コクサッキーBウイルス

関: coxsackievirus B、echovirus、human enterovirus B

WordNet

any of a group of viruses associated with various diseases including viral meningitis and mild respiratory disorders and diarrhea in newborn infants
a harmful or corrupting agency; "bigotry is a virus that must not be allowed to spread"; "the virus of jealousy is latent in everyone"
(virology) ultramicroscopic infectious agent that replicates itself only within cells of living hosts; many are pathogenic; a piece of nucleic acid (DNA or RNA) wrapped in a thin coat of protein
a software program capable of reproducing itself and usually capable of causing great harm to files or other programs on the same computer; "a true virus cannot spread to another computer without human assistance" (同)computer virus
the 2nd letter of the Roman alphabet (同)b
the blood group whose red cells carry the B antigen (同)type_B, group B

PrepTutorEJDIC

ビールス,ろ過性病原体

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/11/12 21:42:52」(JST)

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Coxsackie B is the name of a group of six serotypes of pathogenic enteroviruses that trigger illness ranging from mild gastrointestinal distress to full-fledged pericarditis and myocarditis.^[1]

Geographic distribution

The various members of the Coxsackie B group were discovered almost entirely in the United States, appearing originally in Connecticut, Ohio, New York, and Kentucky, although a sixth member of the group has been found in the Philippines.^[1] That said, all six serotypes have a global distribution and are a relatively common cause of gastrointestinal upset.

Symptoms

Symptoms of infection with viruses in the Coxsackie B grouping include fever, headache, sore throat, gastrointestinal distress, as well as chest and muscle pain. This presentation is known as pleurodynia or Bornholm disease in many areas. Sufferers of chest pain should see a doctor immediately - in some cases, viruses in the Coxsackie B family progress to myocarditis or pericarditis, which can result in permanent heart damage or death. Coxsackie B virus infection may also induce aseptic meningitis. As a group, they are the most common cause of unexpected sudden death, and may account for up to 50% of such cases.^[2] The incubation period for the Coxsackie B viruses is, like most of the Enteroviridae, highly variable, ranging from 2 to 35 days, and illness may last for up to two weeks, but may resolve as quickly as two days. Infection usually occurs between the months of June and October in temperate Northern Hemisphere regions.^[1]

Diagnosis

Enterovirus infection is diagnosed mainly via serological tests such as ELISA^[3] and from cell culture.^[1] Because the same level and type of care is given regardless of type of Coxsackie B infection, it is mostly unnecessary for treatment purposes to diagnose which virus is causing the symptoms in question, though it may be epidemiologically useful.

Viral structure and function

Coxsackie B viruses are single-strand positive-sense RNA viruses that are resistant to a wide variety of chemical treatments. The viral particles themselves are roughly 30 nm icosahedrons.^[4] The virus is most frequently distributed via the fecal-oral route, and infection commonly occurs after eating contaminated food. Coxsackie B viruses are cytolytic, and Coxsackie B2 and B5 viruses have been implicated in hand, foot and mouth disease as well as respiratory infection.^[1] Infection in infants is mostly asymptomatic, but sometimes results in the death of the infant, often due to myocarditis.^[5] Birth defects may also be present in a Coxsackie B infected infant.

Diabetes

Main article: Coxsackie B4 virus

The B4 strain of Coxsackie viruses has been discovered to be a possible cause of Diabetes mellitus type 1.

Treatment and prevention

As of 2008^[update], there is no well-accepted treatment for the Coxsackie B group of viruses.^[1] Palliative care is available, however, and patients suffering chest pain or stiffness of the neck should be examined for signs of cardiac or central nervous system involvement, respectively. Some measure of prevention can usually be achieved by basic sanitation on the part of food-service workers, though the viruses are highly contagious. Care should be taken in washing ones hands and in cleaning the body after swimming. In the event of Coxsackie-induced myocarditis or pericarditis, antiinflammatories can be given to reduce damage to the heart muscle.

