Utilization of Host Proteins as Virus Receptors

Abstract

A general construct in microbiology is that parasites and their hosts continuously evolve to ensure the survival of each. A significant portion of virologic research has been devoted to describing strategies used by different viruses to survive despite attempts by the host to prevent their replication. One hypothesis holds that virus attachment to host cell molecules unique to susceptible cells governs virus spread to, and infection of, specific target organs [1]. Our focus is on the implication of recent research developments that support this hypothesis. The observations have been made with viruses from diverse genera and with cells of different functional types. It may be overly simplistic to state that tissue tropisms are readily defined on the basis of attachment per se, but attachment is a logical starting point in studying the evolution of virus—host interactions, since it has been shown that both virus and host-cell receptors are genetically controlled [1,2]. An excellent review of general principles related to animal virus attachment has been written recently by Holmes [3]. A key issue in relating host-cell molecules to virus attachment is identification of the “productive receptor” [4]. This is the receptor that leads to infection rather than one that binds virus nonspecifically. Many enveloped viruses bind well to a number of nonproductive substrates including inanimate surfaces, such as polystyrene plates, which are not obviously related to tissue tropisms in vivo.