Virus-receptor interactions of coxsackie B viruses and their putative influence on cardiotropism

@article{Selinka2003VirusreceptorIO,
  title={Virus-receptor interactions of coxsackie B viruses and their putative influence on cardiotropism},
  author={H. Selinka and A. Wolde and M. Sauter and R. Kandolf and K. Klingel},
  journal={Medical Microbiology and Immunology},
  year={2003},
  volume={193},
  pages={127-131}
}
Specific virus-receptor interactions are important determinants in the pathogenesis of viral infections, influencing the location and initiation of primary infection as well as the viral spread to other target organs in the postviremic phase. Coxsackieviruses of group B (CVB) specifically interact with at least two receptor proteins, the coxsackievirus-adenovirus receptor (CAR) and the decay-accelerating factor (DAF), and cause a broad spectrum of diseases, including acute and chronic… Expand
Interspecies Differences in Virus Uptake versus Cardiac Function of the Coxsackievirus and Adenovirus Receptor
TLDR
It is shown that chicken CAR expression exclusively in the heart can rescue the otherwise embryonic-lethal CAR knockout phenotype but does not support CVB3 infection of adult cardiomyocytes. Expand
Host immune responses to coxsackievirus B3.
  • S. Huber
  • Biology, Medicine
  • Current topics in microbiology and immunology
  • 2008
TLDR
The interplay between the virus and the cell, which ultimately determines both the type and strength of the adaptive immune response as well as whether autoimmunity will follow the infection, is demonstrated. Expand
Inhibition of coxsackievirus infection in cardiomyocytes by small dsRNA targeting its cognate coxsackievirus adenovirus receptor
TLDR
The inhibition of CAR by siRNA was found to be effective against CVB in cardiomyocytes, however, this treatment strategy has to be evaluated in vivo to develop a new treatment strategy for patients suffering with viral myocarditis. Expand
Coxsackievirus B3 replication and pathogenesis.
Viruses such as coxsackievirus B3 (CVB3) are entirely host cell-dependent parasites. Indeed, they must cleverly exploit various compartments of host cells to complete their life cycle, andExpand
Coxsackie B viruses use multiple receptors to infect human cardiac cells
TLDR
Five new proteins have been identified that are used by Coxsackieviruses for binding to cardiac tissue and are distinct from CAR or CD55, leading us to believe that these viruses may use a different set of receptors for infection of cardiac muscle. Expand
Procoagulant activity during viral infections.
TLDR
Viral infection mediated TLRs activation is both cell type- and species-specific and explains the difficulties in correlating murine model data with the human data, and their contributions to the procoagulant response. Expand
Role of estrogen in suppressing autoimmunity in coxsackievirus B3-induced myocarditis
Picornaviruses are small, nonenveloped, single-stranded, positive-sense RNA viruses that cause multiple diseases including myocarditis/dilated cardiomyopathy, Type 1 diabetes, encephalitis, myositis,Expand
Coxsackievirus B3 infection induced viral myocarditis by regulating the expression pattern of chemokines in cardiac myocytes.
TLDR
Coxsackievirus B3 infection may start viral myocarditis by regulating the expression pattern of chemokines in cardiac myocytes in vitro, and MCP-1 may be one of key chemokine in the initial stage of viralMyocarditis. Expand
Membrane Dynamics and Signaling of the Coxsackievirus and Adenovirus Receptor.
TLDR
The interaction between membrane dynamics, intracellular trafficking, and signaling of CAR is discussed, which includes the molecular mechanisms leading to CAR-specific membrane targeting via the secretory pathway in polarized cells and its internalization are starting to be unraveled. Expand
Differential interferon responses enhance viral epitope generation by myocardial immunoproteasomes in murine enterovirus myocarditis.
TLDR
Type-I IFN- induced myocardial IP activity at early stages coincides with less severe disease manifestation in CVB3-induced myocarditis, and it is proposed that this process may precondition the infected heart for adaptive immune responses. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 33 REFERENCES
Cardiovirulent coxsackieviruses and the decay-accelerating factor (CD55) receptor.
TLDR
DAF is an attachment receptor for cardiovirulent CVB3 and that DAF interaction may be important in the pathogenesis of CVB-mediated heart disease. Expand
Comparative analysis of two coxsackievirus B3 strains: Putative influence of virus‐receptor interactions on pathogenesis
TLDR
Data suggest that even small differences in virus‐receptor interactions, influencing virus binding and virus spread, may have an impact on the pathogenesis of CVB‐induced diseases. Expand
Interaction with Decay-Accelerating Factor Facilitates Coxsackievirus B Infection of Polarized Epithelial Cells
TLDR
Results indicate that interaction with DAF on the apical surface of polarized epithelial cells facilitates infection by a subset of CB virus isolates and suggest a possible role for DAF in infection of epithelial Cells at mucosal surfaces. Expand
Molecular mechanisms in enterovirus and parvovirus B19 associated myocarditis and inflammatory cardiomyopathy
TLDR
Molecular pathology of PVB 19-associated myocarditis is characterized by infection of intracardiac endothelial cells, followed by intravascular accumulation, adhesion and penetration of inflammatory cells, resulting in endothelial dysfunction with secondary myocyte necrosis, which may clinically present with symptoms similar to that of myocardial infarction during acute infection. Expand
Isolation of a Common Receptor for Coxsackie B Viruses and Adenoviruses 2 and 5
TLDR
Identification of CAR as a receptor for these two unrelated and structurally distinct viral pathogens is important for understanding viral pathogenesis and has implications for therapeutic gene delivery with adenovirus vectors. Expand
Comparative analysis of virus-host cell interactions of haemagglutinating and non-haemagglutinating strains of coxsackievirus B3.
TLDR
Findings support the model of preferential interactions of both strains of CBV3 with closely associated DAF and CAR proteins on HeLa cells, despite displaying clear differences in their binding phenotypes. Expand
Clinical coxsackievirus B isolates differ from laboratory strains in their interaction with two cell surface receptors.
TLDR
Interactions between low-passage clinical coxsackie B virus isolates and the two receptors indicate that receptor use by clinical isolates is not strictly related to serotype and that even prototype strains with different passage histories may differ in receptor use. Expand
Human coxsackie-adenovirus receptor is colocalized with integrins alpha(v)beta(3) and alpha(v)beta(5) on the cardiomyocyte sarcolemma and upregulated in dilated cardiomyopathy: implications for cardiotropic viral infections.
TLDR
Low hCAR abundance may render normal human myocardium resistant to CAR-dependent viruses, whereas re-expression of hCAR, such as that observed in DCM, may be a key determinant of cardiac susceptibility to viral infections. Expand
Attachment of coxsackievirus B3 variants to various cell lines: mapping of phenotypic differences to capsid protein VP1.
TLDR
Results suggest that the mutated amino acid residues in VP1 are involved in receptor recognition/binding in coxsackievirus B3 Nancy P and the hybrid virus in various nonpermissive rodent cell lines indicates that cell surface molecules other than CAR and DAF may be involved in attachment of this variant to cell surfaces. Expand
Coxsackieviruses B1, B3, and B5 use decay accelerating factor as a receptor for cell attachment
TLDR
It was concluded that an additional cellular cofactor(s) is required to facilitate cell entry and subsequent replication in virus replication. Expand
...
1
2
3
4
...