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1. Biomedical articles (top 50; 2009 to 2014)
1. |||||||||. 100%  Fechner H, Pinkert S, Geisler A, Poller W, Kurreck J: Pharmacological and biological antiviral therapeutics for cardiac coxsackievirus infections. Molecules; 2011;16(10):8475-503
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacological and biological antiviral therapeutics for cardiac coxsackievirus infections.
  • Damage to the heart is induced both directly by virally mediated cell destruction and indirectly due to the immune and autoimmune processes reacting to virus infection.
  • This review addresses antiviral therapeutics for cardiac coxsackievirus infections discovered over the last 25 years.
  • One group represents pharmacologically active low molecular weight substances that inhibit virus uptake by binding to the virus capsid (e.g., pleconaril) or inactivate viral proteins (e.g., NO-metoprolol and ribavirin) or inhibit cellular proteins which are essential for viral replication (e.g., ubiquitination inhibitors).
  • Soluble receptor analogues (e.g., sCAR-Fc) bind to the virus capsid and block virus uptake.
  • Small interfering RNAs, short hairpin RNAs and antisense oligonucleotides bind to and led to degradation of the viral RNA genome or cellular RNAs, thereby preventing their translation and viral replication.
  • Most recently mesenchymal stem cell transplantation has been shown to possess antiviral activity in CVB3 infections.
  • Taken together, a number of antiviral therapeutics has been developed for the treatment of myocardial CVB infection in recent years.
  • In addition to low molecular weight inhibitors, biological therapeutics have become promising anti-viral agents.
  • [MeSH-major] Coxsackievirus Infections / drug therapy. Coxsackievirus Infections / therapy. Myocarditis / drug therapy. Myocarditis / virology

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  • (PMID = 21989310.001).
  • [ISSN] 1420-3049
  • [Journal-full-title] Molecules (Basel, Switzerland)
  • [ISO-abbreviation] Molecules
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Oligonucleotides, Antisense; 0 / RNA, Small Interfering; 9008-11-1 / Interferons
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2. ||||||.... 60%  Jurgeit A, Moese S, Roulin P, Dorsch A, Lötzerich M, Lee WM, Greber UF: An RNA replication-center assay for high content image-based quantifications of human rhinovirus and coxsackievirus infections. Virol J; 2010;7:264
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  • [Title] An RNA replication-center assay for high content image-based quantifications of human rhinovirus and coxsackievirus infections.
  • BACKGROUND: Picornaviruses are common human and animal pathogens, including polio and rhinoviruses of the enterovirus family, and hepatitis A or food-and-mouth disease viruses.
  • The existing and also emerging HRVs pose severe health risks for patients with asthma or chronic obstructive pulmonary disease.
  • Here, we developed a serotype-independent infection assay using a commercially available mouse monoclonal antibody (mabJ2) detecting double-strand RNA.
  • RESULTS: Immunocytochemical staining for RNA replication centers using mabJ2 identified cells that were infected with either HRV1A, 2, 14, 16, 37 or coxsackievirus (CV) B3, B4 or A21.
  • MabJ2 labeled-cells were immunocytochemically positive for newly synthesized viral capsid proteins from HRV1A, 14, 16, 37 or CVB3, 4.
  • We optimized the procedure for detection of virus replication in settings for high content screening with automated fluorescence microscopy and single cell analysis.
  • Our data show that the infection signal was dependent on multiplicity, time and temperature of infection, and the mabJ2-positive cell numbers correlated with viral titres determined in single step growth curves.
  • The mabJ2 infection assay was adapted to determine the efficacy of anti-viral compounds and small interfering RNAs (siRNAs) blocking enterovirus infections.
  • CONCLUSIONS: We report a broadly applicable, rapid protocol to measure infection of cultured cells with enteroviruses at single cell resolution.
  • This assay can be applied to a wide range of plus-sense RNA viruses, and hence allows comparative studies of viral infection biology without dedicated reagents or procedures.
  • This protocol also allows to directly compare results from small compound or siRNA infection screens for different serotypes without the risk of assay specific artifacts.
  • [MeSH-major] Enterovirus / growth & development. RNA, Viral / metabolism. Rhinovirus / growth & development. Virus Replication
  • [MeSH-minor] Antibodies, Monoclonal / diagnostic use. Antibodies, Viral / diagnostic use. Automation / methods. Cells, Cultured. Humans. Immunohistochemistry / methods. Microbial Sensitivity Tests / methods. Microscopy, Fluorescence / methods. Molecular Sequence Data. Sequence Analysis, DNA. Staining and Labeling / methods. Virus Cultivation / methods

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  • (PMID = 20937137.001).
  • [ISSN] 1743-422X
  • [Journal-full-title] Virology journal
  • [ISO-abbreviation] Virol. J.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ HQ336413/ HQ336414/ HQ336415/ HQ336416/ HQ336417/ HQ336418/ HQ336419/ HQ336420
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Viral; 0 / RNA, Viral
  • [Other-IDs] NLM/ PMC2958916
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3. |......... 10%  Hühn MH, McCartney SA, Lind K, Svedin E, Colonna M, Flodström-Tullberg M: Melanoma differentiation-associated protein-5 (MDA-5) limits early viral replication but is not essential for the induction of type 1 interferons after Coxsackievirus infection. Virology; 2010 May 25;401(1):42-8
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  • [Title] Melanoma differentiation-associated protein-5 (MDA-5) limits early viral replication but is not essential for the induction of type 1 interferons after Coxsackievirus infection.
  • Coxsackievirus infections are associated with severe diseases such as myocarditis, meningitis and pancreatitis.
  • To study the contribution of the intracellular viral sensor melanoma differentiation-associated protein-5 (MDA-5) in the host immune response to Coxsackievirus B3 (CVB3) we infected C57BL/6 and 129/SvJ mice lacking mda-5.
  • Mice deficient in MDA-5 showed a dramatically increased susceptibility to CVB3 infection.
  • The loss of MDA-5 allowed the virus to replicate faster, resulting in increased liver and pancreas damage and heightened mortality.
  • MDA-5 was not absolutely required for the induction of type 1 interferons (IFNs), but essential for the production of maximal levels of systemic IFN-alpha early after infection.
  • Taken together, our findings indicate that MDA-5 plays an important role in the host immune response to CVB3 by preventing early virus replication and limiting tissue pathology.
  • [MeSH-major] Coxsackievirus Infections / immunology. Coxsackievirus Infections / virology. DEAD-box RNA Helicases / physiology. Enterovirus / physiology. Virus Replication
  • [MeSH-minor] Animals. Interferon Type I / biosynthesis. Mice. Mice, Inbred C57BL. Mice, Knockout. Virus Attachment

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  • (PMID = 20206372.001).
  • [ISSN] 1096-0341
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / F30HL096354
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Type I; EC 3.6.1.- / Ifih1 protein, mouse; EC 3.6.4.13 / DEAD-box RNA Helicases
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4. |......... 4%  Burke JD, Sonenberg N, Platanias LC, Fish EN: Antiviral effects of interferon-β are enhanced in the absence of the translational suppressor 4E-BP1 in myocarditis induced by Coxsackievirus B3. Antivir Ther; 2011;16(4):577-84
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  • [Title] Antiviral effects of interferon-β are enhanced in the absence of the translational suppressor 4E-BP1 in myocarditis induced by Coxsackievirus B3.
  • BACKGROUND: Viral myocarditis is most frequently associated with infection by Coxsackievirus B3 (CVB3).
  • METHODS: In the present study we have investigated the role of translational suppression in the context of an IFN-α/β-mediated antiviral immune response to CVB3 infection.
  • Extending these in vitro studies, we examined the effects of CVB3 infection and IFN-β treatment in 4E-BP1(-/-) mice.
  • Similarly, 4E-BP1(-/-) mice are more sensitive to treatment with IFN-β, exhibiting lower viral titres in heart tissue than 4E-BP1(+/+) mice during the course of infection.
  • [MeSH-major] Coxsackievirus Infections / drug therapy

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  • (PMID = 21685545.001).
  • [ISSN] 2040-2058
  • [Journal-full-title] Antiviral therapy
  • [ISO-abbreviation] Antivir. Ther. (Lond.)
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA77816; Canada / Canadian Institutes of Health Research / / MOP 15094; United States / NCI NIH HHS / CA / R01 CA077816-12
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Carrier Proteins; 0 / Eif4ebp1 protein, mouse; 0 / Phosphoproteins; 77238-31-4 / Interferon-beta
  • [Other-IDs] NLM/ NIHMS306798; NLM/ PMC3142995
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5. |......... 4%  Wikswo ME, Khetsuriani N, Fowlkes AL, Zheng X, Peñaranda S, Verma N, Shulman ST, Sircar K, Robinson CC, Schmidt T, Schnurr D, Oberste MS: Increased activity of Coxsackievirus B1 strains associated with severe disease among young infants in the United States, 2007-2008. Clin Infect Dis; 2009 Sep 1;49(5):e44-51
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  • [Title] Increased activity of Coxsackievirus B1 strains associated with severe disease among young infants in the United States, 2007-2008.
  • BACKGROUND: Enterovirus infections are very common and typically cause mild illness, although neonates are at higher risk for severe illness.
  • In 2007, the Centers for Disease Control and Prevention (CDC) received multiple reports of severe neonatal illness and death associated with coxsackievirus B1 (CVB1), a less common enterovirus serotype not previously associated with death in surveillance reports to the CDC.
  • Virus isolates or original specimens obtained from patients from 25 states were referred to the CDC picornavirus laboratory for molecular typing or characterization.
  • RESULTS: During 2007-2008, the NESS received 1079 reports of enterovirus infection.
  • Six neonatal deaths due to CVB1 infection were also reported to the CDC during that time.
  • Phylogenetic analysis of the 2007 and 2008 CVB1 strains indicated that the increase in cases resulted from widespread circulation of a single genetic lineage that had been present in the United States since at least 2001.
  • CONCLUSIONS: Healthcare providers and public health departments should be vigilant to the possibility of continuing CVB1-associated neonatal illness, and testing and continued reporting of enterovirus infections should be encouraged.
  • [MeSH-major] Coxsackievirus Infections / epidemiology. Coxsackievirus Infections / virology. Enterovirus B, Human
  • [MeSH-minor] Centers for Disease Control and Prevention (U.S.). Cluster Analysis. Humans. Infant, Newborn. Phylogeny. Sentinel Surveillance. Serotyping. United States / epidemiology

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  • (PMID = 19622041.001).
  • [ISSN] 1537-6591
  • [Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • [ISO-abbreviation] Clin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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6. |......... 4%  Yoon SY, Ha YE, Choi JE, Ahn J, Lee H, Kim DH: Autophagy in coxsackievirus-infected neurons. Autophagy; 2009 Apr;5(3):388-9
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  • [Title] Autophagy in coxsackievirus-infected neurons.
  • We recently found that coxsackievirus B4 (CVB4) also induces the autophagy pathway and activates the calpain system for replication in neurons.
  • Notably, the inhibition of autophagy with 3-methyladenine (3MA) reduced calpain activation and virus replication.
  • Calpain inhibitors also reduced autophagosome formation and virus replication.
  • This finding indicates that calpain and the autophagy pathway are closely connected with each other during the infection.
  • Interestingly, we also found that 3MA and calpain inhibitors enhanced the caspase-3 specific cleavage of spectrin during CVB4 infection, suggesting that autophagy inhibition by these drugs triggered apoptosis.
  • [MeSH-major] Autophagy / physiology. Coxsackievirus Infections / metabolism. Coxsackievirus Infections / virology
  • [MeSH-minor] Adenine / analogs & derivatives. Adenine / metabolism. Amino Acid Chloromethyl Ketones / pharmacology. Animals. Apoptosis. Calpain / metabolism. Caspases / metabolism. Cysteine Proteinase Inhibitors / pharmacology. Models, Biological. Neurons / metabolism. Neurons / virology. Rats. Sirolimus / pharmacology. Virus Replication / drug effects

