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ConclusionThe initial stage in the viral infectious cycle is the attachment of the virus particle to the host cell membrane. Attachment is mediated by the interaction of a viral surface protein, the VAP, with a normal component of the plasma membrane, of either protein, carbohydrate or lipid, which acts as a virus receptor. Information is accumulating rapidly not only on the nature of the VAPs and of viral receptors but also on the specific domains involved in binding. This knowledge is allowing the development of molecular models for the virus-host cell interaction. Such models permit the rational design of agents which might be effective in preventing virus infection by blocking the attachment stage of the infectious cycle. One group of agents (ligand mimics) will resemble, chemically or structurally, the binding domain of the ligand (in this case the VAP) and competitively inhibit binding of virus to the receptor. The second group of agents will resemble the binding domain of the receptor (receptor mimics) and prevent binding of virus with the host cell by attaching to the binding domain of the VAP.

The recognition event between virus and host cell receptor: a target for antiviral agents