References

^ ^a ^b ^c ^d ^e ^f Fields, Bernard N.; David M. Knipe, Robert M. Chanock, Joseph L. Melnick, Bernard Roizman, Robert E. Shope (1985). Fields Virology. New York: Raven Press. pp. 739–794. ISBN 0-88167-026-X.
^ Maze, S. S.; R. J. Adolph (February 1990). "Myocarditis: unresolved issues in diagnosis and treatment". Clinical Cardiology 13 (2): 69–79. doi:10.1002/clc.4960130203. PMID 2407397.
^ Bell, Eleanor J.; R.A. McCartney, Diane Basquill, A.K.R. Chaudhuri (1986). "Mu-Antibody capture elisa for the rapid diagnosis of enterovirus infections in patients with aseptic meningitis". Journal of Medical Virology 19 (3): 213–217. doi:10.1002/jmv.1890190303. PMID 3016164.
^ Libby, Karen (2000). "Coxsackie B virus pathogen card". http://www.stanford.edu/group/virus/flavi/2000/coxsackieB.htm. Retrieved 2007-09-02.
^ Kaplan, M. H.; Klein S. W., McPhee J., Harper R. G. (1983 November-December). "Group B coxsackievirus infections in infants younger than three months of age: a serious childhood illness". Reviews of Infectious Diseases 5 (6): 1019–1032. PMID 6318288.

UpToDate Contents

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1. エンテロウイルスおよびパレコウイルス感染の臨床症状および診断 clinical manifestations and diagnosis of enterovirus and parechovirus infections
2. 小児における口腔軟部組織病変 soft tissue lesions of the oral cavity in children
3. エンテロウイルスおよびパレコウイルス感染症の疫学、病因、治療、および予防 epidemiology pathogenesis treatment and prevention of enterovirus and parechovirus infections
4. 口腔病変 oral lesions
5. アテローム性動脈硬化症の病因 pathogenesis of atherosclerosis

English Journal

Programmed necrosis in microbial pathogenesis.

Sridharan H1, Upton JW2.Author information 1Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, 2506 Speedway, Stop A5000, Austin, TX 78712-1191, USA.2Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, 2506 Speedway, Stop A5000, Austin, TX 78712-1191, USA. Electronic address: upton@austin.utexas.edu.AbstractProgrammed cell death is an important facet of hostpathogen interactions. Although apoptosis has long been implicated as the major form of programmed cell death in host defense, the past decade has seen the emergence of other forms of regulated death, including programmed necrosis. While the molecular mechanisms of programmed necrosis continue to be unveiled, an increasing number of viral and bacterial pathogens induce this form of death in host cells, with important consequences for infection, control, and pathogenesis. Moreover, pathogen strategies to manipulate or utilize this pathway are now being discovered. In this review, we focus on a variety of viral and bacterial pathogens where a role for programmed necrosis is starting to be appreciated. In particular, we focus on the mechanistic details of how the host or the pathogen might appropriate this pathway for its own benefit.
Trends in microbiology.Trends Microbiol.2014 Feb 21. pii: S0966-842X(14)00017-1. doi: 10.1016/j.tim.2014.01.005. [Epub ahead of print]
Programmed cell death is an important facet of hostpathogen interactions. Although apoptosis has long been implicated as the major form of programmed cell death in host defense, the past decade has seen the emergence of other forms of regulated death, including programmed necrosis. While the molecul
PMID 24565922

Species D Human Adenovirus Type 9 Exhibits Better Virus-Spread Ability for Antitumor Efficacy among Alternative Serotypes.

