A precise map of splice junctions in the mRNAs of minute virus of mice, an autonomous parvovirus.

Parvovirus (PV) is a widespread infection, despite the fact that this pathogen was discovered only recently. The therapeutic effect of PV, in particular its oncolytic activity, is being actively studied now. Notably, PVs causing infections in animals, such as rat PV H-1, caninae PV, and rodent protoparvovirus (minute virus of mice) suppress oncogenesis in these animals. There is an ex vivo evidence of rat glioblastoma and gliosarcoma sensitivity to PV. The affinity of PV B19 to P-antigen located primarily on the membranes of erythroid cells is crucial for the disease pathogenesis. The teratogenic effect of PV B19 is associated with its ability to infect placental cells (P-antigen is present on the cells of chorionic villi and surface of the trophoblast). PV infection can be acquired or congenital, typical or atypical. The outcome of intrauterine infection with PV B19 largely depends on the gestation age when the infection occurred. Women infected during the second trimester are at higher risk of vertical transmission and severe intrauterine pathology with a poor outcome than those infected during the third trimester. Constant contact with young children significantly increases the risk of PV B19 infection among pregnant women with no immunity to this virus. Serum is the most convenient biomaterial for detecting both PV DNA and virus-specific antibodies. One test for anti-PV IgG using enzyme-linked immunosorbent assay is sufficient to determine the immune status of a patient. Polymerase chain reaction with amniotic fluid is used to diagnose intrauterine infection with PV B19. Blood components and products should be checked for PV B19. High frequency of PV B19 detection in the blood of donors necessitates the development of special measures aimed at prevention of virus transmission. Key words: pregnant women, children, parvovirus B19, parvovirus infection

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The Effect of Regulatory Sequence Elements upon the Initiation of DNA Replication of the Minute Virus of Mice

Virology ◽

10.1006/viro.1996.0535 ◽

1996 ◽

Vol 224 (1) ◽

pp. 320-325 ◽

Cited By ~ 9

Author(s):

Nandini Cossons ◽

Maria Zannis-Hadjopoulos ◽

Patrick Tam ◽

Caroline R. Astell ◽

Emmanuel A. Faust

Keyword(s):

Dna Replication ◽

Regulatory Sequence ◽

Minute Virus Of Mice ◽

Sequence Elements ◽

Minute Virus ◽

Initiation Of Dna Replication

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Hypoxic-response elements in the oncolytic parvovirus Minute virus of mice do not allow for increased vector production at low oxygen concentration

Journal of General Virology ◽

10.1099/vir.0.81754-0 ◽

2006 ◽

Vol 87 (5) ◽

pp. 1197-1201 ◽

Cited By ~ 6

Author(s):

Charlotte Servais ◽

Perrine Caillet-Fauquet ◽

Marie-Louise Draps ◽

Thierry Velu ◽

Yvan de Launoit ◽

...

Keyword(s):

Cell Metabolism ◽

Consensus Sequence ◽

High Titre ◽

Host Cells ◽

Low Oxygen ◽

Minute Virus Of Mice ◽

Minute Virus ◽

Responsive Element ◽

Low Oxygen Concentration

Vectors derived from the autonomous parvovirus Minute virus of mice, MVM(p), are promising tools for the gene therapy of cancer. The validation of their in vivo anti-tumour effect is, however, hampered by the difficulty to produce high-titre stocks. In an attempt to increase vector titres, host cells were subjected to low oxygen tension (hypoxia). It has been shown that a number of viruses are produced at higher titres under these conditions. This is the case, among others, for another member of the family Parvoviridae, the erythrovirus B19 virus. Hypoxia stabilizes a hypoxia-inducible transcription factor (HIF-1α) that interacts with a ‘hypoxia-responsive element’ (HRE), the consensus sequence of which (A/GCGTG) is present in the B19 and MVM promoters. Whilst the native P4 promoter was induced weakly in hypoxia, vector production was reduced dramatically, and adding HRE elements to the P4 promoter of the vector did not alleviate this reduction. Hypoxia has many effects on cell metabolism. Therefore, even if the P4 promoter is activated, the cellular factors that are required for the completion of the parvoviral life cycle may not be expressed.

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