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. 2004 Feb 11;320(2):191–194. doi: 10.1016/j.virol.2003.11.025

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Fig. 1 — Caspase-mediated control of ADV replication. Following entry and uncoating of ADV into the host cell (1), early mRNA () is transcribed and translated to produce NS1 (2). During permissive replication (left hand panel), NS1 is cleaved by activated caspases (C) (3) to produce an abbreviated NS1 fragment required for the efficient translocation of NS1 into the nucleus (solid arrow). Once in the nucleus, NS1 can efficiently function in its roles during viral DNA replication () and the control of gene expression (4), as well as the packaging of infectious virions (5). If caspase activation does not occur or is tightly controlled, lack of NS1 cleavage results in restricted virus replication (right hand panel) due to inefficient translocation of NS1 to the nucleus (dotted arrow), and subsequent low levels of viral DNA replication, gene expression, and infectious progeny.

Inline graphic — Caspase-mediated control of ADV replication. Following entry and uncoating of ADV into the host cell (1), early mRNA () is transcribed and translated to produce NS1 (2). During permissive replication (left hand panel), NS1 is cleaved by activated caspases (C) (3) to produce an abbreviated NS1 fragment required for the efficient translocation of NS1 into the nucleus (solid arrow). Once in the nucleus, NS1 can efficiently function in its roles during viral DNA replication () and the control of gene expression (4), as well as the packaging of infectious virions (5). If caspase activation does not occur or is tightly controlled, lack of NS1 cleavage results in restricted virus replication (right hand panel) due to inefficient translocation of NS1 to the nucleus (dotted arrow), and subsequent low levels of viral DNA replication, gene expression, and infectious progeny.