Specific initiation of replication at the right-end telomere of the closed species of minute virus of mice replicative-form DNA.

1997 ◽  
Vol 71 (2) ◽  
pp. 971-980 ◽  
Author(s):  
A Q Baldauf ◽  
K Willwand ◽  
E Mumtsidu ◽  
J P Nüesch ◽  
J Rommelaere
Keyword(s):  
Replicative Form ◽  
Minute Virus Of Mice ◽  
Initiation Of Replication ◽  
Minute Virus ◽  
The Right

scholarly journals Specific interaction of the nonstructural protein NS1 of minute virus of mice (MVM) with [ACCA]2 motifs in the centre of the right-end MVM DNA palindrome induces hairpin-primed viral DNA replication

2002 ◽  
Vol 83 (7) ◽  
pp. 1659-1664 ◽  
Author(s):  
Kurt Willwand ◽  
Adela Moroianu ◽  
Rita Hörlein ◽  
Wolfgang Stremmel ◽  
Jean Rommelaere
Keyword(s):  
Dna Replication ◽  
Structural Transition ◽  
Conformational Transition ◽  
Nonstructural Protein ◽  
Specific Interaction ◽  
Sequence Motifs ◽  
Minute Virus Of Mice ◽  
Minute Virus ◽  
The Right

The linear single-stranded DNA genome of minute virus of mice (MVM) is replicated via a double-stranded replicative form (RF) intermediate DNA. Amplification of viral RF DNA requires the structural transition of the right-end palindrome from a linear duplex into a double-hairpin structure, which serves for the repriming of unidirectional DNA synthesis. This conformational transition was found previously to be induced by the MVM nonstructural protein NS1. Elimination of the cognate NS1-binding sites, [ACCA]2, from the central region of the right-end palindrome next to the axis of symmetry was shown to markedly reduce the efficiency of hairpin-primed DNA replication, as measured in a reconstituted in vitro replication system. Thus, [ACCA]2 sequence motifs are essential as NS1-binding elements in the context of the structural transition of the right-end MVM palindrome.

scholarly journals Depletion of Virion-Associated Divalent Cations Induces Parvovirus Minute Virus of Mice To Eject Its Genome in a 3′-to-5′ Direction from an Otherwise Intact Viral Particle

2009 ◽  
Vol 84 (4) ◽  
pp. 1945-1956 ◽  
Author(s):  
Susan F. Cotmore ◽  
Susan Hafenstein ◽  
Peter Tattersall
Keyword(s):  
Binding Sites ◽  
Prolonged Exposure ◽  
Divalent Cations ◽  
Structural Rearrangement ◽  
Cation Binding ◽  
Minute Virus Of Mice ◽  
Viral Genomes ◽  
Minute Virus ◽  
The Right ◽  
Full Length Genome

ABSTRACT We describe a structural rearrangement that can occur in parvovirus minute virus of mice (MVMp) virions following prolonged exposure to buffers containing 0.5 mM EDTA. Such particles remain stable at 4°C but undergo a conformational shift upon heating to 37°C at pH 7.2 that leads to the ejection of much of the viral genome in a 3′-to-5′ direction, leaving the DNA tightly associated with the otherwise intact capsid. This rearrangement can be prevented by the addition of 1 mM CaCl2 or MgCl2 prior to incubation at 37°C, suggesting that readily accessible divalent cation binding sites in the particle are critical for genome retention. Uncoating was not seen following the incubation of virions at pH 5.5 and 37°C or at pH 7.2 and 37°C in particles with subgenomic DNA, suggesting that pressure exerted by the full-length genome may influence this process. Uncoated genomes support complementary-strand synthesis by T7 DNA polymerase, but synthesis aborts upstream of the right-hand end, which remains capsid associated. We conclude that viral genomes are positioned so that their 3′ termini and coding sequences can be released from intact particles at physiological temperatures by a limited conformational rearrangement. In the presence of divalent cations, incremental heating between 45°C and 65°C induces structural transitions that first lead to the extrusion of VP1 N termini, followed by genome exposure. However, in cation-depleted virions, the sequence of these shifts is blurred. Moreover, cation-depleted particles that have been induced to eject their genomes at 37°C continue to sequester their VP1 N termini within the intact capsid, suggesting that these two extrusion events represent separable processes.

scholarly journals The Expression Strategy of Goose Parvovirus Exhibits Features of both the Dependovirus and Parvovirus Genera

2005 ◽  
Vol 79 (17) ◽  
pp. 11035-11044 ◽  
Author(s):  
Jianming Qiu ◽  
Fang Cheng ◽  
Yuko Yoto ◽  
Zoltán Zádori ◽  
David Pintel
Keyword(s):  
High Efficiency ◽  
Nonstructural Protein ◽  
Nonstructural Proteins ◽  
Coding Region ◽  
Minute Virus Of Mice ◽  
Adeno Associated Virus ◽  
Goose Parvovirus ◽  
Minute Virus ◽  
The Right ◽  
A Site

