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Coxsackie B virus and its interaction with permissive host cells
H C Selinka1, M Huber, A Pasch
1Department of Molecular Pathology, University of Tübingen, Germany. hans-christoph.selinka@med.uni-tuebingen.de
Clinical and Diagnostic Virology
|July 1, 1998
Summary
Coxsackievirus B (CVB) infections involve complex virus-host interactions. Understanding CVB attachment and internalization proteins is key to explaining viral replication, tissue tropism, and pathogenicity in diseases like myocarditis.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Coxsackievirus B (CVB) is a significant cause of viral myocarditis and other diseases in humans and animals.
- Persistent CVB infections are linked to various molecular mechanisms requiring further elucidation.
Purpose of the Study:
- To review molecular mechanisms underlying persistent CVB infections.
- To focus on virus-host cell interactions, particularly CVB receptor usage, and their impact on enteroviral replication.
Main Methods:
- Analysis of CVB interactions with cell surface proteins in cell lines and murine tissues.
- Investigation of virus attachment and internalization processes.
- Examination of intracellular protein interactions, exemplified by p21rasGTPase-activating protein (RasGAP) in CVB3-infected HeLa cells.
Main Results:
- Distinction between CVB attachment and internalization proteins is crucial.
- Multiple proteins may be required for CVB entry into host cells, suggesting a multimeric receptor complex.
- The presence of multiple attachment proteins could influence CVB tissue tropism and pathogenicity.
Conclusions:
- CVB entry involves a complex interplay of specific attachment and internalization proteins.
- A model of a multimeric receptor complex is proposed for CVB uptake.
- Understanding these interactions is vital for comprehending CVB pathogenesis and developing therapeutic strategies.