orthophoric with 200′′ stereopsis and bilateral 20/20 BCVA.Conclusions. To our knowledge, this is the first reported case of orbital myositis associated with Coxsackie virus. This is also the first reported case of isolated strabismus surgery after orbital myositis in pediatric age, highlighting the favourable aesthetic and functional outcomes even in cases of late ocular motility disorders.

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30

Helial, Marwa Naeem, and Ahmed Hasan Mohammed. "Investigation of Coxsackie Virus Type B in Grave’s Thyroiditis." Pakistan Journal of Medical and Health Sciences 16, no. 6 (June 30, 2022): 745–47. http://dx.doi.org/10.53350/pjmhs22166745.

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Thyroiditis is a broad term that refers to a variety of clinical conditions marked by inflammation and damage to thyroid cells. These disorders can be chronic or acute, include lymphocytic infiltration, have a microbial cause, or be linked to autoimmune thyroid disease, such as in Graves’ disease (GD). This cross-sectional study aimed to detect anti-TSH antibodies and investigate Coxsackie virus B (CVB) IgM and IgG antibodies in the serum of patients to know their role in the pathogenesis of thyroiditis. The study included 91 patients suffering from thyroid dysfunction through thyroid hormone tests (FT3, FT4 and TSH) by Snibe Maglumi-800 Chemiluminescence Immunoassay, where they were divided into three groups (subclinical thyroiditis, hypothyroidism and hyperthyroidism). To determine which of them has Graves’ disease, detection of anti-TSH Ab have been performed then detection of antibodies to specific CVB IgM and IgG in the sera of patients by ELISA. The results of serology showed that the percentage of anti-TSH antibodies in the three groups was (68.13%), and the percentage was the highest in the hyperthyroidism group, which amounted to (85%). The serological diagnosis also showed that the presence of antibodies to CVB IgM was (65.93%) while, IgG levels were (20.87%). Conclusions: Coxsackie virus B infection is commonly seen in patients with thyroiditis and may have a role in the its pathogenesis. Keywords: Coxsackie virus B, Graves’ disease, Thyroiditis

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31

Stanisavljević, Sanja, and Divna Kekuš. "Prevention measures and suppression of coxsackie virus infection in health institutions." Sestrinska rec 21, no. 75 (2017): 6–9. http://dx.doi.org/10.5937/sestrec1774006s.

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Ayala Curiel, Javier, Ana Isabel Jiménez Moya, Raúl Gracia Remiro, Carlos Santana Rodríguez, Modesto Herrera Martín, and Soledad Jiménez Casso. "Hemiplejía aguda infantil por virus Coxsackie B." Revista de Neurología 37, no. 08 (2003): 736. http://dx.doi.org/10.33588/rn.3708.2003169.

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WONG, S. N., A. Y. C. TAM, T. H. K. NG, W. F. NG, C. Y. TONG, and T. S. TANG. "Fatal coxsackie B1 virus infection in neonates." Pediatric Infectious Disease Journal 8, no. 9 (September 1989): 638–41. http://dx.doi.org/10.1097/00006454-198909000-00015.

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Berlacher, Mark, Amber Oberle, and Khalil Diab. "Coxsackie B Virus: The Enigmatic Effusion Culprit." Chest 148, no. 4 (October 2015): 102A. http://dx.doi.org/10.1378/chest.2221961.

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35

Bowles, N. E., C. A. Sewry, V. Dubowitz, and L. C. Archard. "DERMATOMYOSITIS, POLYMYOSITIS, AND COXSACKIE-B-VIRUS INFECTION." Lancet 329, no. 8540 (May 1987): 1004–7. http://dx.doi.org/10.1016/s0140-6736(87)92271-9.

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LEVI, G., S. SCALVINI, M. VOLTERRANI, S. MARANGONI, G. AROSIO, and A. QUADRI. "Coxsackie virus heart disease: 15 years after." European Heart Journal 9, no. 12 (December 1988): 1303–7. http://dx.doi.org/10.1093/oxfordjournals.eurheartj.a062447.

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37

Gin, Alexander, Emma King, Emma Scardamaglia, and David Orchard. "Eczema exacerbation caused by Coxsackie virus A6." Australasian Journal of Dermatology 59, no. 1 (July 20, 2017): 64–65. http://dx.doi.org/10.1111/ajd.12677.

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38

Starakis, Ioannis, Markos Marangos, Sofia Giali, and Harry Bassaris. "Acute transverse myelitis due to Coxsackie virus." Journal of Clinical Neuroscience 12, no. 3 (April 2005): 296–98. http://dx.doi.org/10.1016/j.jocn.2004.03.031.

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39

Eggers, H. J., and TH Mertens. "PERSISTENCE OF COXSACKIE B VIRUS-SPECIFIC IgM." Lancet 328, no. 8501 (August 1986): 284. http://dx.doi.org/10.1016/s0140-6736(86)92102-1.

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40

Mancia, D., F. Geminiani, A. Fiocchi, D. Medici, A. Marbini, G. Magnani, and G. Pavesi. "Pandysautonomic neuropathy associated with coxsackie virus infection." Electroencephalography and Clinical Neurophysiology 75 (January 1990): S90. http://dx.doi.org/10.1016/0013-4694(90)92044-w.

