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The immunodominant epitopes of HCV are likely to be localized to the structural, rather than the nonstructural proteins, of the virus. The

HCV envelope glycoproteins (GP), designated E1 and E2, are the putative sites of the immunodominant epitope. Antibodies to the envelope proteins are present in low titer in most HCV-infected individuals. At the N-terminal portion of E2, a hypervariable region I (HVR I) is present, and may play a key role in the emergence of HCV variants that escape immune recognition by neutralizing antibody activity. Antibodies to HVR I may have neutralizing ability, since they have been shown to block the attachment of HCV to human fibroblasts in tissue culture (33). Despite these observations, it remains uncertain whether HVR I is the principal target of the neutralizing immune response to HCV. In studies of HCV infection in both chimpanzees and human beings, antibodies to E2 could not be correlated with self-limited infection (34). In fact, persistence of these antibodies correlated with chronic infection. Other immune epitopes, in other portions of the structural proteins, also may function in the neutralization of the virus. The critical immune epitopes, their sites on the genome, and their specific sequences need to be identified.

Theoretically, if circulating neutralizing antibodies, directed to the immunodominant epitopes of HCV, are present prior to infection (as a consequence of vaccination or passive administration of antibodies), they may serve to protect susceptible hepatocytes from HCV infection during the initial viremic phase, by interfering with viral attachment and/or entry. Additionally, they may protect uninfected hepatocytes during the likely secondary viremia or contiguous exposure to virus that results from production and release of virus from infected, injured cells, early in infection. However, if HCV is capable of evading neutralizing antibodies, a HCV vaccine that simultaneously elicited cell-mediated immunity might prove more effective than one that only evokes antibodies, because cellmediated immune responses may detect and destroy the initially infected cells, resulting in self-limited infection. This remains speculative, since the role of cell-mediated immunity in preventing HCV infection is still uncertain.

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