RGD Reference Report - Coxsackievirus B3-associated myocardial pathology and viral load reduced by recombinant soluble human decay-accelerating factor in mice. - Rat Genome Database

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Coxsackievirus B3-associated myocardial pathology and viral load reduced by recombinant soluble human decay-accelerating factor in mice.

Authors: Yanagawa, Bobby  Spiller, O Brad  Choy, Jonathan  Luo, Honglin  Cheung, Paul  Zhang, Huifang M  Goodfellow, Ian G  Evans, David J  Suarez, Agripina  Yang, Decheng  McManus, Bruce M 
Citation: Yanagawa B, etal., Lab Invest. 2003 Jan;83(1):75-85.
RGD ID: 13702890
Pubmed: (View Article at PubMed) PMID:12533688

Coxsackievirus B3 (CVB3) infection can result in myocarditis, which in turn may lead to a protracted immune response and subsequent dilated cardiomyopathy. Human decay-accelerating factor (DAF), a binding receptor for CVB3, was synthesized as a soluble IgG1-Fc fusion protein (DAF-Fc). In vitro, DAF-Fc was able to inhibit complement activity and block infection by CVB3, although blockade of infection varied widely among strains of CVB3. To determine the effects of DAF-Fc in vivo, 40 adolescent A/J mice were infected with a myopathic strain of CVB3 and given DAF-Fc treatment 3 days before infection, during infection, or 3 days after infection; the mice were compared with virus alone and sham-infected animals. Sections of heart, spleen, kidney, pancreas, and liver were stained with hematoxylin and eosin and submitted to in situ hybridization for both positive-strand and negative-strand viral RNA to determine the extent of myocarditis and viral infection, respectively. Salient histopathologic features, including myocardial lesion area, cell death, calcification and inflammatory cell infiltration, pancreatitis, and hepatitis were scored without knowledge of the experimental groups. DAF-Fc treatment of mice either preceding or concurrent with CVB3 infection resulted in a significant decrease in myocardial lesion area and cell death and a reduction in the presence of viral RNA. All DAF-Fc treatment groups had reduced infectious CVB3 recoverable from the heart after infection. DAF-Fc may be a novel therapeutic agent for active myocarditis and acute dilated cardiomyopathy if given early in the infectious period, although more studies are needed to determine its mechanism and efficacy.

Annotation

Disease Annotations    
Viral Myocarditis  (IMP,ISO)

Objects Annotated

Genes (Rattus norvegicus)
Cd55  (CD55 molecule (Cromer blood group))

Genes (Mus musculus)
Cd55  (CD55 molecule, decay accelerating factor for complement)

Genes (Homo sapiens)
CD55  (CD55 molecule (Cromer blood group))


Additional Information