ABSTRACT The RNA transcription profile of the goose parvovirus (GPV) was determined, and it is a surprising hybrid of features of the Parvovirus and Dependovirus genera of the Parvovirinae subfamily of the Parvoviridae. Similar to the Dependovirus adeno-associated virus type 5, RNAs transcribed from the GPV upstream P9 promoter, which encode the viral nonstructural proteins, were polyadenylated at a high efficiency at a polyadenylation site [(pA)p] located within an intron in the center of the genome. Efficient usage of (pA)p required a downstream element that overlaps with the polypyrimidine tract of the A2 3′ splice site of the central intron. An upstream element required for efficient use of (pA)p was also identified. RNAs transcribed from the P42 promoter, presumed to encode the viral capsid proteins, primarily extended through (pA)p and were polyadenylated at a site, (pA)d, located at the right end of the genome and ultimately spliced at a high efficiency. No promoter analogous to the Dependovirus P19 promoter was detected; however, similar to minute virus of mice and other members of the Parvovirus genus, a significant portion of pre-mRNAs generated from the P9 promoter were additionally spliced within the putative GPV Rep1 coding region and likely encode an additional, smaller, nonstructural protein. Also similar to members of the Parvovirus genus, detectable activity of the GPV P42 promoter was highly dependent on transactivation by the GPV Rep1 protein in a manner dependent on binding to a cis-element located in the P42 promoter.

scholarly journals Chimeric and Pseudotyped Parvoviruses Minimize the Contamination of Recombinant Stocks with Replication-Competent Viruses and Identify a DNA Sequence That Restricts Parvovirus H-1 in Mouse Cells

2003 ◽  
Vol 77 (6) ◽  
pp. 3851-3858 ◽  
Author(s):  
Claudia Wrzesinski ◽  
Lia Tesfay ◽  
Nathalie Salomé ◽  
Jean-Claude Jauniaux ◽  
Jean Rommelaere ◽  
...  
Keyword(s):  
Early Stage ◽  
Pseudotyped Virus ◽  
Minute Virus Of Mice ◽  
Viral Dna Replication ◽  
Recombinant Vector ◽  
Virus Capsids ◽  
Minute Virus ◽  
Mouse Cells ◽  
Hand Region ◽  
The Right

ABSTRACT Recent studies demonstrated the ability of the recombinant autonomous parvoviruses MVMp (fibrotropic variant of the minute virus of mice) and H-1 to transduce therapeutic genes in tumor cells. However, recombinant vector stocks are contaminated by replication-competent viruses (RCVs) generated during the production procedure. To reduce the levels of RCVs, chimeric recombinant vector genomes were designed by replacing the right-hand region of H-1 virus DNA with that of the closely related MVMp virus DNA and conversely. Recombinant H-1 and MVMp virus pseudotypes were also produced with this aim. In both cases, the levels of RCVs contaminating the virus stocks were considerably reduced (virus was not detected in pseudotyped virus stocks, even after two amplification steps), while the yields of vector viruses produced were not affected. H-1 virus could be distinguished from MVMp virus by its restriction in mouse cells at an early stage of infection prior to detectable viral DNA replication and gene expression. The analysis of the composite viruses showed that this restriction could be assigned to a specific genomic determinant(s). Unlike MVMp virus, H-1 virus capsids were found to be a major determinant of the greater permissiveness of various human cell lines for this virus.

scholarly journals Genome Packaging Sense Is Controlled by the Efficiency of the Nick Site in the Right-End Replication Origin of Parvoviruses Minute Virus of Mice and LuIII

2005 ◽  
Vol 79 (4) ◽  
pp. 2287-2300 ◽  
Author(s):  
Susan F. Cotmore ◽  
Peter Tattersall
Keyword(s):  
Replication Origin ◽  
Close Relative ◽  
Transfer Model ◽  
Minute Virus Of Mice ◽  
Positive Sense ◽  
Minute Virus ◽  
Nick Site ◽  
The Right

ABSTRACT The parvovirus minute virus of mice (MVM) packages predominantly negative-sense single strands, while its close relative LuIII encapsidates strands of both polarities with equal efficiency. Using genomic chimeras and mutagenesis, we show that the ability to package positive strands maps not, as originally postulated, to divergent untranslated regions downstream of the capsid gene but to the viral hairpins and predominantly to the nick site of OriR, the right-end replication origin. In MVM, the sequence of this site is 5′-CTAT▾TCA-3′, while in LuIII a two-base insertion (underlined) changes it to 5′-CTAT AT ▾TCA-3′. Matched LuIII genomes differing only at this position (designated LuIII and LuΔ2) packaged 47 and <8% positive-sense strands, respectively. OriR sequences from these viruses were both able to support NS1-mediated nicking in vitro, but initiation efficiency was consistently two- to threefold higher for LuΔ2 derivatives, suggesting that LuIII's ability to package positive strands is determined by a suboptimal right-end origin rather than by strand-specific packaging sequences. These observations support a mathematical “kinetic hairpin transfer” model, previously described by Chen and colleagues (K. C. Chen, J. J. Tyson, M. Lederman, E. R. Stout, and R. C. Bates, J. Mol. Biol. 208:283-296, 1989), that postulates that preferential excision of particular strands is solely responsible for packaging specificity. By analyzing replicative-form (RF) DNA generated in vivo during LuIII and LuΔ2 infections, we extend this model, showing that positive-sense strands do accumulate in LuΔ2 infections as part of duplex RF DNA, but these do not support packaging. However, replication is biphasic, so that accumulation of positive-sense strands is ultimately suppressed, probably because the onset of packaging removes newly displaced single strands from the replicating pool.

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