Uchino J1, Curiel DT2, Ugai H1.Author information 1Cancer Biology Division, School of Medicine, Washington University in St. Louis, St. Louis, Missouri, United States of America.2Cancer Biology Division, School of Medicine, Washington University in St. Louis, St. Louis, Missouri, United States of America ; Biologic Therapeutics Center, Department of Radiation Oncology, School of Medicine, Washington University in St. Louis, St. Louis, Missouri, United States of America.AbstractSpecies C human adenovirus serotype 5 (HAdV-C5) is widely used as a vector for cancer gene therapy, because it efficiently transduces target cells. A variety of HAdV-C5 vectors have been developed and tested in vitro and in vivo for cancer gene therapy. While clinical trials with HAdV-C5 vectors resulted in effective responses in many cancer patients, administration of HAdV-C5 vectors to solid tumors showed responses in a limited area. A biological barrier in tumor mass is considered to hinder viral spread of HAdV-C5 vectors from infected cells. Therefore, efficient virus-spread from an infected tumor cell to surrounding tumor cells is required for successful cancer gene therapy. In this study, we compared HAdV-C5 to sixteen other HAdV serotypes selected from species A to G for virus-spread ability in vitro. HAdV-D9 showed better virus-spread ability than other serotypes, and its viral progeny were efficiently released from infected cells during viral replication. Although the HAdV-D9 fiber protein contains a binding site for coxsackie B virus and adenovirus receptor (CAR), HAdV-D9 showed expanded tropism for infection due to human CAR (hCAR)-independent attachment to target cells. HAdV-D9 infection effectively killed hCAR-negative cancer cells as well as hCAR-positive cancer cells. These results suggest that HADV-D9, with its better virus-spread ability, could have improved therapeutic efficacy in solid tumors compared to HAdV-C5.
PloS one.PLoS One.2014 Feb 4;9(2):e87342. doi: 10.1371/journal.pone.0087342. eCollection 2014.
Species C human adenovirus serotype 5 (HAdV-C5) is widely used as a vector for cancer gene therapy, because it efficiently transduces target cells. A variety of HAdV-C5 vectors have been developed and tested in vitro and in vivo for cancer gene therapy. While clinical trials with HAdV-C5 vectors res
PMID 24503714

Infection of human islets of langerhans with two strains of coxsackie B virus serotype 1: Assessment of virus replication, degree of cell death and induction of genes involved in the innate immunity pathway.

Anagandula M1, Richardson SJ, Oberste MS, Sioofy-Khojine AB, Hyöty H, Morgan NG, Korsgren O, Frisk G.Author information 1Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.AbstractType 1 diabetes mellitus is believed to be triggered, in part, by one or more environmental factors and human enteroviruses (HEVs) are among the candidates. Therefore, this study has examined whether two strains of HEV may differentially affect the induction of genes involved in pathways leading to the synthesis of islet hormones, chemokines and cytokines in isolated, highly purified, human islets. Isolated, purified human pancreatic islets were infected with strains of Coxsackievirus B1.Viral replication and the degree of CPE/islet dissociation were monitored. The expression of insulin, glucagon, CXCL10, TLR3, IF1H1, CCL5, OAS-1, IFNβ, and DDX58 was analyzed. Both strains replicated in islets but only one of strain caused rapid islet dissociation/CPE. Expression of the insulin gene was reduced during infection of islets with either viral strain but the gene encoding glucagon was unaffected. All genes analyzed which are involved in viral sensing and the development of innate immunity were induced by Coxsackie B viruses, with the notable exception of TLR3. There was no qualitative difference in the expression pattern between each strain but the magnitude of the response varied between donors. The lack of virus induced expression of TLR3, together with the differential regulation of IF1H1, OAS1 and IFNβ, (each of which has polymorphic variants influence the predisposition to type 1 diabetes), that might result in defective clearance of virus from islet cells. The reduced expression of the insulin gene and the unaffected expression of the gene encoding glucagon by Coxsackie B1 infection is consistent with the preferential β-cell tropism of the virus. J. Med. Virol. 9999: XX-XX, 2013. © 2013 Wiley Periodicals, Inc.
Journal of medical virology.J Med Virol.2013 Nov 19. doi: 10.1002/jmv.23835. [Epub ahead of print]
Type 1 diabetes mellitus is believed to be triggered, in part, by one or more environmental factors and human enteroviruses (HEVs) are among the candidates. Therefore, this study has examined whether two strains of HEV may differentially affect the induction of genes involved in pathways leading to
PMID 24249667