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41

NIKOSKELAINEN, JUKKA, J. LENNART KALLIOMÁKI, KAISA LAPINLEIMU, MIRJA STENVIK, and PEKKA E. HALONEN. "Coxsackie B Virus Antibodies in Myocardial Infarction." Acta Medica Scandinavica 214, no. 1 (April 24, 2009): 29–32. http://dx.doi.org/10.1111/j.0954-6820.1983.tb08566.x.

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42

Paul, F. M., and M. Yin-Murphy. "Coxsackie B. Virus Infection in Singapore Children." Journal of Tropical Pediatrics 31, no. 2 (April 1, 1985): 96–100. http://dx.doi.org/10.1093/tropej/31.2.96.

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Badurdeen, Dilhana, Magdy Girgis, Andrew Sanderson, and Adeyinka Laiyemo. "Coxsackie Virus: An Unusual Cause of Pancreatitis." American Journal of Gastroenterology 108 (October 2013): S88. http://dx.doi.org/10.14309/00000434-201310001-00290.

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Muir, P., F. Nicholson, J. E. Banatvala, and P. J. Bingley. "Coxsackie B virus and postviral fatigue syndrome." BMJ 302, no. 6777 (March 16, 1991): 658–59. http://dx.doi.org/10.1136/bmj.302.6777.658-b.

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Chun-yan, Guo, Han Bo, Chang Hong, Jiang Hong-lei, and Han Xiu-zhen. "Anti-perforin neutralizing antibody reduces myocardial injury in viral myocarditis." Cardiology in the Young 19, no. 6 (October 14, 2009): 601–7. http://dx.doi.org/10.1017/s104795110999182x.

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AbstractAimTo investigate the role of anti-perforin neutralizing antibody in viral myocarditis.MethodsWe divided 45 Balb/c mice randomly into 3 groups, a normal control group, a control group inoculated with coxsackie virus B3, and a group inoculated with anti-perforin neutralizing antibody. The second group was inoculated with 0.15 milliliters coxsackie virus B3, and the third group additionally with 0.1milligrams/kilogram anti-perforin neutralizing antibody at time points of 6 hours and 3 days after infection. Histopathology was performed using haematoxylin and eosin, with apoptosis examined by the terminal transferase-mediated 2′-deoxyuridine 5′-triphosphate-biotin nick, end-labeling method, or Tunel. The expression of caspase-3 in myocardium was investigated by immunohistochemistry and reverse-transcription polymerase chain reaction.ResultsThe pathologic score, myocardial viral titers, average percentages of apoptotic cardiomyocytes, expression of active caspase-3 protein and messenger ribonucleic acid in the myocardium of the mice receiving anti-PFP neutralizing antibody therapy were all significantly reduced when compared to values from the group inoculated with coxsackie virus B3. The rates of expression of Caspase-3 and myocardial apoptosis were positively correlated with the scores for myocardial pathology.ConclusionOur results suggest that anti- perforin neutralizing antibody can reduce the myocardial damage by blocking the perforin/granzyme pathway, and downregulating the expression of messenger ribonucleic acid and protein of Caspase-3. These approaches may offer promising novel therapeutic strategies for the clinical treatment of viral myocarditis.

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Ivanova, Stefka Kr, Svetla G. Angelova, Asya P. Stoyanova, Irina L. Georgieva, Lubomira K. Nikolaeva-Glomb, Zafira G. Mihneva, and Neli St Korsun. "Serological and Molecular Biological Studies of Parvovirus B19, Coxsackie B Viruses, and Adenoviruses as Potential Cardiotropic Viruses in Bulgaria." Folia Medica 58, no. 4 (December 1, 2016): 250–56. http://dx.doi.org/10.1515/folmed-2016-0036.

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AbstractBackground:Inflammatory diseases of the heart (myocarditis, pericarditis) are commonly caused by viruses. Among the human cardiotropic viruses, parvovirus B19, Coxsackie B viruses, and adenoviruses play a leading role.Aim:The aim of the present study was to determine the presumptive causative role of parvovirus B19, Coxsackie B viruses, and adenoviruses in the development of myocarditis, pericarditis and dilated cardiomyopathy by demonstrating the presence of specific antiviral antibodies or viral DNA in patients’ serum samples.Materials and methods:We tested serum samples collected between 2010 and 2014 from 235 patients with myocarditis (n=108), pericarditis (n=79), myopericarditis (n=19), dilated cardiomyopathy (n=7), and fever of unknown origin accompanied by cardiac complaints (n=22). The mean age of patients with the standard deviation was 33 ± 18 years. Serological and molecular methods (ELISA for specific IgM/IgG antibodies to parvovirus B19 and IgM antibodies to Coxsackie B viruses and adenoviruses, and PCR for detection of parvovirus B19 in serum samples, respectively) were used in the study.Results:Of all tested 235 serum samples, in 60 (25.5%) positive results for at least one of the three tested viruses were detected. Forty out of these 235 serum samples (17%) were Coxsackie B virus IgM positive. They were found in 17% (18/108) of the patients with myocarditis, in 15% (12/79) of those with pericarditis, in 16% (3/19) of those with myopericarditis and in 32% (7/22) in those with fever of unknown origin. The 63 Coxsackie B virus IgM negative patient’s serum samples were tested by ELISA for presence of adenovirus IgM antibodies. Such were found in 4 patients with pericarditis and in 2 patients with fever of unknown origin. Every IgM negative sample (n=189) for Coxsackie B and adenovirus was further tested by ELISA for parvovirus B19 IgM/IgG antibodies. B19-IgM antibodies were detected in 14 patients (7.4%). The percentages for B19-IgM antibodies was 8% (7/90), 5% (3/63) and 31% (4/13) in the patients affected with myocarditis, pericarditis, and fever of unknown origin, respectively. Protective B19-IgG antibodies were found in 108 (57%) of the samples. A B19-PCR signal was detected in all the patients who were B19-IgM positive, and in only 1 patient with positive B19-IgG result, the latter presenting with dilated cardiomyopathy.Conclusion:The present study shows the involvement of Coxsackie B, parvovirus B19 and adenoviruses in the development of inflammatory diseases of the heart (myocarditis and pericarditis). It is the first ever study in the country that simultaneously analyzes the prevalence of the three major human cardiotropic viruses.

