Abstract
Because of the close coupling of the replication of animal viruses and host cell functions, successful antiviral therapy has demanded agents specifically directed against virus infected cells. In addition, the spread of virus within an infected individual involves a wide variety of cells in which antiviral drugs may or may not act with similar efficacy. Recent studies (1) have demonstrated that host defense to viral infection involves a multitiered series of interrelated, but yet independent responses, which act on virus infected cells as well as on extracellular virus to diminish spread of the agent within the host. Various host defenses act both at the portal of entry and in the target organs with relative efficacy which differs from one virus to another -- or even between strains. In addition to local action of IgA antibody and macrophages, systemic IgM and IgG antibodies and antibody-dependent cellular cytotoxic mechanisms come into play, together with thymus-derived lymphocyte cytotoxicity and lymphoidne production. Such host factors are clearly critical in dictating the pathogenesis of infection of any particular virus. The proper function of all of these events obviously depends on a complex series of host biosynthetic and differentiation steps.
Supported by a grant from the US public Health Service (AI 05629)
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Merigan, T.C., Renis, H.E. (1979). Success of Antiviral Therapy Involves Cooperative Immune Responses. In: Walker, R.T., De Clercq, E., Eckstein, F. (eds) Nucleoside Analogues. NATO Advanced Study Institutes Series, vol 26. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-9137-5_13
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