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Research at Vanderbilt

Target cell entry to halt Chikungunya virus

by | Posted on Monday, Apr. 28, 2014 — 8:00 AM

Atomic model of chikungunya virion. (Voss JE et al., Nature 2010)

Chikungunya virus (CHIKV) is transmitted to humans by virus-carrying mosquitoes and has caused recent outbreaks in Asia, Africa and the Caribbean. CHIKV infection is characterized by fever, rash and polyarthritis that can persist for months or years. There are no licensed vaccines or antiviral therapies for CHIKV.

Laurie Silva, Ph.D., and colleagues have discovered that CHIKV binds to glycosaminoglycan (GAG) molecules on the surfaces of host cells. The investigators tested two CHIKV strains – a pathogenic clinical isolate and an attenuated vaccine-candidate strain – for binding to cultured cells. Both strains required GAG expression, but they differed in affinity for GAGs (the vaccine strain binds with higher affinity than the clinical isolate). The researchers also identified a residue in the CHIKV attachment protein that influences binding to GAGs.

The findings, reported in the March Journal of Virology, improve understanding of the viral and host cell determinants of CHIKV cell entry – a key step in viral infection and possible target for new antivirals.

This research was supported by National Institutes of Health grants AI096833 and AI057157, which supports the Southeast Regional Center for Excellence for Emerging Infections and Biodefense, and by the Elizabeth B. Lamb Center for Pediatric Research.

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Contact:
Leigh MacMillan, (615) 322-4747
leigh.macmillan@vanderbilt.edu


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