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Richardson, Ciarán, Paul Brennan, Martin Powell, Stuart Prince, Yun-Hsiang Chen, O. Brad Spiller, and Martin Rowe. "Susceptibility of B lymphocytes to adenovirus type 5 infection is dependent upon both coxsackie–adenovirus receptor and αvβ5 integrin expression." Journal of General Virology 86, no. 6 (June 1, 2005): 1669–79. http://dx.doi.org/10.1099/vir.0.80806-0.

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Human lymphocytes are resistant to genetic modification, particularly from recombinant adenoviruses, thus hampering the analysis of gene function using adenoviral vectors. This study engineered an Epstein–Barr virus-transformed B-lymphoblastoid cell line permissive to adenovirus infection and elucidated key roles for both the coxsackie–adenovirus receptor and αvβ5 integrin in mediating entry of adenoviruses into these cells. The work identified a strategy for engineering B cells to become susceptible to adenovirus infection and showed that such a strategy could be useful for the introduction of genes to alter lymphoblastoid-cell gene expression.

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48

McIntyre, J. P., and G. A. Keen. "Laboratory surveillance of viral meningitis by examination of cerebrospinal fluid in Cape Town, 1981–9." Epidemiology and Infection 111, no. 2 (October 1993): 357–71. http://dx.doi.org/10.1017/s095026880005706x.

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SummaryNine years accumulated laboratory data derived from the culture of the cerebrospinal fluid of 11 360 aseptic meningitis cases were retrospectively reviewed to establish the epidemiology of viral meningitis in Cape Town. Virus was isolated from 3406 of the cases (91% enteroviruses and 9% mumps).Five major summer viral meningitis episodes were documented: two of echovirus 4 (706 and 445 cases), echovirus 9 (223), coxsackie A9 (104) and one of unidentified enterovirus (324 cases – probably echo 9). Although coxsackie B was endemic, clusters of one or other type were dominant at any one time. Mumps was endemic. Sixty-two percent of all viral cases were <5 years old. The median ages of 4 and 5 years in echoviruses 9 and 4 (the epidemic strains) contrasted with that of 1 year in coxsackie B (with many cases <3 months old). Mumps peaked at 3–4 years of age. Males dominated overall, particularly in mumps.

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Hohn, Arno R., and Robert E. Stanton. "Myocarditis in Children." Pediatrics In Review 9, no. 3 (September 1, 1987): 83–88. http://dx.doi.org/10.1542/pir.9.3.83.

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Acute myocarditis may go undetected. Nearly half of the known cases of myocarditis are caused by coxsackie B virus. Findings in myocarditis are often nonspecific. Echo cardiograms show reduced function. Some cases of myocarditis progress to cardiomyopathy.

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50

Schoub, Barry D., Sylvia Johnson, Jo M. McAnerney, Isabel L. Dos Santos, and Katalin I. M. Klaassen. "Epidemic Coxsackie B virus infection in Johannesburg, South Africa." Journal of Hygiene 95, no. 2 (October 1985): 447–55. http://dx.doi.org/10.1017/s0022172400062872.

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SUMMARYA particularly extensive epidemic of Coxsackie B3 virus infection occurred in Johannesburg in the spring and summer of 1984. A total of 142 positive cases were diagnosed by isolation of the virus from stools and other specimens (60) or by serology (82). Coxsackie B3 accounted for 87% of the isolations and was also the dominant serotype on serology.The outbreak involved predominantly children and young adults, with no apparent sex differences being noted. The majority of specimens came from the white population and no significant difference in age or sex distribution could be observed between the two race groups. The major clinical presentation in the white group was Bornholm disease followed by cardiac involvement and then meningoencephalitis. In the black group, however, myocarditis was the major clinical presentation, which is of particular interest taking into account the extremely high incidence of acute rheumatic carditis in this population and the prevalence of chronic cardiomyopathy.

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