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  • (PMID = 19158511.001).
  • [ISSN] 1554-8635
  • [Journal-full-title] Autophagy
  • [ISO-abbreviation] Autophagy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Cysteine Proteinase Inhibitors; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 5142-23-4 / 3-methyladenine; EC 3.4.22.- / Calpain; EC 3.4.22.- / Caspases; JAC85A2161 / Adenine; W36ZG6FT64 / Sirolimus
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7. |......... 8%  Yen FB, Chang LY, Kao CL, Lee PI, Chen CM, Lee CY, Shao PL, Wang SC, Lu CY, Huang LM: Coxsackieviruses infection in northern Taiwan--epidemiology and clinical characteristics. J Microbiol Immunol Infect; 2009 Feb;42(1):38-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coxsackieviruses infection in northern Taiwan--epidemiology and clinical characteristics.
  • BACKGROUND AND PURPOSE: The epidemiology of coxsackievirus has rarely been investigated in Taiwan.
  • This study was performed to ascertain the epidemiological and clinical characteristics of coxsackievirus infections in Taiwan.
  • METHODS: 457 patients treated at a medical center in northern Taiwan who were positive for coxsackievirus were enrolled in this retrospective study.
  • Patients' medical charts were reviewed for clinical diagnosis, physical examination, laboratory findings, and clinical manifestations.
  • RESULTS: Three serotypes of coxsackievirus A (A9, 5.3%; A10, 7.2%; A16, 87.5%) were identified among 265 patients, 27.4% of whom were admitted to hospital.
  • All 6 serotypes of coxsackievirus B (B1, 2.6%; B2, 7.8%; B3, 55.7%; B4, 2.1%; B5, 12.5%; B6, 1.0%; non-typable, 18.2%) were identified in 192 patients, 45.3% of whom were admitted to hospital.
  • Patients with coxsackievirus B infection had higher hospital admission rates (p < 0.001), more CNS involvement (p < 0.001), and longer fever duration (p < 0.001) than those with coxsackievirus A infection.
  • Patients with coxsackievirus A infection tended to have more skin manifestations (p < 0.001) and oral ulcers (p < 0.001).
  • Patients with coxsackievirus B infection were more likely to be admitted to hospital, had longer fever duration, and more CNS involvement than patients with coxsackievirus A infection.
  • [MeSH-major] Coxsackievirus Infections. Enterovirus

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  • (PMID = 19424557.001).
  • [ISSN] 1995-9133
  • [Journal-full-title] Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi
  • [ISO-abbreviation] J Microbiol Immunol Infect
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
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8. |......... 5%  Lind K, Svedin E, Utorova R, Stone VM, Flodström-Tullberg M: Type III interferons are expressed by Coxsackievirus-infected human primary hepatocytes and regulate hepatocyte permissiveness to infection. Clin Exp Immunol; 2014 Sep;177(3):687-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Type III interferons are expressed by Coxsackievirus-infected human primary hepatocytes and regulate hepatocyte permissiveness to infection.
  • Hepatitis is a common and potentially fatal manifestation of severe Coxsackievirus infections, particularly in newborn children.
  • Little is known of the immune-mediated mechanisms regulating permissiveness to liver infection.
  • It is well established that type I interferons (IFNs) play an important role in the host innate immune response to Coxsackievirus infections.
  • Recent studies have highlighted a role for another IFN family, the type III IFNs (also called IFN-λ), in anti-viral defence.
  • Whether type III IFNs are produced by hepatocytes during a Coxsackievirus infection remains unknown.
  • Moreover, whether or not type III IFNs protects hepatocytes from a Coxsackievirus infection has not been addressed.
  • In this study, we show that primary human hepatocytes respond to a Coxsackievirus B3 (CVB3) infection by up-regulating the expression of type III IFNs.
  • We also demonstrate that type III IFNs induce an anti-viral state in hepatocytes characterized by the up-regulated expression of IFN-stimulated genes, including IFN-stimulated gene (ISG15), 2'-5'-oligoadenylate synthetase 2 (OAS2), protein kinase regulated by dsRNA (PKR) and myxovirus resistance protein 1 (Mx1).
  • Our studies suggest that human hepatocytes express type III IFNs in response to a Coxsackievirus infection and highlight a novel role for type III IFNs in regulating hepatocyte permissiveness to this clinically relevant type of virus.

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  • [Copyright] © 2014 British Society for Immunology.
  • (PMID = 24773058.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Keywords] NOTNLM ; Coxsackievirus / anti-viral defence / enterovirus / hepatocytes / interferons
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9. |......... 4%  Sun Y, Wang X, Yuan S, Dang M, Li X, Zhang XC, Rao Z: An open conformation determined by a structural switch for 2A protease from coxsackievirus A16. Protein Cell; 2013 Oct;4(10):782-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An open conformation determined by a structural switch for 2A protease from coxsackievirus A16.
  • Coxsackievirus A16 belongs to the family Picornaviridae, and is a major agent of hand-foot-and-mouth disease that infects mostly children, and to date no vaccines or antiviral therapies are available.
  • Here we present the crystal structure of coxsackievirus A16 2A protease, which interestingly forms hexamers in crystal as well as in solution.
  • This structure shows an open conformation, with its active site accessible, ready for substrate binding and cleavage activity.
  • In addition, we compared the in vitro cleavage efficiency of 2A proteases from coxsackievirus A16 and enterovirus 71 upon the same substrates by fluorescence resonance energy transfer (FRET), and observed higher protease activity of enterovirus 71 compared to that of coxsackievirus A16.
  • In conclusion, our study shows an open conformation of coxsackievirus A16 2A protease and the underlying mechanisms for conformational conversion and substrate specificity.
  • [MeSH-major] Cysteine Endopeptidases / chemistry. Hand, Foot and Mouth Disease / enzymology. Picornaviridae / enzymology. Protein Conformation. Viral Proteins / chemistry
  • [MeSH-minor] Coxsackievirus Infections / virology. Crystallography, X-Ray. Fluorescence Resonance Energy Transfer. Humans. Structure-Activity Relationship. Substrate Specificity

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  • (PMID = 24026848.001).
  • [ISSN] 1674-8018
  • [Journal-full-title] Protein & cell
  • [ISO-abbreviation] Protein Cell
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Viral Proteins; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.22.29 / picornain 2A, Picornavirus
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10. |......... 4%  Chen SP, Huang YC, Li WC, Chiu CH, Huang CG, Tsao KC, Lin TY: Comparison of clinical features between coxsackievirus A2 and enterovirus 71 during the enterovirus outbreak in Taiwan, 2008: a children's hospital experience. J Microbiol Immunol Infect; 2010 Apr;43(2):99-104
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of clinical features between coxsackievirus A2 and enterovirus 71 during the enterovirus outbreak in Taiwan, 2008: a children's hospital experience.
  • BACKGROUND/PURPOSE: Coxsackievirus A2 (Cox A2) was the predominant serotype in the enterovirus outbreak in Taiwan, 2008.
  • However, detailed clinical features of Cox A2 infection have not been reported.
  • METHODS: A total of 280 hospitalized patients (97 with culture-proven EV71 infection and 183 with culture-proven Cox A2 infection) in 2008 at the Chang Gung Children's Medical Center were enrolled in this study.
  • Patients with EV71 infection had a significantly longer hospitalization period (4.1 vs. 3.0 days, p< 0.001).
  • Fever, fever for more than 3 days with a temperature above 39 degrees C, lethargy, poor activity, poor appetite and a myoclonic jerk were significantly associated with EV71 infection.
  • Fever, or fever with a temperature above 39 degrees C, febrile seizure, elevated white cell counts, and elevated serum C-reactive protein concentrations were significantly associated with Cox A2 infection.
  • Most patients with EV71 infection presented with hand-foot-mouth disease (78.3%), while most Cox A2-infected patients presented with herpangina (83.6%).
  • All the patients with Cox A2 infection showed total recovery.
  • One patient with EV71 infection died from encephalitis with cardiopulmonary failure, and 6.2% of EV71-infected children had neurologic sequelae.
  • Compared with those infected by EV71, the children with Cox A2 infection mostly presented with herpangina, had fewer central nervous system complications, and had better overall outcome.
  • [MeSH-major] Coxsackievirus Infections / epidemiology. Coxsackievirus Infections / pathology. Disease Outbreaks. Enterovirus / isolation & purification. Enterovirus Infections / epidemiology. Enterovirus Infections / pathology
  • [MeSH-minor] Central Nervous System Diseases / epidemiology. Central Nervous System Diseases / virology. Child. Child, Preschool. Female. Hand, Foot and Mouth Disease / epidemiology. Hand, Foot and Mouth Disease / pathology. Hand, Foot and Mouth Disease / virology. Herpangina / epidemiology. Herpangina / pathology. Herpangina / virology. Hospitals. Humans. Infant. Length of Stay. Male. Seasons. Sex Factors. Taiwan / epidemiology

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  • [Copyright] Copyright 2010 Taiwan Society of Microbiology. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20457425.001).
  • [ISSN] 1995-9133
  • [Journal-full-title] Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi
  • [ISO-abbreviation] J Microbiol Immunol Infect
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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11. |......... 4%  Huang WT, Lee PI, Chang LY, Kao CL, Huang LM, Lu CY, Chen JM, Lee CY: Epidemic pleurodynia caused by coxsackievirus B3 at a medical center in northern Taiwan. J Microbiol Immunol Infect; 2010 Dec;43(6):515-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epidemic pleurodynia caused by coxsackievirus B3 at a medical center in northern Taiwan.
  • Patients with known heart diseases or pulmonary consolidations were excluded.
  • Coxsackievirus B3 (CB3) was isolated in 15 (60%) of the 25 throat swab specimens.
  • Six patients were observed with tonsillar exudates and one was confirmed to have a CB3 urinary tract infection.
  • The clinical features and radiological findings suggest that CB3-associated epidemic pleurodynia might be a disease of the pleura and occasionally spreads to nearby tissues, resulting in chest wall myositis, pulmonary infiltrates and myopericarditis.
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Coxsackievirus Infections / epidemiology. Coxsackievirus Infections / physiopathology. Coxsackievirus Infections / radiography. Coxsackievirus Infections / virology. Female. Hospitals, University. Humans. Infant. Infant, Newborn. Male. Pharynx / virology. Pleurisy / epidemiology. Pleurisy / physiopathology. Pleurisy / radiography. Pleurisy / virology. Taiwan / epidemiology. Tonsillitis / epidemiology. Tonsillitis / physiopathology. Tonsillitis / virology. Urinary Tract Infections / epidemiology. Urinary Tract Infections / physiopathology. Urinary Tract Infections / virology

