Mouse polyomavirus late region mutants expressing a defective VP2 capsid protein exhibit an enhanced viral DNA replication.
We have constructed mouse polyomavirus mutants with deletions or insertions in the late region. These viral constructs exhibit two different phenotypes, characterized by a differential replication ability. The first type shows a twofold higher level of DNA synthesis with respect to wild type, while mutants of the second type are virtually unable to replicate. In this paper we investigate the replicative behavior of the first class of mutants, which expresses defective viral coat proteins. Our data raise the possibility that, of the three late gene viral products, VP2 is involved in the formation of an encapsidation intermediate that, in an indirect fashion, affects the rate of viral DNA synthesis.
Melucci-Vigo
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Dipartimento di Genetica e Biologia Molecolare, Università di Roma La Sapienza, Italy.
Magnusson
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Risuleo
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D000818:Animals; D002213:Capsid / Q000235:genetics* / Q000502:physiology; D036022:Capsid Proteins; D004261:DNA Replication / Q000235:genetics*; D005814:Genes, Viral / Q000235:genetics; D051379:Mice; D009154:Mutation / Q000235:genetics; D010641:Phenotype; D011120:Polyomavirus / Q000235:genetics* / Q000502:physiology; D015678:Viral Structural Proteins / Q000235:genetics; D014779:Virus Replication / Q000235:genetics*
D036022:Capsid Proteins; C442543:VP2 protein, Polyomavirus; D015678:Viral Structural Proteins