9 research outputs found

    Chronic Fatigue Syndrome and Viral Infections

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    Hypoxia enhances human B19 erythrovirus gene expression in primary erythroid cells

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    AbstractHuman B19 erythrovirus replicates in erythroid progenitors present in bone marrow and fetal tissues where partial oxygen tension is low. Here we show that infected human primary erythroid progenitor cells exposed to hypoxia (1% O2) in vitro increase viral capsid protein synthesis, virus replication, and virus production. Hypoxia-inducible factor-1 (HIF-1), the main transcription factor involved in the cellular response to reduced oxygenation, is shown to bind an HIF binding site (HBS) located in the distal part of the B19 promoter region, but the precise mechanism involved in the oxygen-sensitive upregulation of viral gene expression remains to be elucidated

    ETUDE IN VITRO DE LA TOXICITE CELLULAIRE DE PEPTIDES DERIVES DE LA PROTEINE NS1 DU PARVOVIRUS B19 (DES BIOL. MED.)

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    CHATENAY M.-PARIS 11-BU Pharma. (920192101) / SudocSudocFranceF

    Advances in Human B19 Erythrovirus Biologyâ–¿

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    Since its discovery, human parvovirus B19 (B19V), now termed erythrovirus, has been associated with many clinical situations (neurological and myocardium infections, persistent B19V DNAemia) in addition to the prototype clinical manifestations, i.e., erythema infectiosum and erythroblastopenia crisis. In 2002, the use of new molecular tools led to the characterization of three different genotypes of human B19 erythrovirus. Although the genomic organization is conserved, the geographic distribution of the different genotypes varies worldwide, and the nucleotidic divergences can impact the molecular diagnosis of B19 virus infection. The cell cycle of the virus remains partially unresolved; however, recent studies have shed light on the mechanism of cell entry and the interactions of B19V proteins with apoptosis pathways
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