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Sequences within the early and late promoters of archetype JC virus restrict viral DNA replication and infectivity.

Abstract：

:Two forms of JC virus (JCV) have been isolated from its human host, an archetype found in kidney tissue and urine of nonimmunocompromised individuals and a rearranged type detected in lymphocytes and brain tissue of patients with and without progressive multifocal leukoencephalopathy. To investigate the hypothesis that alterations to the archetype transcriptional control region yield rearranged forms of the virus exhibiting new tissue tropic and pathogenic potentials, attempts were made to propagate archetype JCV in human renal and glial cell cultures. Although rearranged forms of JCV multiplied in these cells, archetype JCV failed to do so. Through the use of chimeric and mutant viral genomes, and a cell line that constitutively expresses viral T protein, we demonstrated that archetype's inactivity relative to that of rearranged forms was due to differences in the promoter-enhancer and not in the protein coding regions or origin of DNA replication. Additional analyses revealed that the absence of a large tandem duplication and the presence of a 23- and a 66-base pair sequence in the archetype transcriptional control region were responsible for this restricted lytic behavior. We discuss the possibility that deletion and duplication events within the archetype promoter-enhancer might yield more active viral variants via the loss of a negative, or the creation of a positive, transcriptional control signal(s).

journal_name

Virology

journal_title

Virology

authors

Daniel AM,Swenson JJ,Mayreddy RP,Khalili K,Frisque RJ

doi

10.1006/viro.1996.0037

subject

Has Abstract

pub_date

1996-02-01 00:00:00

pages

90-101

issue

1

eissn

0042-6822

issn

1096-0341

pii

S0042682296900379

journal_volume

216

pub_type

杂志文章

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