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  • [Copyright] Copyright © 2010 Taiwan Society of Microbiology. Published by Elsevier B.V. All rights reserved.
  • (PMID = 21195979.001).
  • [ISSN] 1995-9133
  • [Journal-full-title] Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi
  • [ISO-abbreviation] J Microbiol Immunol Infect
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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12. |......... 3%  Teng S, Zhao SY, Wei Y, Shao QM, Jiang MY, Cui DW, Xie GL: [Observation on virus shedding periods of enterovirus-71 and coxsackievirus A 16 monitored by nucleic acids determination in stool samples of children with hand, foot and mouth disease]. Zhonghua Er Ke Za Zhi; 2013 Oct;51(10):787-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Observation on virus shedding periods of enterovirus-71 and coxsackievirus A 16 monitored by nucleic acids determination in stool samples of children with hand, foot and mouth disease].
  • OBJECTIVE: To observe the duration of enterovirus-71 (EV71) and coxsackievirus A 16 (CoxA16) viral shedding in stool samples of children with hand, foot and mouth disease (HFMD) infected with EV71 and CoxA16 and to explore the relationship between the duration of intestinal virus shedding and the severity of illness of children with HFMD.
  • The stool samples were collected with the interval of 4 to7 days and the viral nucleic acids were detected by fluorescent PCR until the stool viral nucleic acids of infected children turned to be negative.
  • The positive rates of viral nucleic acid and the differences of distribution among different groups were analyzed by Kaplan-Meier survival analysis during the follow-up period.
  • RESULT: The 113 cases of infected children were grouped as follows: 65 cases of EV71 positive children, 44 cases of CoxA16 positive children, 4 cases of EV71/CoxA16 mixed infection.
  • The median duration of the stool viral nucleic acids turning to negative was 26 (18.25-32.50) days in EV71 group and 27 (14.50-33.75) days in CoxA16 group (Z = 1.51, P > 0.05).
  • At 1, 4, 6 and 10 weeks, the positive rates of stool viral nucleic acid of children with HFMD in EV71 group were 100%, 48.1%, 17.2% and 0 respectively.
  • At 1, 4 and 6 weeks, the positive rates of stool viral nucleic acid of children with HFMD in CoxA16 group were 95.5%, 53.8% and 0 respectively (χ(2) = 0.18, P > 0.05).
  • At 1, 4 and 6 weeks, the positive rates of stool viral nucleic acid of children with HFMD in ordinary EV71 group were 100%, 23.5% and 0 respectively, while at 1, 4, 6 and 10 weeks, the positive rates of stool viral nucleic acid of children with HFMD in severe EV71 group were 100%, 62.4%, 26.0% and 0 respectively (χ(2) = 5.689, P < 0.05).
  • The duration of intestinal virus shedding of children with HFMD infected with EV71 was related with the severity of the illness.
  • [MeSH-major] Enterovirus A, Human / isolation & purification. Feces / virology. Hand, Foot and Mouth Disease / virology. Nucleic Acids / isolation & purification. Virus Shedding
  • [MeSH-minor] Child. Child, Preschool. China / epidemiology. Coxsackievirus Infections / diagnosis. Coxsackievirus Infections / epidemiology. Enterovirus / genetics. Enterovirus / isolation & purification. Female. Humans. Infant. Male. Polymerase Chain Reaction. RNA, Viral / genetics

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  • (PMID = 24406235.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi. Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Nucleic Acids; 0 / RNA, Viral
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13. |......... 3%  Saikia UN, Mishra B, Sharma M, Nada R, Radotra B: Disseminated coxsackievirus B fulminant myocarditis in an immunocompetent adult: a case report: case of disseminated coxsackievirus myocarditis. Diagn Microbiol Infect Dis; 2014 Jan;78(1):98-100
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  • [Title] Disseminated coxsackievirus B fulminant myocarditis in an immunocompetent adult: a case report: case of disseminated coxsackievirus myocarditis.
  • We report a case of fulminant myocarditis along with dissemination of coxsackievirus, which was clinically unrecognized.
  • [MeSH-major] Coxsackievirus Infections / diagnosis. Coxsackievirus Infections / pathology. Enterovirus B, Human / isolation & purification. Myocarditis / diagnosis. Myocarditis / pathology

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  • [Copyright] © 2013.
  • (PMID = 24182898.001).
  • [ISSN] 1879-0070
  • [Journal-full-title] Diagnostic microbiology and infectious disease
  • [ISO-abbreviation] Diagn. Microbiol. Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Coxsackievirus / Dissemination / Fulminant / Myocarditis
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14. |......... 3%  Zhu B, Zhong JY, Xia HM, Gong ST, Xiao MS, Xie JH, Zhang YY, Hua L, Lian GW: [Etiology of hand, foot and mouth disease in Guangzhou in 2008]. Zhonghua Er Ke Za Zhi; 2010 Feb;48(2):127-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Etiology of hand, foot and mouth disease in Guangzhou in 2008].
  • OBJECTIVE: To understand the etiology of hand, foot and mouth disease (HFMD) in Guangzhou area in 2008.
  • TaqMan real-time RT-PCR were used for detection of enterovirus 71 (EV71), Coxsackievirus A16 (CA16) and other enteroviruses.
  • RESULT: Enterovirus was identified from 434 of 1023 samples and detection rate of enterovirus was 42.42%; of the 434 samples, 276 were positive for EV71 (63.6%), 126 for CA16 (29%), 4 samples for enterovirus 84, 3 for Echovirus 11, 2 for Echovirus 9, 3 for Coxsackievirus B3, 4 for Coxsackievirus A10, 3 for Coxsackievirus A6, 6 for Coxsackievirus A12 or A5, and for 7 samples typing was difficult.
  • [MeSH-major] Enterovirus A, Human / isolation & purification. Hand, Foot and Mouth Disease / virology
  • [MeSH-minor] Child. Child, Preschool. China / epidemiology. Coxsackievirus Infections / epidemiology. DNA Primers. Female. Humans. Infant. Male. RNA, Viral. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20426938.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi. Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Viral
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15. |......... 3%  Richer MJ, Horwitz MS: The innate immune response: an important partner in shaping coxsackievirus-mediated autoimmunity. J Innate Immun; 2009;1(5):421-34
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  • [Title] The innate immune response: an important partner in shaping coxsackievirus-mediated autoimmunity.
  • To protect against viral infection, the immune response is critically dependent on innate sensing mechanisms to provide rapid detection of pathogens and allow for the development of an appropriate adaptive immune response.
  • Coxsackieviruses are common human pathogens that have been linked to the induction of autoimmune diseases such as chronic autoimmune myocarditis and type 1 diabetes.
  • In this review, we will discuss the current knowledge of the interactions between coxsackievirus and the innate immune system and how these interactions can potentially lead to the induction of autoimmune diseases.
  • [MeSH-major] Autoimmune Diseases. Coxsackievirus Infections / immunology. Diabetes Mellitus, Type 1. Immunity, Innate. Myocarditis

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 20375600.001).
  • [ISSN] 1662-8128
  • [Journal-full-title] Journal of innate immunity
  • [ISO-abbreviation] J Innate Immun
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 117
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16. |......... 3%  Shi HJ, Liu JS, Wang LC, Zhang XM, Liu LD, Liao Y, Na RX, Li QH: [Biological characters of a coxsackievirus B3 variant strain isolated from a hand-foot-mouth disease patient with severe clinical symptoms]. Zhonghua Yi Xue Za Zhi; 2010 Apr 27;90(16):1141-4
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  • [Title] [Biological characters of a coxsackievirus B3 variant strain isolated from a hand-foot-mouth disease patient with severe clinical symptoms].
  • OBJECTIVE: To analyze the genetic and biological characters of a new isolate of coxsackievirus B3 (CoxB3), i.e.
  • FY-19 strain, and investigate its mechanistic role in causing different clinical symptoms of hand-foot-mouth disease (HFMD).
  • The viral replication kinetic analysis suggested that the FY-19 proliferation increased rapidly and peaked at 14 hours post-infection.
  • [MeSH-major] Enterovirus B, Human / classification. Enterovirus B, Human / genetics. Hand, Foot and Mouth Disease / virology
  • [MeSH-minor] Animals. Cell Line. Cercopithecus aethiops. Coxsackievirus Infections. Genotype. Humans. Mice. RNA, Viral. Vero Cells. Viral Proteins / genetics

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  • (PMID = 20646436.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Viral; 0 / Viral Proteins
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17. |......... 3%  Lott JP, Liu K, Landry ML, Nix WA, Oberste MS, Bolognia J, King B: Atypical hand-foot-and-mouth disease associated with coxsackievirus A6 infection. J Am Acad Dermatol; 2013 Nov;69(5):736-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical hand-foot-and-mouth disease associated with coxsackievirus A6 infection.
  • BACKGROUND: Hand-foot-and-mouth disease (HFMD) is an acute viral illness commonly caused by coxsackievirus (CV)-A16 and enterovirus 71 infections.
  • OBJECTIVE: We sought to describe the clinical features of atypical HFMD associated with CV-A6 infection and its diagnostic laboratory evaluation.
  • Enterovirus infection was assessed by reverse transcriptase polymerase chain reaction of biologic specimens.
  • Enterovirus type was determined by viral capsid protein 1 gene sequencing.
  • Infection with CV-A6 was confirmed in all patients.
  • CONCLUSION: Consideration of the expanded range of cutaneous findings in atypical HFMD caused by CV-A6 infection may assist clinicians in diagnosis and management.
  • [MeSH-major] Coxsackievirus Infections / complications. Enterovirus A, Human. Hand, Foot and Mouth Disease / complications. Hand, Foot and Mouth Disease / virology

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  • [Copyright] Copyright © 2013 American Academy of Dermatology, Inc. Published by Mosby, Inc. All rights reserved.
  • (PMID = 24035209.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; AD / CDC / CV / Centers for Disease Control and Prevention / ED / HFMD / PCR / RT / atopic dermatitis / atypical / coxsackievirus / coxsackievirus A6 / diagnosis / emergency department / enterovirus / evaluation / exanthem / hand-foot-and-mouth disease / polymerase chain reaction / reverse transcriptase
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18. |......... 3%  Lo SH, Huang YC, Huang CG, Tsao KC, Li WC, Hsieh YC, Chiu CH, Lin TY: Clinical and epidemiologic features of Coxsackievirus A6 infection in children in northern Taiwan between 2004 and 2009. J Microbiol Immunol Infect; 2011 Aug;44(4):252-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical and epidemiologic features of Coxsackievirus A6 infection in children in northern Taiwan between 2004 and 2009.
  • BACKGROUND: Isolates of Coxsackievirus A6 (Cox A6) is increasing clinically in 2009 in Taiwan but detailed clinical features of Cox A6 infections in children have not been reported.
  • This study is to define clinical manifestations and laboratory findings of Cox A6 infection in children.
  • METHODS: From January 2004 to December 2009, a total of 4,664 children with enterovirus infections, based on throat virus culture, were treated in Chang Gung Children's hospital.
  • Two hundred and ninety-six (6.3%) patients positive for Cox A6 infection were included in this study.
  • RESULTS: There were two peaks of Cox A6 infection in 2007 and 2009 during the study period, especially during the warm season.
  • One hundred and eight (76.6%) inpatients were diagnosed as herpangina and 18 (12.8%) hand-foot-mouth disease.
  • CONCLUSIONS: Cox A6 is among the major serotypes of enteroviruses in Taiwan and most cases presented as herpangina and hand-foot-mouth disease.
  • [MeSH-major] Coxsackievirus Infections / diagnosis. Coxsackievirus Infections / epidemiology. Enterovirus / isolation & purification

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  • [Copyright] Copyright © 2011. Published by Elsevier B.V.
  • (PMID = 21524960.001).
  • [ISSN] 1995-9133
  • [Journal-full-title] Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi
  • [ISO-abbreviation] J Microbiol Immunol Infect
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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19. |......... 3%  Stewart CL, Chu EY, Introcaso CE, Schaffer A, James WD: Coxsackievirus A6-induced hand-foot-mouth disease. JAMA Dermatol; 2013 Dec;149(12):1419-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coxsackievirus A6-induced hand-foot-mouth disease.
  • IMPORTANCE: Hand-foot-mouth disease (HFMD) is an acute, self-limited, highly contagious viral illness that commonly affects children younger than 5 years.
  • It is most typically caused by enterovirus 71 or coxsackievirus A16 and results in asymptomatic infection or mild disease.
  • Recently, there have been increasing reports of a more severe form of HFMD associated with fevers, joint pains, and widespread painful eruptions.
  • These severe cases were most commonly caused by coxsackievirus A6.
  • His infection with coxsackievirus A6 was confirmed based on polymerase chain reaction from his oral mucosa and cutaneous vesicle fluid.
  • CONCLUSIONS AND RELEVANCE: Dermatologists should be familiar with the severe variant of HFMD caused by coxsackievirus A6, include it in their differential diagnosis of acute febrile blistering diseases, and be aware that certain patients may require hospitalization.
  • [MeSH-major] Coxsackievirus Infections / physiopathology. Enterovirus A, Human / isolation & purification. Hand, Foot and Mouth Disease / physiopathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Hospitalization. Humans. Male. Polymerase Chain Reaction. Severity of Illness Index

