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L-SIGN (CD209L) isoforms differently mediate trans-infection of hepatoma cells by hepatitis C virus pseudoparticles

Jason P. Gardner^2,

¹ Albert Einstein College of Medicine, Microbiology and Immunology Department, 1300 Morris Park Avenue, Bronx, NY 10461, USA
² Progenics Pharmaceuticals Inc., 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA

Correspondence
Tatjana Dragic
tdragic{at}aecom.yu.edu

L-SIGN is a C-type lectin that is expressed on liver sinusoidal endothelial cells. Capture of Hepatitis C virus (HCV) by this receptor results in trans-infection of hepatoma cells. L-SIGN alleles have been identified that encode between three and nine tandem repeats of a 23 residue stretch in the juxtamembrane oligomerization domain. Here, it was shown that these repeat-region isoforms are expressed at the surface of mammalian cells and variably bind HCV envelope glycoprotein E2 and HCV pseudoparticles. Differences in binding were reflected in trans-infection efficiency, which was highest for isoform 7 and lowest for isoform 3. These findings provide a molecular mechanism whereby L-SIGN polymorphism could influence the establishment and progression of HCV infection.

Present address: GlaxoSmithKline R&D, B38 2 58, Greenford Road, London UB6 0HE, UK.

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