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Pathogenic hantaviruses selectively inhibit beta3 integrin directed endothelial cell migration
I N Gavrilovskaya1, T Peresleni, E Geimonen
1Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, USA.
Archives of Virology
|October 12, 2002
Summary
Pathogenic hantaviruses disrupt endothelial cell migration via beta3 integrins, contributing to hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Non-pathogenic hantaviruses do not affect this process.
Area of Science:
- Virology
- Cell Biology
- Pathogenesis
Background:
- Hantaviruses cause HFRS and HPS in humans.
- Pathogenic hantaviruses utilize beta3 integrins, while non-pathogenic strains use beta1 integrins for endothelial cell entry.
- Beta3 integrins are implicated in regulating vascular permeability.
Purpose of the Study:
- To investigate how pathogenic and non-pathogenic hantaviruses affect beta3 and beta1 integrin-mediated endothelial cell functions.
- To determine the role of hantavirus-integrin interactions in viral pathogenesis.
Main Methods:
- Assessing endothelial cell migration on beta3 and beta1 integrin ligands after infection with various hantaviruses.
- Utilizing antibodies against beta3 integrins to block specific cell migration pathways.
Main Results:
- Pathogenic hantaviruses (NY-1, SNV, HTN, SEO, PUU) selectively inhibited endothelial cell migration on beta3 integrin ligands.
- Non-pathogenic hantaviruses (PH, TUL) did not affect endothelial cell migration on either beta3 or beta1 integrin ligands.
- Inhibition of migration by pathogenic viruses occurred as early as 24-48 hours post-infection.
Conclusions:
- Hantaviruses that use beta3 integrins, associated with HFRS and HPS, functionally impair endothelial cell migration.
- Hantaviruses specifically regulate beta3 integrin functions, not beta1 integrin functions.
- Dysregulation of beta3 integrin-mediated endothelial cell functions by hantaviruses may contribute to disease pathogenesis.