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  • (PMID = 24172861.001).
  • [ISSN] 2168-6084
  • [Journal-full-title] JAMA dermatology
  • [ISO-abbreviation] JAMA Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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20. |......... 3%  Feuer R, Ruller CM, An N, Tabor-Godwin JM, Rhoades RE, Maciejewski S, Pagarigan RR, Cornell CT, Crocker SJ, Kiosses WB, Pham-Mitchell N, Campbell IL, Whitton JL: Viral persistence and chronic immunopathology in the adult central nervous system following Coxsackievirus infection during the neonatal period. J Virol; 2009 Sep;83(18):9356-69
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  • [Title] Viral persistence and chronic immunopathology in the adult central nervous system following Coxsackievirus infection during the neonatal period.
  • Coxsackieviruses are significant human pathogens, and the neonatal central nervous system (CNS) is a major target for infection.
  • Despite the extreme susceptibility of newborn infants to coxsackievirus infection and viral tropism for the CNS, few studies have been aimed at determining the long-term consequences of infection on the developing CNS.
  • We previously described a neonatal mouse model of coxsackievirus B3 (CVB3) infection and determined that proliferating stem cells in the CNS were preferentially targeted.
  • Here, we describe later stages of infection, the ensuing inflammatory response, and subsequent lesions which remain in the adult CNS of surviving animals.
  • High levels of type I interferons and chemokines (in particular MCP-5, IP10, and RANTES) were upregulated following infection and remained at high levels up to day 10 postinfection (p.i).
  • CVB3 RNA was detected in the CNS up to 3 months p.i at high abundance ( approximately 10(6) genomes/mouse brain), and viral genomic material remained detectable in culture after two rounds of in vitro passage.
  • These data suggest that CVB3 may persist in the CNS as a low-level, noncytolytic infection, causing ongoing inflammatory lesions.
  • Thus, the effects of a relatively common infection during the neonatal period may be long lasting, and the prognosis for newborn infants recovering from acute infection should be reexplored.
  • [MeSH-major] Central Nervous System / virology. Coxsackievirus Infections / pathology. Enterovirus / pathogenicity
  • [MeSH-minor] Animals. Animals, Newborn. Cerebral Cortex / pathology. Cerebral Cortex / virology. Chemokines / analysis. Chronic Disease. Enterovirus B, Human. Genome, Viral. Hippocampus / pathology. Hippocampus / virology. Humans. Inflammation. Interferon Type I / analysis. Mice. RNA, Viral / blood. Time Factors. Up-Regulation

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  • (PMID = 19570873.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / F32 AI-065095; United States / NIMH NIH HHS / MH / MH62331; United States / NINDS NIH HHS / NS / NS036979; United States / NIAID NIH HHS / AI / R01 AI-42314; United States / NIAID NIH HHS / AI / R01 AI042314-13; United States / NINDS NIH HHS / NS / R01 NS054108-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokines; 0 / Interferon Type I; 0 / RNA, Viral
  • [Other-IDs] NLM/ PMC2738251
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21. |......... 3%  Chu PY, Ke GM, Chen YS, Lu PL, Chen HL, Lee MS, Chen BC, Huang TS, Li YC, Chou LC, Wang SY, Lin KH: Molecular epidemiology of Coxsackievirus B3. Infect Genet Evol; 2010 Aug;10(6):777-84
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  • [Title] Molecular epidemiology of Coxsackievirus B3.
  • Molecular epidemiological characteristics are needed to understand the impact of Coxsackievirus B3 (CV-B3) infection, since no CV-B3 genotyping literature is available.
  • Half of them contracted respiratory tract infection (12/24).
  • CNS infections were not associated with a specific strain or genotype.
  • [MeSH-major] Coxsackievirus Infections / epidemiology. Coxsackievirus Infections / virology. Enterovirus B, Human / genetics
  • [MeSH-minor] Americas / epidemiology. Amino Acid Sequence. Amino Acid Substitution. Child. Child, Preschool. Disease Outbreaks. Europe / epidemiology. Female. Genotype. Humans. Infant. Infant, Newborn. Male. Molecular Epidemiology. Molecular Sequence Data. Phylogeny. Sequence Homology, Amino Acid. Taiwan / epidemiology

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  • [Copyright] Copyright 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20398802.001).
  • [ISSN] 1567-7257
  • [Journal-full-title] Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases
  • [ISO-abbreviation] Infect. Genet. Evol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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22. |......... 3%  Chu PY, Tsai YL, Chen HL, Ke GM, Hsu CY, Chen YT, Wang CF, Su HJ, Chou LC, Hsu LC, Lin KH: Coxsackievirus B4 in southern Taiwan: molecular epidemiology. J Clin Virol; 2009 May;45(1):16-22
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  • [Title] Coxsackievirus B4 in southern Taiwan: molecular epidemiology.
  • BACKGROUND: Enterovirus outbreaks caused by Coxsackievirus B4 (CB4) in Taiwan in 2004 and 2008.
  • The clinical manifestations of CB4 infection were examined by retrospectively reviewing medical records of infected patients.
  • In this retrospective follow-up study of sixteen patients with CB4 infection, the median patient age at the time of infection diagnosis was 4-year-old (range, 18 days to 10-year-old), and male-female ratio was 1:1.
  • None of the sixteen patients suffered IDDM or myocarditis after their B4 infection episodes; four had Attention Deficit Hyperactivity Disorder (ADHD) and/or tic disorders (TDs) at follow-up.
  • Controlled studies are needed to evaluate a possible association between ADHD and TDs with CB4 infection.
  • [MeSH-major] Coxsackievirus Infections / epidemiology. Coxsackievirus Infections / virology. Enterovirus B, Human / genetics
  • [MeSH-minor] Child. Child, Preschool. Cluster Analysis. Disease Outbreaks. Female. Genes, Viral. Genotype. Humans. Infant. Infant, Newborn. Male. Molecular Epidemiology. Molecular Sequence Data. Phylogeny. Retrospective Studies. Sequence Analysis, RNA. Taiwan / epidemiology

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  • (PMID = 19375382.001).
  • [ISSN] 1873-5967
  • [Journal-full-title] Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
  • [ISO-abbreviation] J. Clin. Virol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB455912/ AB455913/ AB455914/ AB455915/ AB455916/ AB455917/ AB455918/ AB455919/ AB455920/ AB455921/ AB455922/ AB455923/ AB455924/ AB455925/ AB455926/ AB455927/ AB455928/ AB455929/ AB455930/ AB455931/ AB455932/ AB455933/ AB455934/ AB455935/ AB455936/ AB455937/ AB455938/ AB455939/ AB455940/ AB455941/ AB455942/ AB455943/ AB455944/ AB455945/ AB455946/ AB455947/ AB455948/ AB455949/ AB455950/ AB455951/ AB455952/ AB455953/ AB455954/ AB455955/ AB455956/ AB455957/ AB455958/ AB455959/ AB455960/ AB455961/ AB455962/ AB455963/ AB455964/ AB455965/ AB455966/ AB455967/ AB455968/ AB455969/ AB455970/ AB455971/ AB455972/ AB455973/ AB455974/ AB455975/ AB455976/ AB455977/ AB455978/ AB455979/ AB455980/ AB455981/ AB455982/ AB455983/ AB455984/ AB455985/ AB455986/ AB455987/ AB455988/ AB455989/ AB455990/ AB455991/ AB455992/ AB455993/ AB455994/ AB455995/ AB455996/ AB455997/ AB455998/ AB455999/ AB456000/ AB456001/ AB456002/ AB456003/ AB456004/ AB456005/ AB456006/ AB456007/ AB456008/ AB456009/ AB456010/ AB456011/ AB456012/ AB456013/ AB456014/ AB456015/ AB456016/ AB456017/ AB456018/ AB456019/ AB456020/ AB456021/ AB456022/ AB456023/ AB456024/ AB456025/ AB456026/ AB456027/ AB456028/ AB456029/ AB456030/ AB456031/ AB456032/ AB456033/ AB456034
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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23. |......... 3%  Inal JM, Jorfi S: Coxsackievirus B transmission and possible new roles for extracellular vesicles. Biochem Soc Trans; 2013 Feb 1;41(1):299-302
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  • [Title] Coxsackievirus B transmission and possible new roles for extracellular vesicles.
  • Coxsackievirus B1, a member of the Picornaviridae family is a non-enveloped single-stranded RNA virus associated with human diseases including myocarditis and pancreatitis.
  • Infection of the intestinal mucosa, lined by polarized epithelial cells, requires interaction of coxsackievirus with apically located DAF (decay-accelerating factor) before transport to the basolaterally located CAR (coxsackie and adenovirus receptor), where entry is mediated by endocytosis.
  • As with many other non-enveloped viruses, coxsackievirus has to induce lysis of host cells in order to perpetuate infection.
  • However, recent evidence indicates that virus spread to secondary sites is not only achieved by a lytic mechanism and a non-lytic cell-cell strategy has been suggested for coxsackievirus B3.
  • Calpain-mediated depolymerization of the actin cytoskeleton, as a result of increases in intracellular calcium concentration during coxsackievirus infection, would result in a release of host cell-derived microvesicles.
  • [MeSH-major] Coxsackievirus Infections / transmission. Enterovirus B, Human / isolation & purification

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  • (PMID = 23356301.001).
  • [ISSN] 1470-8752
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
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24. |......... 3%  Dorobantu CM, van der Schaar HM, Ford LA, Strating JR, Ulferts R, Fang Y, Belov G, van Kuppeveld FJ: Recruitment of PI4KIIIβ to coxsackievirus B3 replication organelles is independent of ACBD3, GBF1, and Arf1. J Virol; 2014 Mar;88(5):2725-36
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  • [Title] Recruitment of PI4KIIIβ to coxsackievirus B3 replication organelles is independent of ACBD3, GBF1, and Arf1.
  • Members of the Enterovirus (poliovirus [PV], coxsackieviruses, and human rhinoviruses) and Kobuvirus (Aichi virus) genera in the Picornaviridae family rely on PI4KIIIβ (phosphatidylinositol-4-kinase IIIβ) for efficient replication.
  • Although ACBD3 interacted directly with coxsackievirus B3 (CVB3) 3A, its depletion from cells by RNA interference did not affect PI4KIIIβ recruitment to replication organelles and did not impair CVB3 RNA replication.
  • Together, our findings indicate that unlike originally envisaged, coxsackievirus recruits PI4KIIIβ to replication organelles independently of ACBD3 and GBF1/Arf1.
  • IMPORTANCE: A hallmark of enteroviral infection is the generation of new membranous structures to support viral RNA replication.
  • The functionality of these "replication organelles" depends on the concerted actions of both viral nonstructural proteins and co-opted host factors.
  • This study shows that the strategy employed by coxsackievirus to recruit PI4KIIIβ to replication organelles is far more complex than initially anticipated.
  • [MeSH-major] ADP-Ribosylation Factor 1 / metabolism. Adaptor Proteins, Signal Transducing / metabolism. Enterovirus B, Human / physiology. Guanine Nucleotide Exchange Factors / metabolism. Membrane Proteins / metabolism. Phosphotransferases (Alcohol Group Acceptor) / metabolism. Virus Replication
  • [MeSH-minor] Animals. Cell Line. Coxsackievirus Infections / metabolism. Coxsackievirus Infections / virology. Humans. Protein Binding. RNA, Viral / genetics. RNA, Viral / metabolism. Viral Proteins / metabolism

