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Our preliminary data suggest that Epstein-Barr virus (EBV) is able to bind to and fuse with the surface membranes of hepatoma cell line Li7A. In order to obtain further evidence, we utilized the relief of rhodamine fluorescence to monitor whether fusion would also take place when Li7A cells were exposed to experimental conditions such as neutral or low pH. It is well known that for some viruses, protonation in the endosomal compartment is needed to trigger the fusion. We show, furthermore, that the rate and extent of fusion are not affected by pretreatment of the cells with agents known to elevate the lysosomal and ensodomal pH, such as chloroquine or NH4Cl (lysosomotropic agent). By indirect immunofluorescence assay, in addition, we confirmed the binding of the EBV to the Li7A cell surface membrane. We attempted finally to correlate the above processes with successful infection of Li7A cells by EBV detected using the polymerase chain reaction technique. In spite of the apparent lack of viral receptor CD21, these nonlymphoid cells appeared susceptible to EBV penetration and infection through fusion with the plasma membrane at the surface of the cells.

The TOFE lymphoid cell line from normal human bone marrow is susceptible to infection by a hepatitis C virus (HCV) serum strain. A sequence analysis of the 5' untranslated region (UTR) of HCV before and after long-term in vitro infection revealed one base substitution at position -158 (C > T) of the 5' UTR. We performed the direct sequencing of 5' UTR polymerase chain reaction-amplified sequences of the HCV genome: a) from the original serum-derived strain; b) from TOFE cell extracts 6 months post infection. This base substitution in the regulatory elements of the 5' UTR might be related to the ability of the virus to grow in cell culture.