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Analysis of the binding of hepatitis C virus genotype 1a and 1b E2 glycoproteins to peripheral blood mononuclear cell subsets

¹ The Edward Jenner Institute for Vaccine Research, Compton, Newbury RG20 7NN, UK
² Institute of Medical Virology, Justus Liebig University, Giessen, Germany
³ Division of Microbiology and Infectious Diseases, The University of Nottingham, Nottingham, UK
⁴ Istituto di Ricerche di Biologia Moleculare P. Angeletti, Rome, Italy
⁵ CNRS-UPR2511, Institut Pasteur de Lille, Lille, France
⁶ MRC Virology Unit, Institute of Virology, Glasgow, UK

Correspondence
Persephone Borrow
persephone.borrow{at}jenner.ac.uk

Hepatitis C virus (HCV) binding to hepatocytes is thought to be mediated via interaction of the E2 glycoprotein with (co-)receptors including CD81 and scavenger receptor class B type I (SR-BI). Here, the expression of CD81 and SR-BI was analysed on peripheral blood mononuclear cell (PBMC) subsets, and the binding of genotype 1 soluble truncated E2 (sE2) proteins to these cells was investigated. All PBMC subsets expressed CD81, although at varying levels. In contrast, SR-BI was only detected on monocytes and dendritic cells (DCs). The genotype 1a H77c sE2 protein showed higher PBMC binding than other genotype 1a/b sE2s. H77c sE2 binding to different PBMC subsets largely paralleled their level of CD81 expression, and could be inhibited by blocking E2–CD81 interaction. However, those PBMC subsets reported to be infected by HCV in vivo (monocytes, DCs and B cells) also exhibited residual, CD81-independent binding, indicating roles for SR-BI/other receptor(s) in mediating haematopoietic cell infection.

Supplementary material is available in JGV Online.

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