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  • (PMID = 24352456.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3A protein, coxsackievirus B; 0 / ACBD3 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / GBF1 protein, human; 0 / Guanine Nucleotide Exchange Factors; 0 / Membrane Proteins; 0 / RNA, Viral; 0 / Viral Proteins; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.67 / phosphatidylinositol 4-kinase IIIbeta, human; EC 3.6.5.2 / ADP-Ribosylation Factor 1
  • [Other-IDs] NLM/ PMC3958084 [Available on 09/01/14]
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25. |......... 3%  Shea YF, Chan CY, Hung IF, Chan KH: Hand, foot and mouth disease in an immunocompetent adult due to Coxsackievirus A6. Hong Kong Med J; 2013 Jun;19(3):262-4
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  • [Title] Hand, foot and mouth disease in an immunocompetent adult due to Coxsackievirus A6.
  • Hand, foot and mouth disease most commonly occurs in children less than 10 years old, but can occur in immunocompetent adults.
  • Real-time polymerase chain reaction revealed Coxsackievirus A6 in the vesicle fluid from the feet, throat swab, and rectal swab.
  • Since the disease is highly contagious, to contain the infection it is prudent to recognise that hand, foot and mouth disease can occur in immunocompetent adults.
  • [MeSH-major] Coxsackievirus Infections / complications. Enterovirus A, Human / isolation & purification. Hand, Foot and Mouth Disease / virology

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  • (PMID = 23732432.001).
  • [ISSN] 1024-2708
  • [Journal-full-title] Hong Kong medical journal = Xianggang yi xue za zhi / Hong Kong Academy of Medicine
  • [ISO-abbreviation] Hong Kong Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Keywords] NOTNLM ; Hand, foot and mouth disease
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26. |......... 3%  Rassmann A, Martin U, Saluz HP, Peter S, Munder T, Henke A: Identification of gene expression profiles in HeLa cells and HepG2 cells infected with Coxsackievirus B3. J Virol Methods; 2013 Jan;187(1):190-4
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  • [Title] Identification of gene expression profiles in HeLa cells and HepG2 cells infected with Coxsackievirus B3.
  • Viral infections of host cells cause multiple changes of cellular metabolism including immediate defense mechanisms as well as processes to support viral replication.
  • Coxsackievirus B3 (CVB3) is a member of the Picornavirus family and is responsible for a wide variety of mild or severe infections including acute and chronic inflammations.
  • Expression analysis of HeLa cells and HepG2 cells infected with CVB3 identified 34 genes whose mRNA levels were altered significantly upon infection.
  • All genes expressed differentially were sorted with regard to their functions and interpreted in view of known contributors to the infection process.
  • [MeSH-major] Coxsackievirus Infections / genetics. Coxsackievirus Infections / metabolism. Enterovirus B, Human / genetics. RNA, Messenger / biosynthesis
  • [MeSH-minor] Apoptosis / genetics. Cell Line, Tumor. Enzyme Activation. Gene Expression. Gene Expression Profiling. HeLa Cells / virology. Hep G2 Cells / virology. Humans. Oligonucleotide Array Sequence Analysis. Signal Transduction / genetics. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism. Virus Replication / genetics

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  • [Copyright] Copyright © 2012 Elsevier B.V. All rights reserved.
  • (PMID = 23000448.001).
  • [ISSN] 1879-0984
  • [Journal-full-title] Journal of virological methods
  • [ISO-abbreviation] J. Virol. Methods
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
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27. |......... 3%  Roberts BJ, Moussawi M, Huber SA: Sex differences in TLR2 and TLR4 expression and their effect on coxsackievirus-induced autoimmune myocarditis. Exp Mol Pathol; 2013 Feb;94(1):58-64
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  • [Title] Sex differences in TLR2 and TLR4 expression and their effect on coxsackievirus-induced autoimmune myocarditis.
  • Coxsackievirus B3 (CVB3) infection of C57Bl/6 mice shows a sex bias with males developing more severe cardiac inflammation than females because males develop a Th1 inflammatory response, whereas females develop a Th2 response.
  • To assess the role of TLRs in coxsackievirus-induced myocarditis wild type and Toll-like receptor 2-/- male and female mice were infected and assessed for viral replication, myocarditis, helper T-cell generation, and regulatory T-cell generation.
  • [MeSH-major] Coxsackievirus Infections / immunology. Myocarditis / immunology. Myocarditis / virology. Sex Characteristics. Toll-Like Receptor 2 / metabolism. Toll-Like Receptor 4 / metabolism
  • [MeSH-minor] Animals. Autoimmune Diseases / immunology. Autoimmune Diseases / metabolism. Disease Susceptibility / immunology. Enterovirus / immunology. Female. Lipopeptides / pharmacology. Lipopolysaccharides / pharmacology. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. Nerve Tissue Proteins / biosynthesis. Nuclear Proteins / biosynthesis. T-Lymphocytes, Regulatory / immunology. T-Lymphocytes, Regulatory / metabolism. Th1 Cells / metabolism

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  • [Copyright] Copyright © 2012 Elsevier Inc. All rights reserved.
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  • (PMID = 22750431.001).
  • [ISSN] 1096-0945
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL108371; United States / NIAID NIH HHS / AI / P01 AI045666; United States / NCRR NIH HHS / RR / P20 RR021905; United States / NHLBI NIH HHS / HL / R01 HL108371; United States / NCRR NIH HHS / RR / T20-RR021905
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipopeptides; 0 / Lipopolysaccharides; 0 / Nerve Tissue Proteins; 0 / NeuN protein, mouse; 0 / Nuclear Proteins; 0 / Pam(3)CSK(4) peptide; 0 / Tlr2 protein, mouse; 0 / Tlr4 protein, mouse; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptor 4
  • [Other-IDs] NLM/ NIHMS390723; NLM/ PMC3485413
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28. |......... 3%  Kim DS, Nam JH: Characterization of attenuated coxsackievirus B3 strains and prospects of their application as live-attenuated vaccines. Expert Opin Biol Ther; 2010 Feb;10(2):179-90
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  • [Title] Characterization of attenuated coxsackievirus B3 strains and prospects of their application as live-attenuated vaccines.
  • Coxsackievirus strain CVB3 is widespread in the human population and causes myocarditis or pancreatitis.
  • [MeSH-minor] Animals. Antibodies, Viral / biosynthesis. Coxsackievirus Infections / immunology. Coxsackievirus Infections / prevention & control. Coxsackievirus Infections / virology. Genetic Vectors. Humans. Mutation / genetics. Receptors, Virus / genetics

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  • (PMID = 20088713.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Receptors, Virus; 0 / Vaccines, Attenuated; 0 / coxsackievirus B receptor
  • [Number-of-references] 96
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29. |......... 3%  Chen Z, Yang L, Liu Y, Tang A, Li X, Zhang J, Yang Z: LY294002 and Rapamycin promote coxsackievirus-induced cytopathic effect and apoptosis via inhibition of PI3K/AKT/mTOR signaling pathway. Mol Cell Biochem; 2014 Jan;385(1-2):169-77
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  • [Title] LY294002 and Rapamycin promote coxsackievirus-induced cytopathic effect and apoptosis via inhibition of PI3K/AKT/mTOR signaling pathway.
  • Coxsackievirus B3 (CVB3) is a common human pathogen for acute myocarditis, pancreatitis, non-septic meningitis, and encephalitis; it induces a direct cytopathic effect (CPE) and apoptosis on infected cells.
  • The activity of downstream targets of PI3K and mTOR is attenuated after CVB3 infection and inhibitors of PI3K and mTOR made their activity to decrease more significantly.
  • Taken together, these data illustrate a new and imperative role for PI3K/AKT/mTOR signaling in CVB3 infection in HeLa cells and suggest an useful approach for the therapy of CVB3 infection.
  • [MeSH-major] Apoptosis / drug effects. Chromones / pharmacology. Cytopathogenic Effect, Viral / drug effects. Morpholines / pharmacology. Phosphatidylinositol 3-Kinase / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Sirolimus / pharmacology. TOR Serine-Threonine Kinases / antagonists & inhibitors
  • [MeSH-minor] Coxsackievirus Infections / enzymology. Coxsackievirus Infections / pathology. Enterovirus / drug effects. Enterovirus / physiology. Gene Expression Regulation, Neoplastic / drug effects. HeLa Cells. Humans. Signal Transduction / drug effects

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  • (PMID = 24072614.001).
  • [ISSN] 1573-4919
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chromones; 0 / Morpholines; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.137 / Phosphatidylinositol 3-Kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; W36ZG6FT64 / Sirolimus
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30. |......... 3%  Tabor-Godwin JM, Tsueng G, Sayen MR, Gottlieb RA, Feuer R: The role of autophagy during coxsackievirus infection of neural progenitor and stem cells. Autophagy; 2012 Jun;8(6):938-53
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  • [Title] The role of autophagy during coxsackievirus infection of neural progenitor and stem cells.
  • Coxsackievirus B3 (CVB3) has previously been shown to utilize autophagy in an advantageous manner during the course of infection of the host cell.
  • However, few studies have determined whether stem cells induce autophagy in a similar fashion, and whether virus-induced autophagy occurs following infection of stem cells.
  • Therefore, we compared the induction of autophagy following CVB3 infection of neural progenitor and stem cells (NPSCs), which we have recently shown to be highly susceptible to CVB3 infection, to HL-1 cells, a transformed cardiomyocyte cell line.
  • As previously demonstrated for other susceptible host cells, HL-1 cells showed an increase in the activity of autophagic signaling following infection with a CVB3 expressing dsRed protein (dsRed-CVB3).
  • Furthermore, viral titers in HL-1 cells increased in the presence of an inducer of autophagy (CCPA), while viral titers decreased in the presence of an inhibitor of autophagy (3-MA).
  • In contrast, no change in autophagic signaling was seen in NPSCs following infection with dsRed-CVB3.
  • In differentiated NPSC precursors, autophagy was activated during the differentiation process, and a decrease in autophagic signaling was observed within all three CNS lineages following dsRed-CVB3 infection.
  • Hence, we conclude that the role of autophagy in modulating CVB3 replication appears cell type-specific, and stem cells may uniquely regulate autophagy in response to infection.
  • [MeSH-major] Autophagy. Coxsackievirus Infections / pathology. Neural Stem Cells / pathology. Neural Stem Cells / virology
  • [MeSH-minor] Adenine / analogs & derivatives. Adenine / pharmacology. Adenosine / analogs & derivatives. Adenosine / pharmacology. Animals. Cell Differentiation / drug effects. Enterovirus B, Human / drug effects. Enterovirus B, Human / physiology. Fibroblast Growth Factors / pharmacology. Green Fluorescent Proteins / metabolism. HeLa Cells. Humans. Mice. Mice, Inbred C57BL. Microtubule-Associated Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction / drug effects. Sirolimus / pharmacology. Transduction, Genetic. Viral Load / drug effects. Viral Proteins / metabolism. Virus Replication / drug effects

