Soluble coxsackie- and adenovirus receptor (sCAR-Fc); a highly efficient compound against laboratory and clinical strains of coxsackie-B-virus

2016 ◽  
Vol 136 ◽  
pp. 1-8 ◽  
Author(s):  
Sandra Pinkert ◽  
Babette Dieringer ◽  
Sabine Diedrich ◽  
Heinz Zeichhardt ◽  
Jens Kurreck ◽  
...  
Keyword(s):  
Coxsackie And Adenovirus Receptor ◽  
Clinical Strains ◽  
Highly Efficient ◽  
B Virus ◽  
Coxsackie B Virus ◽  
Adenovirus Receptor ◽  
Coxsackie B

scholarly journals The Coxsackie B Virus and Adenovirus Receptor Resides in a Distinct Membrane Microdomain

2003 ◽  
Vol 77 (4) ◽  
pp. 2559-2567 ◽  
Author(s):  
Katherine J. D. Ashbourne Excoffon ◽  
Thomas Moninger ◽  
Joseph Zabner
Keyword(s):  
Lipid Raft ◽  
Density Lipoprotein ◽  
Cellular Adhesion ◽  
Immunoglobulin Superfamily ◽  
Viral Receptor ◽  
Membrane Microdomain ◽  
B Virus ◽  
Coxsackie B Virus ◽  
Adenovirus Receptor ◽  
Coxsackie B

ABSTRACT The coxsackie B virus and adenovirus receptor (CAR) is a member of the immunoglobulin superfamily. In addition to activity as a viral receptor, it may play a role in cellular adhesion. We asked what determines the cell membrane microdomain of CAR. We found that CAR is localized to a novel lipid-rich microdomain similar to that of the low-density lipoprotein receptor (LDLR) but distinct from that of a CAR variant that exhibited traditional lipid raft localization via fusion to a glycosylphosphatidylinositol (GPI) tail. The cytoplasmic tail determines its membrane localization, since deletion of this domain resulted in mislocalization. Results indicate that CAR, CAR-LDLR, and LDLR reside in a novel lipid raft that is distinct from caveolin-1-containing caveolae and GPI-linked proteins. Residence in a lipid-rich domain provides a mechanism that allows CAR to interact with other cell adhesion proteins and yet function as an adenovirus receptor.

scholarly journals A Zebrafish Coxsackievirus and Adenovirus Receptor Homologue Interacts with Coxsackie B Virus and Adenovirus

2002 ◽  
Vol 76 (20) ◽  
pp. 10503-10506 ◽  
Author(s):  
JenniElizabeth Petrella ◽  
Christopher J. Cohen ◽  
Jedidiah Gaetz ◽  
Jeffrey M. Bergelson
Keyword(s):  
Adenovirus Type ◽  
Extracellular Domain ◽  
Receptor Interaction ◽  
Transfected Cells ◽  
B Virus ◽  
Coxsackie B Virus ◽  
Coxsackievirus And Adenovirus Receptor ◽  
Adenovirus Receptor ◽  
Adenovirus Type 5 ◽  
Coxsackie B

ABSTRACT In this study, a zebrafish homologue of the coxsackievirus and adenovirus receptor (CAR) protein was identified. Although the extracellular domain of zebrafish CAR (zCAR) is less than 50% identical to that of human CAR (hCAR), zCAR mediated infection of transfected cells by both adenovirus type 5 and coxsackievirus B3. CAR residues interacting deep within the coxsackievirus canyon are highly conserved in zCAR and hCAR, which is consistent with the idea that receptor contacts within the canyon are responsible for coxsackievirus attachment. In contrast, CAR residues contacting the south edge of the canyon are not conserved, suggesting that receptor interaction with the viral “puff region” is not essential for attachment.

Myocarditis in Children

1987 ◽  
Vol 9 (3) ◽  
pp. 83-88
Author(s):  
Arno R. Hohn ◽  
Robert E. Stanton
Keyword(s):  
Acute Myocarditis ◽  
B Virus ◽  
Coxsackie B Virus ◽  
Coxsackie B

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

TRANSIENT SYNOVITIS OF THE HIP JOINT IN CHILDREN

PEDIATRICS ◽  
1959 ◽  
Vol 24 (6) ◽  
pp. 1042-1049 ◽  
Author(s):  
Alexander Spock
Keyword(s):  
Hip Joint ◽  
Streptococcal Infection ◽  
Weight Bearing ◽  
Bed Rest ◽  
Transient Synovitis ◽  
Treatment Results ◽  
B Virus ◽  
Coxsackie B Virus ◽  
Roentgenographic Examination ◽  
Coxsackie B

A clinical review of 47 eases of transient synovitis of the hip joint occurring in patients less than 14 years of age is presented. Evidence from clinical, bacteriologic and serologic data is presented to show that in four patients acute streptococcal infection was associated with the development of transient synovitis. In one other patient clinical and serologic data disclosed a similar parallelism with an infection by the Coxsackie B virus. These findings suggest that these agents may be among those etiologically responsible for this syndrome. An obese or stocky physique probably predisposes a child to this disease. Patients with transient synovitis do not have any diagnostic abnormalities which can be detected by roentgenographic examination. Prevention of weight bearing by bed rest until the patient is completely asymptomatic provides the best form of therapy, and failure to follow such treatment results in prolongation of the illness. Antibiotics do not appear to influence the course of the disease. Three patients in this series developed Legg-Perthes disease within an interval of 3 to 17 months after convalescing from transient synovitis of the hip.

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