Japanese Journal

コクサッキーウイルス感染を伴ったunilateral acute idiopathic maculopathy(UAIM)の1例 (特集第67回日本臨床眼科学会講演集(8))

山田章悟,平本裕盛,三木克朗 [他]
臨床眼科 68(10), 1433-1439, 2014-10
NAID 40020219561

職員スキー旅行後に発生した手足口病の集団感染

加藤徳子,北野十喜一,竹尾友宏,秋田洋一,渡辺大輔,山岸由佳,三鴨廣繁
日本皮膚科学会雑誌 124(7), 1301-1304, 2014
2013年2月に愛知医科大学病院職員30名が参加したスキー合宿旅行後，4名に発症した手足口病の事例を経験した．NT法を用いたペア血清では4名ともにコクサッキーウイルスA10（coxsackievirus A10：CA10）抗体価の有意な上昇が認められたが，CA6, 16およびエンテロウイルス71（enterovirus71：EV71）の上昇がみられたものもいた．当院ICT（Infection Co …
NAID 130005055503

Coxsackie A16 Virus-associated Atypical Hand-foot-and-mouth Disease

Matsuzawa Michiko,Ishii Akira,Demitsu Toshio,Sugawara Hitoshi
Internal Medicine 53(6), 643-644, 2014
NAID 130003392723

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リンク元	「コクサッキーBウイルス」「coxsackievirus B」「human enterovirus B」
関連記事	「B」「virus」

「コクサッキーBウイルス」

Coxsackie B virus
	Coxsackie B4 virus
Virus classification
Group:	Group IV ((+)ssRNA)
Family:	Picornaviridae
Genus:	Enterovirus
Species:	Human enterovirus B
Subtype
	Coxsackie B virus

　　[★]

英: Coxsackie B virus
関: エコーウイルス、B型ヒトエンテロウイルス、コクサッキーウイルスB

「coxsackievirus B」

　　[★]

コクサッキーウイルスB

関: Coxsackie B virus、echovirus、human enterovirus B

「human enterovirus B」

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B型ヒトエンテロウイルス

関: Coxsackie B virus、coxsackievirus B、echovirus

「B」

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気管分岐部下緑
補体のalternative pathwayに関わる蛋白質

Mg2+存在下でC3, B, Dが反応してC3bBbとなり、これがC3転換酵素(C3bBb)あるいはC5転換酵素(C3bBb3b)を形成する。これらはP(properdin)と結合して活性化し、それぞれC3、C5を活性化する

「virus」

　　[★] ウイルス

[Fields_Virology-0] ^ ^a ^b ^c ^d ^e ^f Fields, Bernard N.; David M. Knipe, Robert M. Chanock, Joseph L. Melnick, Bernard Roizman, Robert E. Shope (1985). Fields Virology. New York: Raven Press. pp. 739–794. ISBN 0-88167-026-X.

[1] Maze, S. S.; R. J. Adolph (February 1990). "Myocarditis: unresolved issues in diagnosis and treatment". Clinical Cardiology 13 (2): 69–79. doi:10.1002/clc.4960130203. PMID 2407397.

[2] Bell, Eleanor J.; R.A. McCartney, Diane Basquill, A.K.R. Chaudhuri (1986). "Mu-Antibody capture elisa for the rapid diagnosis of enterovirus infections in patients with aseptic meningitis". Journal of Medical Virology 19 (3): 213–217. doi:10.1002/jmv.1890190303. PMID 3016164.

[3] Libby, Karen (2000). "Coxsackie B virus pathogen card". http://www.stanford.edu/group/virus/flavi/2000/coxsackieB.htm. Retrieved 2007-09-02.

[4] Kaplan, M. H.; Klein S. W., McPhee J., Harper R. G. (1983 November-December). "Group B coxsackievirus infections in infants younger than three months of age: a serious childhood illness". Reviews of Infectious Diseases 5 (6): 1019–1032. PMID 6318288.

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案内

Coxsackie B virus