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  • (PMID = 22751470.001).
  • [ISSN] 1554-8635
  • [Journal-full-title] Autophagy
  • [ISO-abbreviation] Autophagy
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 3R01NS054108-01A2S1; United States / NHLBI NIH HHS / HL / R01 HL092136; United States / NHLBI NIH HHS / HL / R01 HL092136; United States / NINDS NIH HHS / NS / R01 NS054108; United States / NIMH NIH HHS / MH / R24 MH065515
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Microtubule-Associated Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Viral Proteins; 147336-22-9 / Green Fluorescent Proteins; 37739-05-2 / 2-chloro-N(6)cyclopentyladenosine; 5142-23-4 / 3-methyladenine; 62031-54-3 / Fibroblast Growth Factors; JAC85A2161 / Adenine; K72T3FS567 / Adenosine; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC3427259
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31. |......... 3%  Wu YD, Shang SQ, Chen ZM, Yang ZH: [Analysis of the epidemic characteristics of the etiological agents in children with hand, foot and mouth disease and its clinical significance]. Zhonghua Er Ke Za Zhi; 2010 Jul;48(7):535-9
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  • [Title] [Analysis of the epidemic characteristics of the etiological agents in children with hand, foot and mouth disease and its clinical significance].
  • OBJECTIVE: To investigate the epidemic characteristics of etiological agents in children with hand, foot and mouth disease (HFMD) and analyze the differences between the severe and mild cases with HFMD seen from 2008 to 2009 in the Children's Hospital.
  • Enterovirus universal type, enterovirus type 71 (EV71) and coxsackie virus group A 16 (CA16) were detected by real-time RT-PCR respectively.
  • EV71 positive rate in these 126 patients with enterovirus universal type infection was 57.14%(72/126).
  • There was no EV71 infection in these 80 cases with suspected herpangina.
  • EV71 infection was mainly popular in 2008.
  • The epidemic characteristics of enterovirus infection with HFMD between 2008 and 2009 had significant differences (χ(2) = 23.50, P = 0.000) (P < 0.01).
  • The epidemic characteristics of enterovirus infection between severe and mild HFMD patients also had significant differences (χ(2) = 29.85, P < 0.01).
  • There was no significant difference in the gender (χ(2) = 0.135, P = 0.714) and virus load (t = 0.141, P = 0.889) between the mild and severe HFMD cases.
  • CONCLUSION: HFMD showed different epidemic characteristics at different times of enterovirus infection.
  • There was no significant difference in the gender and virus load between the mild and severe cases with HFMD.
  • Children under 3 years of age with EV71 infection were at high risk for severe HFMD.
  • [MeSH-major] Coxsackievirus Infections / epidemiology. Hand, Foot and Mouth Disease / epidemiology. Hand, Foot and Mouth Disease / virology
  • [MeSH-minor] Child. Child, Preschool. China / epidemiology. Enterovirus. Female. Humans. Infant. Male. Viral Load

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  • (PMID = 21055092.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi. Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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32. |......... 3%  Sinclair C, Gaunt E, Simmonds P, Broomfield D, Nwafor N, Wellington L, Templeton K, Willocks L, Schofield O, Harvala H: Atypical hand, foot, and mouth disease associated with coxsackievirus A6 infection, Edinburgh, United Kingdom, January to February 2014. Euro Surveill; 2014;19(12):20745
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  • [Title] Atypical hand, foot, and mouth disease associated with coxsackievirus A6 infection, Edinburgh, United Kingdom, January to February 2014.
  • In January to February 2014, 16 hand, foot and mouth disease (HFMD) cases were identified in Edinburgh, United Kingdom.
  • Coxsackievirus A6 (CV-A6) was identified in all the typed cases (n=11).
  • [MeSH-major] Coxsackievirus Infections / complications. Enterovirus A, Human / genetics. Hand, Foot and Mouth Disease / complications. Hand, Foot and Mouth Disease / virology
  • [MeSH-minor] Adult. Chickenpox / etiology. Child, Preschool. Diagnosis, Differential. Disease Outbreaks. Female. Great Britain / epidemiology. Humans. Infant. Kaposi Varicelliform Eruption / etiology. Male. Middle Aged. RNA, Viral / genetics. Real-Time Polymerase Chain Reaction. Retrospective Studies. Sentinel Surveillance. Sequence Analysis, DNA

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  • (PMID = 24698138.001).
  • [ISSN] 1560-7917
  • [Journal-full-title] Euro surveillance : bulletin Européen sur les maladies transmissibles = European communicable disease bulletin
  • [ISO-abbreviation] Euro Surveill.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / RNA, Viral
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33. |......... 3%  Thibaut HJ, van der Schaar HM, Lanke KH, Verbeken E, Andrews M, Leyssen P, Neyts J, van Kuppeveld FJ: Fitness and virulence of a coxsackievirus mutant that can circumnavigate the need for phosphatidylinositol 4-kinase class III beta. J Virol; 2014 Mar;88(5):3048-51
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  • [Title] Fitness and virulence of a coxsackievirus mutant that can circumnavigate the need for phosphatidylinositol 4-kinase class III beta.
  • We show that mutant coxsackievirus is not outcompeted by wild-type virus during 10 passages in vitro.
  • In mice, the mutant virus proved as virulent as wild-type virus, even when mice were treated with a PI4KIIIβ inhibitor.
  • Our data suggest that upon emergence, the 3A-H57Y mutant has the fitness to establish a resistant population with a virulence similar to that of wild-type virus.
  • [MeSH-minor] Animals. Coxsackievirus Infections / metabolism. Coxsackievirus Infections / virology. Host-Pathogen Interactions. Mice. Viral Proteins / genetics. Viral Proteins / metabolism. Virulence / genetics. Virus Replication

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  • (PMID = 24371067.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Viral Proteins; EC 2.7.1.67 / 1-Phosphatidylinositol 4-Kinase
  • [Other-IDs] NLM/ PMC3958056 [Available on 09/01/14]
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34. |......... 3%  Yi L, Lu J, Kung HF, He ML: The virology and developments toward control of human enterovirus 71. Crit Rev Microbiol; 2011 Nov;37(4):313-27
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  • Enterovirus 71 (EV71), a member of the Enterovirus genus in the Picornaviridae family, was first recognized as a dermotrophic virus that usually cause mild, self-limiting hand-foot-and-mouth disease (HFMD).
  • However, EV71 infection can sometimes induce a variety of severe neurological complications and even death.
  • Current large outbreaks of EV71 make this virus being a major public health issue.
  • Intense effort has been made to address its underlying pathogenesis and to develop effective means for combating EV71 infections.
  • Here, we aimed to provide an overview of cellular mechanisms underlying EV71 infection and to assess potential agents for prevention and treatment of EV71 infections.
  • [MeSH-major] Coxsackievirus Infections / prevention & control. Enterovirus A, Human
  • [MeSH-minor] Disease Outbreaks / prevention & control. Humans

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  • (PMID = 21651436.001).
  • [ISSN] 1549-7828
  • [Journal-full-title] Critical reviews in microbiology
  • [ISO-abbreviation] Crit. Rev. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
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35. |......... 3%  Poffenberger MC, Straka N, El Warry N, Fang D, Shanina I, Horwitz MS: Lack of IL-6 during coxsackievirus infection heightens the early immune response resulting in increased severity of chronic autoimmune myocarditis. PLoS One; 2009;4(7):e6207
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  • [Title] Lack of IL-6 during coxsackievirus infection heightens the early immune response resulting in increased severity of chronic autoimmune myocarditis.
  • BACKGROUND: Chronic myocarditis is often initiated by viral infection, the most common of which is coxsackievirus infection.
  • The precise mechanism by which viral infection leads to chronic autoimmune pathology is poorly understood, however it is clear that the early immune response plays a critical role.
  • However, the function of IL-6 during viral-mediated autoimmunity has yet to be elucidated.
  • METHODS AND RESULTS: To address the requirement of IL-6 during disease induction, IL-6 deficient mice were infected with coxsackievirus B3 (CB3).
  • Following infection, mice lacking IL-6 developed increased chronic autoimmune disease pathology compared to wild type controls without a corresponding change in the level of viral replication in the heart.
  • This increase in disease severity was accompanied by elevated levels of TNF-alpha, MCP-1, IL-10, activated T cells and cardiac infiltrating macrophage/monocytes.
  • Injection of recombinant IL-6 early following infection in the IL-6 deficient mice was sufficient to lower the serum cytokines TNF-alpha and IL-10 as well as the serum chemokines MCP-1, MIP-1beta, RANTES and MIG with a corresponding decrease in the chronic disease pathology strongly suggests an important regulatory role for IL-6 during the early response.
  • CONCLUSIONS: While IL-6 plays a pathogenic role in experimental-induced autoimmune disease, its function following viral-induced autoimmunity is not reprised.
  • By regulating the early immune response and thereby controlling the severity of chronic disease, IL-6 directs the outcome of chronic autoimmune myocarditis.
  • [MeSH-major] Autoimmune Diseases / physiopathology. Coxsackievirus Infections / immunology. Interleukin-6 / physiology. Myocarditis / physiopathology
  • [MeSH-minor] Animals. Chronic Disease. Enterovirus B, Human / physiology. Mice. Mice, Inbred C57BL. Mice, Knockout. Recombinant Proteins / administration & dosage. Severity of Illness Index. Virus Replication


36. |......... 3%  Cai Y, Liu Q, Huang X, Li D, Ku Z, Zhang Y, Huang Z: Active immunization with a Coxsackievirus A16 experimental inactivated vaccine induces neutralizing antibodies and protects mice against lethal infection. Vaccine; 2013 Apr 26;31(18):2215-21
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  • [Title] Active immunization with a Coxsackievirus A16 experimental inactivated vaccine induces neutralizing antibodies and protects mice against lethal infection.
  • Coxsackievirus A16 (CA16) is one of the main pathogens that cause hand, foot and mouth disease, which frequently occurs in young children.
  • We show that immunization with β-propiolactone-inactivated whole-virus vaccines derived from two CA16 clinical isolates were able to induce CA16-specific antibody and IFN-secreting T-cell responses in mice.
  • More significantly, active immunization of mice with the inactivated vaccines conferred complete protection against lethal infection with CA16-MAV.
  • Collectively, these results provide a solid foundation for further development of inactivated whole-virus CA16 vaccines for human use.
  • [MeSH-major] Coxsackievirus Infections / immunology. Coxsackievirus Infections / prevention & control. Enterovirus / immunology. Viral Vaccines / immunology
  • [MeSH-minor] Animals. Antibodies, Neutralizing / blood. Antibodies, Viral / blood. Cercopithecus aethiops. Disease Models, Animal. Female. Immunization, Passive. Interferon-gamma / immunology. Mice. Mice, Inbred ICR. Neutralization Tests. Propiolactone. T-Lymphocytes / immunology. Vaccination. Vaccines, Inactivated / immunology. Vero Cells

  • HSDB. structure - BETA-PROPIOLACTONE.
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  • [Copyright] Copyright © 2013 Elsevier Ltd. All rights reserved.
  • (PMID = 23499596.001).
  • [ISSN] 1873-2518
  • [Journal-full-title] Vaccine
  • [ISO-abbreviation] Vaccine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Neutralizing; 0 / Antibodies, Viral; 0 / Vaccines, Inactivated; 0 / Viral Vaccines; 6RC3ZT4HB0 / Propiolactone; 82115-62-6 / Interferon-gamma
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37. |......... 3%  Osterback R, Vuorinen T, Linna M, Susi P, Hyypiä T, Waris M: Coxsackievirus A6 and hand, foot, and mouth disease, Finland. Emerg Infect Dis; 2009 Sep;15(9):1485-8
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  • [Title] Coxsackievirus A6 and hand, foot, and mouth disease, Finland.
  • During fall 2008, an outbreak of hand, foot, and mouth disease (HFMD) with onychomadesis (nail shedding) as a common feature occurred in Finland.
  • We identified an unusual enterovirus type, coxsackievirus A6 (CVA6), as the causative agent.
  • CVA6 infections may be emerging as a new and major cause of epidemic HFMD.
  • [MeSH-major] Communicable Diseases, Emerging / virology. Coxsackievirus Infections / virology. Disease Outbreaks. Enterovirus. Hand, Foot and Mouth Disease / virology

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  • (PMID = 19788821.001).
  • [ISSN] 1080-6059
  • [Journal-full-title] Emerging infectious diseases
  • [ISO-abbreviation] Emerging Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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  • [Other-IDs] NLM/ PMC2819858
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38. |......... 3%  Jia L, Zhao CS, Zhang L, Li S, Zhang DT, Liu BW, Wang QY, Li XY: [Comparisons of epidemiological and clinical characteristics in children with hand-foot-mouth disease caused by Enterovirus 71 and Coxackievirus A16]. Zhongguo Dang Dai Er Ke Za Zhi; 2011 Aug;13(8):635-7
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  • [Title] [Comparisons of epidemiological and clinical characteristics in children with hand-foot-mouth disease caused by Enterovirus 71 and Coxackievirus A16].
  • OBJECTIVE: To compare the differences of epidemiological and clinical characteristics in children with hand-foot-mouth disease (HFMD) caused by Coxsackievirus A16 (CA16) and Enterovirus 71 (EV71).
  • The clinical data of children with EV71 and CA16 infection were retrospectively reviewed and compared.
  • The multivariate logistic regression analysis showed that the HFMD children who had erythra of knees had higher probability of CA16 infection.
  • [MeSH-major] Coxsackievirus Infections / epidemiology. Enterovirus A, Human. Hand, Foot and Mouth Disease / epidemiology

