Abstract
Infection by a virus usually initiates an immune response to the virus, as a result of which the infection is cleared. Viruses have, therefore, evolved ways of evading immune recognition which allow them to persist in individuals or, if clearance with lifelong protection is the outcome of initial contact with the host, to maintain themselves within the population. Examples of such mechanisms include infection in early childhood, as new susceptible hosts appear every 2–3 years (e.g. measles virus); the availability of a secondary host (often an animal reservoir, e.g. influenza virus)1,2; and modification of viral coat proteins by antigenic shift and drift (e.g. influenza virus haemagglutinin)1. It is also possible for a virus to persist in cells or animals of a species other than the natural host2. Although this may be an artificial phenomenon it provides important clues as to the nature of persistence in the intact host. Lastly, viruses may become persistent in a single host. The maintenance of such persistence requires a complex series of interactions between host and virus to be established and maintained to provide an asymptomatic virus–host equilibrium. This latter mechanism is the subject of this chapter.
Keywords
- Natural Killer
- Persistent Infection
- Chronic Active Hepatitis
- Delay Type Hypersensitivity
- Herpes Simplex Virus Infection
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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Alp, N., Borysiewicz, L.K. (1994). The Immunology and Pathogenesis of Persistent Virus Infections. In: Sissons, J.G.P., Borysiewicz, L.K., Cohen, J. (eds) Immunology of Infection. Immunology and Medicine Series, vol 25. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1430-1_5
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