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Blood, 15 October 2001, Vol. 98, No. 8, pp. 2293-2300
PLENARY PAPER
The dynamics of hepatitis C virus binding to platelets and 2 mononuclear cell lines
Samir Hamaia,
Chengyao Li, and
Jean-Pierre Allain
From the Division of Transfusion Medicine, Department
of Haematology, University of Cambridge, Cambridge, United Kingdom, and
the East Anglia Blood Centre, National Blood Service, Cambridge, United
Kingdom.
Hepatitis C virus (HCV) binds to platelets in chronically infected
patients where free HCV constitutes only about 5% of total circulating
virus. Free HCV preferentially binds to human mononuclear cell lines
but free and complexed virus binds equally to platelets. The extent of
free HCV binding to human Molt-4 T cells (which express CD81) and to
human promonocytic U937 cells or to platelets (which do not express
CD81) was similar. The binding of free HCV to the cell lines was
saturated at a virus dose of 1 IU HCV RNA per cell but binding to
platelets was not saturable. Human anti-HCV IgG, but not anti-CD81,
markedly inhibited HCV binding to target cells in a dose-dependent
manner. Human antibodies to HCV hypervariable region 1 of E2
glycoprotein partially inhibited viral binding to target cells.
Recombinant E2 also inhibited viral binding to target cells in a
dose-dependent manner, with the efficacy of this decreasing in the rank
order of Molt-4 cells more than U937 cells more than platelets. In
contrast to HCV, recombinant E2 bound to Molt-4 cells to an extent
markedly greater than that apparent with U937 cells or platelets. These
results suggest that the binding of HCV to blood cells is mediated by
multiple cell surface receptors and that recombinant E2 binding may not
be representative of the interaction of the intact virus with target cells.
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