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Molecular anatomy of viral persistence

can persist in their hosts and what the consequences are in terms of producing disease requires new insights. Yet, much current thinking is based on information gathered over the past century from studies of acute viral infections. These began with the primary observations of Beijerinck and Ivanovski (5, 18) that material responsible for tobacco mosaic disease passed through the pores of a Pasteur-Chamberlin filter without losing infectivity and that this soluble residue of filtration replicated when reintroduced onto healthy tobacco leaves. Correspondingly, Loeffler and Frosch (20) determined the same series of events for the pathogen causing bovine foot-and-mouth disease. These observations provided the basis for defining viruses as subcellular entities that could cause a distinct, often pathognomonic form of tissue destruction. Documentation during the years that followed and up to the present affirmed that many diseases with a proven viral cause were accompanied by cellular necrosis and inflammatory infiltrates. Thus, the histopathologic hallmarks of acute infection, tissue destruction, cell necrosis, and lymphoid infiltration, have served as signals to begin attempts to isolate virus. Accordingly, when these hallmarks are not present, the problem is assumed to originate from a source other than viral. However, we are now aware of significant differences between persistent and acute virus infections. For example, their histopathologic pictures often differ dramatically. Lymphoid cell infiltration and destruction of virally infected cells, the signs of acute infection, need not occur and frequently do not, with persistent infections. Another example lies with immune responses; the immune system consists of humoral (antibody) and cellular (lymphocyte, monocyte) components that function to protect the host from invading microbes. Immunization, primarily developed and used most successfully against agents causing acute infection in humans and domestic animals, has been focused toward enhancing antibody responses to glycoprotein or structural protein antigens present on surface virions, although cytotoxic T lymphocytes (CTL) also play roles in control of acute infection (24). However, the dilemma in protection from persistent infections is more complex. The viruses often are cell associated, and surface glycoproteins are usually not expressed or are expressed to minimal degrees on such persistently infected cells (29). In this scenario, antibodies are not efficient in lysing infected cells. Further, several million antibody molecules are needed, along with effector molecules of the