Tandem mengovirus 5' pseudoknots are linked to viral RNA synthesis, not poly(C)-mediated virulence.

Abstract:

:The RNA genomes from the cardioviruses, hepatoviruses, and aphthoviruses encode two to five tandem pseudoknots within their 5' untranslated regions. These pseudoknots lie adjacent to a pyrimidine-rich sequence, which in cardio- and aphthoviruses takes the form of a homopolymeric poly(C) tract. Seven deletion mutations within mengovirus pseudoknots PK(B) and PK(C) were created and characterized. tested in tissue culture, mengovirus genomes with alterations in PK(C) were viable but had small plaque phenotypes. Larger plaque revertants were isolated and partially characterized, and each proved to be a second-site pseudorevertant with (unmapped) changes elsewhere in the genome. The infectious PK(C) mutant viruses were highly lethal to mice, and deletions in this motif did not affect mengovirus virulence in the same manner as deletions in the adjacent poly(C) tract. In contrast, deletions in PK(B), or deletions which spanned PK(B) + PK(C), produced nonviable genomes. Cell-free translations directed by any of the altered PK sequences gave normal polyprotein amounts relative to wild-type mengovirus. But viral RNA accumulation during HeLa cell infection was dramatically impaired, even with the least disruptive of the PK(C) changes, suggesting the pseudoknots play an essential though undefined role in RNA synthesis and moreover that an intact PK(B) structure is critical to this function.

journal_name

J Virol

journal_title

Journal of virology

authors

Martin LR,Palmenberg AC

doi

10.1128/JVI.70.11.8182-8186.1996

subject

Has Abstract

pub_date

1996-11-01 00:00:00

pages

8182-6

issue

11

eissn

0022-538X

issn

1098-5514

journal_volume

70

pub_type

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