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  • (PMID = 21849112.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] China
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39. |......... 3%  Zong W, He Y, Yu S, Yang H, Xian H, Liao Y, Hu G: Molecular phylogeny of Coxsackievirus A16 in Shenzhen, China, from 2005 to 2009. J Clin Microbiol; 2011 Apr;49(4):1659-61
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  • [Title] Molecular phylogeny of Coxsackievirus A16 in Shenzhen, China, from 2005 to 2009.
  • Phylogenetic analysis of a Coxsackievirus A16 (CA16) sequence from Shenzhen, China, and other Chinese and international CA16 sequences revealed a pattern of endemic cocirculation of strains of clusters B2a and B2b within subtype B2 viruses.
  • [MeSH-major] Coxsackievirus Infections / epidemiology. Coxsackievirus Infections / virology. Enterovirus / classification. Enterovirus / genetics
  • [MeSH-minor] Amino Acid Substitution / genetics. China / epidemiology. Cluster Analysis. Evolution, Molecular. Humans. Molecular Epidemiology. Molecular Sequence Data. Mutation, Missense. Phylogeny. RNA, Viral / genetics. Sequence Analysis, DNA

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  • (PMID = 21325543.001).
  • [ISSN] 1098-660X
  • [Journal-full-title] Journal of clinical microbiology
  • [ISO-abbreviation] J. Clin. Microbiol.
  • [Language] eng
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HM777114/ HM777115/ HM777116/ HM777117/ HM777118/ HM777119/ HM777120/ HM777121/ HM777122/ HM777123/ HM777124/ HM777125/ HM777126/ HM777127/ HM777128/ HM777129/ HM777130/ HM777131/ HM777132/ HM777133/ HM777134/ HM777135/ HM777136/ HM777137/ HM777138/ HM777139/ HM777140/ HM777141/ HM777142/ HM777143/ HM777144/ HM777145/ HM777146/ HM777147/ HM777148/ HM777149/ HM777150/ HM777151/ HM777152/ HM777153/ HM777154/ HM777155/ HM777156/ HM777157/ HM777158/ HM777159/ HM777160/ HM777161/ HM777162/ HM777163/ HM777164/ HM777165/ HM777166/ HM777167/ HM777168/ HM777169/ HM777170/ HM777171/ HM777172/ HM777173/ HM777174/ HM777175/ HM777176/ HM777177/ HM777178/ HM777179/ HM777180/ HM777181/ HM777182/ HM777183/ HM777184/ HM777185/ HM777186/ HM777187/ HM777188/ HM777189/ HM777190/ HM777191/ HM777192/ HM777193/ HM777194/ HM777195/ HM777196/ HM777197/ HM777198/ HM777199/ HM777200/ HM777201/ HM777202/ HM777203/ HM777204/ HM777205/ HM777206/ HM777207/ HM777208/ HM777209/ HM777210/ HM777211/ HM777212/ HM777213/ HM777214/ HM777215/ HM777216/ HM777217/ HM777218
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Viral
  • [Other-IDs] NLM/ PMC3122795
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40. |......... 3%  Sauter P, Hober D: Mechanisms and results of the antibody-dependent enhancement of viral infections and role in the pathogenesis of coxsackievirus B-induced diseases. Microbes Infect; 2009 Apr;11(4):443-51
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  • [Title] Mechanisms and results of the antibody-dependent enhancement of viral infections and role in the pathogenesis of coxsackievirus B-induced diseases.
  • The mechanisms of the antibody-dependent enhancement (ADE) of viral infection are presented, particularly within the Picornaviridae family.
  • The ADE of infection has been described in both human and animal models, worsens viral infections and compromises vaccine safety.
  • The ADE of coxsackievirus B infection can also be implied in the pathogenesis of diseases like chronic dilated cardiomyopathy or insulin-dependent type 1 diabetes.
  • [MeSH-major] Antibody-Dependent Enhancement. Cardiomyopathy, Dilated / etiology. Coxsackievirus Infections / complications. Coxsackievirus Infections / immunology. Diabetes Mellitus, Type 1 / etiology. Enterovirus B, Human / immunology

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  • [ErratumIn] Microbes Infect. 2009 Dec;11(14-15):1219
  • (PMID = 19399964.001).
  • [ISSN] 1769-714X
  • [Journal-full-title] Microbes and infection / Institut Pasteur
  • [ISO-abbreviation] Microbes Infect.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] France
  • [Number-of-references] 52
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41. |......... 3%  Li-Sha G, Yi-He C, Na-Dan Z, Teng Z, Yue-Chun L: Effects of carvedilol treatment on cardiac cAMP response element binding protein expression and phosphorylation in acute coxsackievirus B3-induced myocarditis. BMC Cardiovasc Disord; 2013;13:100
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  • [Title] Effects of carvedilol treatment on cardiac cAMP response element binding protein expression and phosphorylation in acute coxsackievirus B3-induced myocarditis.
  • BACKGROUND: The role of β-adrenergic stimulation on viral myocarditis has been investigated in animal models of viral myocarditis.
  • However, the CREB expression and phosphorylation have not been studied, and the effects of carvedilol (a nonselective β-adrenoceptor antagonist) on the CREB has not been investigated in the setting of acute viral myocarditis.
  • METHODS: This study was therefore designed to examine the effects of carvedilol on the transcriptional factor CREB in a murine model of acute viral myocarditis.
  • In a coxsackievirus B3 murine myocarditis model (Balb/c), effects of carvedilol on plasma noradrenaline, heart rate and blood pressure, myocardial histopathological changes and fibrosis, cardiomyocyte apoptosis, cardiac CREB and phosphorylated CREB, cytokine levels, and viral RNA were studied.
  • RESULTS: The expression and phosphorylation of CREB were decreased with concomitant increase of IL-6 and TNF-α in murine coxsackievirus-induced acute viral myocarditis.
  • Carvedilol increased the cardiac CREB expression and phosphorylation and decreased the plasma catecholamine levels and the production of IL-6 and TNF-α with amelioration of acute viral myocarditis.
  • CONCLUSION: These results show that CREB may be involved in the pathophysiology of viral myocarditis and carvedilol exerts some of its beneficial effects by increasing the CREB expression and phosphorylation.
  • [MeSH-major] CREB-Binding Protein / biosynthesis. Carbazoles / therapeutic use. Coxsackievirus Infections / drug therapy. Coxsackievirus Infections / metabolism. Myocarditis / drug therapy. Myocarditis / metabolism. Propanolamines / therapeutic use
  • [MeSH-minor] Acute Disease. Adrenergic beta-Antagonists / pharmacology. Adrenergic beta-Antagonists / therapeutic use. Animals. Gene Expression Regulation. Male. Mice. Mice, Inbred BALB C. Phosphorylation / drug effects. Phosphorylation / physiology. Treatment Outcome. Viral Proteins / drug effects

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  • (PMID = 24225056.001).
  • [ISSN] 1471-2261
  • [Journal-full-title] BMC cardiovascular disorders
  • [ISO-abbreviation] BMC Cardiovasc Disord
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenergic beta-Antagonists; 0 / Carbazoles; 0 / Crebbp protein, mouse; 0 / Propanolamines; 0 / Viral Proteins; 0 / coxsackie B3 virus protein 2B; 0K47UL67F2 / carvedilol; EC 2.3.1.48 / CREB-Binding Protein
  • [Other-IDs] NLM/ PMC3840656
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42. |......... 2%  Kim H, Kang B, Hwang S, Hong J, Chung J, Kim S, Jeong YS, Kim K, Cheon DS: Molecular characteristics of human coxsackievirus B1 infection in Korea, 2008-2009. J Med Virol; 2013 Jan;85(1):110-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular characteristics of human coxsackievirus B1 infection in Korea, 2008-2009.
  • This study was performed to analyze epidemiological and molecular characteristics of coxsakievirus (CV) B1 infection associated with severe neonatal illness cases and death in Korea during 2008-2009.
  • The other clinical symptoms were herpangina or hand-foot-mouth disease (22.1%) and neonatal sepsis (7.7%).
  • The identification of CVB1 in South Korea shows the potential of EVs to cause serious disease in an unpredictable fashion.
  • [MeSH-major] Coxsackievirus Infections / epidemiology. Coxsackievirus Infections / virology. Enterovirus / classification. Enterovirus / isolation & purification
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cluster Analysis. Female. Genotype. Humans. Infant. Male. Molecular Epidemiology. Molecular Sequence Data. Phylogeny. Polymerase Chain Reaction. RNA, Viral / genetics. Real-Time Polymerase Chain Reaction. Republic of Korea / epidemiology. Sequence Analysis, DNA. Sequence Homology, Amino Acid. Viral Structural Proteins / genetics

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  • [Copyright] Copyright © 2012 Wiley Periodicals, Inc.
  • [ErratumIn] J Med Virol. 2013 Aug;85(8):1498
  • [ErratumIn] J Med Virol. 2013 May;85(5):939
  • (PMID = 23073968.001).
  • [ISSN] 1096-9071
  • [Journal-full-title] Journal of medical virology
  • [ISO-abbreviation] J. Med. Virol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ JN638300/ JN638301/ JN638302/ JN638303/ JN638304/ JN638305/ JN638306/ JN638307/ JN638308/ JN638309/ JN638310/ JQ235663/ JQ235664/ JQ235665/ JQ235666/ JQ235667/ JQ235668/ JQ235669/ JQ235670/ JQ235671/ JQ235672/ JQ235673/ JQ235674/ JQ235675/ JQ235676/ JQ235677/ JQ235678/ JQ235679/ JQ235680/ JQ235681/ JQ235682/ JQ235683/ JQ235684/ JQ235685/ JQ235686/ JQ235687/ JQ235688/ JQ235689
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Viral; 0 / Viral Structural Proteins
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43. |......... 2%  Verma NA, Zheng XT, Harris MU, Cadichon SB, Melin-Aldana H, Khetsuriani N, Oberste MS, Shulman ST: Outbreak of life-threatening coxsackievirus B1 myocarditis in neonates. Clin Infect Dis; 2009 Sep 1;49(5):759-63
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  • [Title] Outbreak of life-threatening coxsackievirus B1 myocarditis in neonates.
  • In the summer and fall of 2007, we observed a unique cluster of cases of severe coxsackievirus B1 (CVB1) infection among Chicago area neonates.
  • Eight neonates had closely related strains of CVB1 that were typed at the Centers of Disease Control and Prevention; 2 other neonates had CVB infections, 1 of which was further identified as serotype CVB1.
  • [MeSH-major] Coxsackievirus Infections / epidemiology. Disease Outbreaks. Enterovirus B, Human / classification. Myocarditis / epidemiology. Myocarditis / virology

