Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2006-9-28
pubmed:abstractText
Coxsackie adenovirus receptor (CAR) is involved in immunological processes, and its soluble isoforms have antiviral effects on coxsackievirus B3 (CVB3) infection in vitro. We explored in this study the impact of CAR4/7, a soluble CAR isoform, on CVB3-induced myocarditis in BALB/c mice. BALB/c mice were treated daily with recombinant CAR4/7, beta-galactosidase (beta-Gal; as control protein) or buffer for 9 days. Half of each group was infected with CVB3 on day 3, and all mice were killed on day 9. Myocardial CVB3 titer, histology, and serology were analyzed. Treatment with CAR4/7 led to a significant reduction of myocardial CVB3 titer, whereas the application of beta-Gal had no detectable effect on the myocardial virus load. CAR4/7 application, however, resulted in increased myocardial inflammation and tissue damage in CVB3-infected hearts, whereas beta-Gal caused a degree of cardiac inflammation and injury similar to that in buffer-treated CVB3-infected control animals. CAR4/7 and beta-Gal treatment induced the production of antibodies against the respective antigens. CAR4/7-, but not beta-Gal-specific, virus-negative sera reacted against myocardial tissue and cellular membranous CAR, and significantly inhibited CVB3 infection in vitro. Thus, CAR4/7 suppressed CVB3 infection in vivo, supporting the concept of receptor analog in antiviral therapy. However, CAR4/7 treatment also leads to an aggravation of myocardial inflammation and injury most likely secondary to an autoimmune process.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0946-2716
pubmed:author
pubmed:issnType
Print
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
842-51
pubmed:dateRevised
2011-7-8
pubmed:meshHeading
pubmed-meshheading:16924471-Animals, pubmed-meshheading:16924471-Antiviral Agents, pubmed-meshheading:16924471-Cell Survival, pubmed-meshheading:16924471-Coxsackievirus Infections, pubmed-meshheading:16924471-Creatine Kinase, pubmed-meshheading:16924471-Enterovirus B, Human, pubmed-meshheading:16924471-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:16924471-HeLa Cells, pubmed-meshheading:16924471-Humans, pubmed-meshheading:16924471-Immune Sera, pubmed-meshheading:16924471-Immunohistochemistry, pubmed-meshheading:16924471-Injections, Intraperitoneal, pubmed-meshheading:16924471-Male, pubmed-meshheading:16924471-Mice, pubmed-meshheading:16924471-Mice, Inbred BALB C, pubmed-meshheading:16924471-Myocarditis, pubmed-meshheading:16924471-Random Allocation, pubmed-meshheading:16924471-Receptors, Virus, pubmed-meshheading:16924471-Recombinant Proteins, pubmed-meshheading:16924471-Serum Amyloid A Protein, pubmed-meshheading:16924471-Solubility
pubmed:year
2006
pubmed:articleTitle
Treatment of coxsackievirus-B3-infected BALB/c mice with the soluble coxsackie adenovirus receptor CAR4/7 aggravates cardiac injury.
pubmed:affiliation
Department of Cardiology and Pneumonology, Charité University of Medicine, Campus Benjamin Franklin, Hindenburgdamm 30, 12200, Berlin, Germany. andrea.doerner@charite.de
pubmed:publicationType
Journal Article