Abstract
Infection of mammalian cells by human adenoviruses induces dramatic alterations in the cells’ abilities to continue their normal business. Indeed, adenoviruses were first recognised by their ability to kill cells which supported the efficient replication of the virus (1, 2). Such cell death is the culmination of several processes which redirect the host cells’ biosynthetic apparatus. Thus, when adenoviruses infect rapidly-dividing, fully permissive cells, they induce rapid and complete inhibition of synthesis of both cellular DNA and cellular proteins. At first sight, such redirection of cellular functions appears of obvious advantage to the virus: the relevant cellular machinery becomes devoted to the production of the components which will form progeny virions, the raison d’etre of the infectious cycle. The complete cessation of cellular DNA or protein synthesis and the vast quantities of viral macromolecules produced attest to the efficiency of the molecular mechanisms by which the virus carries out such usurption. It is, therefore, quite surprising that as little as 10% of the newly made viral material is assembled into virions (see ref. 3 for a review).
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Flint, J. (1986). Alterations in Cellular Functions in Adenovirus-Infected and Transformed Cells. In: Doerfler, W. (eds) Adenovirus DNA. Developments in Molecular Virology, vol 8. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2293-1_9
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