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  • (PMID = 19622042.001).
  • [ISSN] 1537-6591
  • [Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • [ISO-abbreviation] Clin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. |......... 2%  Rose NR: Critical cytokine pathways to cardiac inflammation. J Interferon Cytokine Res; 2011 Oct;31(10):705-10
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  • Infectious disease is frequently cited as a precursor of subsequent autoimmune disease in genetically susceptible hosts.
  • However, the precise mechanisms required for the transition from infection to autoimmunity have not been well defined.
  • We have developed a mouse model of autoimmune myocarditis initiated by infection with Coxsackievirus B3 to trace the cytokine pathways involved.
  • We found that greater production of interleukin-1β (IL-1β) and tumor necrosis factor-α during the early innate response to virus infection is necessary and sufficient to induce a later heart-specific autoimmune disease.
  • Severity of the autoimmune myocarditis is determined by the profile of a number of T helper 1 (Th1) and Th2 cytokines.
  • Th17 cytokines also contribute to disease, but the signature Th17 cytokine, IL-17A, is not required for cardiac inflammation.
  • These findings may provide useful markers to identify individuals prone to develop an autoimmune sequel after infection and suggest future early interventions.
  • [MeSH-major] Autoimmune Diseases / immunology. Cytokines / immunology. Immunity, Innate. Myocarditis / immunology. Myocardium / immunology. T-Lymphocytes, Helper-Inducer / immunology
  • [MeSH-minor] Animals. Coxsackievirus Infections / complications. Coxsackievirus Infections / immunology. Coxsackievirus Infections / pathology. Disease Models, Animal. Enterovirus B, Human / immunology. Humans. Mice

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  • (PMID = 21861699.001).
  • [ISSN] 1557-7465
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI151835; United States / NHLBI NIH HHS / HL / HL67290; United States / NHLBI NIH HHS / HL / HL70729
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines
  • [Other-IDs] NLM/ PMC3189548
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45. |......... 2%  Fairweather D, Stafford KA, Sung YK: Update on coxsackievirus B3 myocarditis. Curr Opin Rheumatol; 2012 Jul;24(4):401-7
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  • [Title] Update on coxsackievirus B3 myocarditis.
  • PURPOSE OF REVIEW: To present recent findings on the pathogenesis of coxsackievirus B3 (CVB3) myocarditis based on animal models, with a focus on the role of T helper (Th) immune responses in disease progression.
  • RECENT FINDINGS: Acute CVB3 myocarditis is known to be increased by Th1 immune responses, but recent findings indicate that Th1-type immunity protects against acute myocarditis by reducing viral replication and prevents the progression to chronic myocarditis and dilated cardiomyopathy (DCM) by inhibiting Th2 responses.
  • Th1 responses protect against CVB3 myocarditis by inhibiting Th2 responses and viral replication, but increase acute inflammation.
  • [MeSH-major] Autoimmune Diseases / virology. Coxsackievirus Infections / complications. Enterovirus B, Human. Myocarditis / virology
  • [MeSH-minor] Animals. Disease Models, Animal. Mice. T-Lymphocytes, Helper-Inducer / immunology

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  • (PMID = 22488075.001).
  • [ISSN] 1531-6963
  • [Journal-full-title] Current opinion in rheumatology
  • [ISO-abbreviation] Curr Opin Rheumatol
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL087033
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
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46. |......... 2%  Cooper IF, Siadaty MS: 'Pharmacologic Substances' associated with 'Coxsackie Virus Infection': Top Publications. BioMedLib Review; PharmacologicSubstance;CoxsackieVirusInfection:706082900. ISSN: 2331-5717. 2014/12/22
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  • [Title] 'Pharmacologic Substances' associated with 'Coxsackie Virus Infection': Top Publications.
  • There are articles published each month which present 'Pharmacologic Substance' for 'coxsackie virus infection'.
  • Cooper IF et al: 'Amino Acids, Peptides, or Proteins' associated with 'Coxsackie Virus Infection': Top Publications.
  • Rager-Zisman B et al: Effects of immunosuppression on coxsackie B-3 virus infection in mice, and passive protection by circulating antibody.
  • Rager-Zisman B et al: The role of antibody and host cells in the resistance of mice against infection by coxsackie B-3 virus.
  • Fechner H et al: Pharmacological and biological antiviral therapeutics for cardiac coxsackievirus infections.
  • Galabov AS et al: Antiviral activity of N-phenyl-N'-aryl- or alkylthiourea derivatives in Coxsackie virus infections in mice.
  • Wessely R et al: Cardioselective infection with coxsackievirus B3 requires intact type I interferon signaling: implications for mortality and early viral replication.
  • Huber SA et al: Influence of sex hormones on Coxsackie B-3 virus infection in Balb/c mice.
  • Al-Hello H et al: Amino acids of Coxsackie B5 virus are critical for infection of the murine insulinoma cell line, MIN-6.
  • Berg AK et al: Antiviral treatment of Coxsackie B virus infection in human pancreatic islets.
  • Yuan W: [Effects of Coxsackie B-2 virus infection on electrophysiologic properties of beating cultured rat heart cells].

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  • [Copyright] Copyright 2014 Siadaty and Cooper; licensee BioMedLib LLC.
  • (UID = 706082900.001).
  • [ISSN] 2331-5717
  • [Journal-full-title] BioMedLib Review
  • [Language] eng
  • [Publication-type] Review
  • [Publication-country] UNITED STATES
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47. |......... 2%  Jun EJ, Ye JS, Hwang IS, Kim YK, Lee H: Selenium deficiency contributes to the chronic myocarditis in coxsackievirus-infected mice. Acta Virol; 2011;55(1):23-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selenium deficiency contributes to the chronic myocarditis in coxsackievirus-infected mice.
  • Both coxsackievirus B3 (CVB3) infection and selenium (Se) deficiency play a pivotal role in Keshan disease of the heart.
  • The Se deficiency was known to contribute to the CVB3-induced myocarditis in acute and subacute phase of infection.
  • However, its effect on the myocarditis in chronic phase of infection has not been examined yet.
  • To address this question, we kept mice on a Se-replete or Se-deficient diet for 28 days, infected them intraperitoneally with CVB3 and maintaining previous diets, we examined them for next 90 days for several parameters indicative of the infection or disease.
  • We found out that the mice on the Se-deficient diet exhibited a higher mortality, lower serum glutathione peroxidase (GPx) activity, evident histopathological changes indicative of myocarditis, and a higher level of viral RNA in the heart.
  • Summing up, these data suggest that the Se-deficiency creates a chronic myocarditis-prone condition by fostering the active virus replication.
  • [MeSH-major] Coxsackievirus Infections / metabolism. Coxsackievirus Infections / virology. Enterovirus / physiology. Myocarditis / metabolism. Myocarditis / virology. Selenium / deficiency
  • [MeSH-minor] Animals. Cardiomyopathies / pathology. Cardiomyopathies / virology. Cercopithecus aethiops. Enterovirus Infections / pathology. Enterovirus Infections / virology. Glutathione Peroxidase / blood. Heart / virology. Mice. Myocardium / pathology. RNA, Viral / genetics. Vero Cells

  • HSDB. structure - SELENIUM, ELEMENTAL.
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  • (PMID = 21434702.001).
  • [ISSN] 0001-723X
  • [Journal-full-title] Acta virologica
  • [ISO-abbreviation] Acta Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / RNA, Viral; EC 1.11.1.9 / Glutathione Peroxidase; H6241UJ22B / Selenium; Keshan disease
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48. |......... 2%  Cooper IF, Siadaty MS: 'Laboratory Procedures' associated with 'Coxsackie Virus Infection': Top Publications. BioMedLib Review; LaboratoryProcedure;CoxsackieVirusInfection:705463118. ISSN: 2331-5717. 2014/8/18
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  • [Title] 'Laboratory Procedures' associated with 'Coxsackie Virus Infection': Top Publications.
  • There are articles published each month which present 'Laboratory Procedure' for 'coxsackie virus infection'.
  • Cooper IF et al: 'Laboratory Procedures' associated with 'Coxsackie Virus Infection': Top Publications.
  • E W et al: [Detection of Coxsackie B3 virus infection in newborn care unit using reverse transcriptase polymerase chain reaction method].
  • Shafren DR et al: Mouse cells expressing human intercellular adhesion molecule-1 are susceptible to infection by coxsackievirus A21.
  • Dörries R et al: Specificity of IgM antibodies in acute human coxsackievirus B infections, analysed by indirect solid phase enzyme immunoassay and immunoblot technique.
  • Chan D et al: Comparison of serodiagnosis of group B coxsackievirus infections by an immunoglobulin M capture enzyme immunoassay versus microneutralization.
  • MacWilliam KM et al: Counterelectrophoresis on human serum in coxsackie virus infections.
  • Sachtleben P et al: [The electrokinetic potentials of tissue culture cells after infection with coxsackie B3 virus].
  • Kaznacheev VP et al: [Electron microscopic study of the myocardium of mice with experimental infection caused by Coxsackie virus A13].
  • Yang YZ et al: Coxsackie B-2 virus infection in rat beating heart cell culture.
  • Angela GC et al: [Cytomorphology and enzymocytochemistry of Coxsackie virus A9 infection in cell cultures].

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  • [Copyright] Copyright 2014 Siadaty and Cooper; licensee BioMedLib LLC.
  • (UID = 705463118.001).
  • [ISSN] 2331-5717
  • [Journal-full-title] BioMedLib Review
  • [Language] eng
  • [Publication-type] Review
  • [Publication-country] UNITED STATES
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49. |......... 2%  Yip CC, Lau SK, Woo PC, Yuen KY: Human enterovirus 71 epidemics: what's next? Emerg Health Threats J; 2013;6:19780
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • EV71 commonly causes hand, foot and mouth disease (HFMD) in children, but can result in neurological and cardiorespiratory complications in severe cases.
  • In particular, 'double-recombinant' EV71 strains belonging to a novel genotype D have been predominant in mainland China and Hong Kong over the last decade, though co-circulating with a minority of other EV71 subgenotypes and coxsackie A viruses.
  • [MeSH-major] Coxsackievirus Infections / epidemiology. Coxsackievirus Infections / virology. Enterovirus A, Human / genetics. Hand, Foot and Mouth Disease / epidemiology. Hand, Foot and Mouth Disease / virology
  • [MeSH-minor] Child. China / epidemiology. Disease Outbreaks / statistics & numerical data. Evolution, Molecular. Genotype. Humans. Mutation. Recombination, Genetic. Sequence Analysis, DNA

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  • (PMID = 24119538.001).
  • [ISSN] 1752-8550
  • [Journal-full-title] Emerging health threats journal
  • [ISO-abbreviation] Emerg Health Threats J
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Sweden
  • [Other-IDs] NLM/ PMC3772321
  • [Keywords] NOTNLM ; evolution / genotype / hand, foot and mouth disease / human enterovirus 71 / mutation / recombination
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50. |......... 2%  Li X, Mao C, Ma S, Wang X, Sun Z, Yi Y, Guo M, Shen X, Sun L, Bi S: Generation of neutralizing monoclonal antibodies against Enterovirus 71 using synthetic peptides. Biochem Biophys Res Commun; 2009 Dec 25;390(4):1126-8
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  • Enterovirus 71 (EV71) has led to recent outbreaks of hand, foot and mouth disease (HFMD) in China, resulting in high mortality.
  • The specificities of the anti-EV71 peptide monoclonal antibodies were confirmed by Western blot analysis and immunocytochemistry against EV71 virus.
  • Because there is no vaccine available and treatment is very limited, mouse anti-EV71 monoclonal antibody, clone 22A12, could be a promising candidate to be humanized and used for treatment of EV71 infection.
  • [MeSH-major] Antibodies, Monoclonal / biosynthesis. Antibodies, Neutralizing / biosynthesis. Antibodies, Viral / biosynthesis. Enterovirus A, Human / immunology. Viral Vaccines / immunology
  • [MeSH-minor] Animals. Coxsackievirus Infections / immunology. Coxsackievirus Infections / therapy. Coxsackievirus Infections / virology. Hand, Foot and Mouth Disease / immunology. Hand, Foot and Mouth Disease / therapy. Hand, Foot and Mouth Disease / virology. Humans. Mice. Neutralization Tests. Peptides / immunology

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  • (PMID = 19799860.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Neutralizing; 0 / Antibodies, Viral; 0 / Peptides; 0 / Viral Vaccines
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