2006
DOI: 10.1002/hep.21220
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Hepatitis B virus genotype G monoinfection and its transmission by blood components

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Cited by 53 publications
(56 citation statements)
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“…Our experiments demonstrated that genotype G clones were replication competent whether driven by the strong actin promoter (1.1-mer genomes in pTriEx vector) or by the endogenous promoter (SphI dimers in pUC18 vector), as evidenced by RNA transcription, envelope protein expression (our unpublished observations), core protein expression and particle assembly, genome replication, and virion secretion. These findings confirm an earlier report of the replication capacity of an SpeI dimer of genotype G (25) and are fully compatible with a recent report of genotype G monoinfection in a blood donor and several transfusion recipients (12). Those authors were unable to detect genotype A sequence in blood samples by a variety of sensitive methods, thus demonstrating convincingly that genotype G can be transmitted and propagated in patients without the need for a helper virus.…”
Section: Discussionsupporting
confidence: 91%
“…Our experiments demonstrated that genotype G clones were replication competent whether driven by the strong actin promoter (1.1-mer genomes in pTriEx vector) or by the endogenous promoter (SphI dimers in pUC18 vector), as evidenced by RNA transcription, envelope protein expression (our unpublished observations), core protein expression and particle assembly, genome replication, and virion secretion. These findings confirm an earlier report of the replication capacity of an SpeI dimer of genotype G (25) and are fully compatible with a recent report of genotype G monoinfection in a blood donor and several transfusion recipients (12). Those authors were unable to detect genotype A sequence in blood samples by a variety of sensitive methods, thus demonstrating convincingly that genotype G can be transmitted and propagated in patients without the need for a helper virus.…”
Section: Discussionsupporting
confidence: 91%
“…The presence of HBV/A significantly increases the rate of HBV/G replication in hepatocytes, although infection with HBV/G alone is possible. [46][47][48][49] Genetic rearrangements between HBV/A and HBV/G can occur during persistent coinfection. Therefore, we examined how novel Ae/G recombinants were generated and transmitted in the Japanese MSM population.…”
Section: Discussionmentioning
confidence: 99%
“…Epidemiological and clinical data regarding this genotype are limited, likely due to the low prevalence of HBV/G throughout the world . HBV/G infection has been frequently reported to be detected along with a co-infecting functional HBV strain, such as genotype A (Kato et al, 2002a) or genotype H (Sánchez et al, 2007); however, HBV/G monoinfection has also been described (Alvarado-Esquivel et al, 2006;Chudy et al, 2006;Pas et al, 2008). Recombination between HBV/ G and the co-infecting genotype has been observed, but normally as a minority species within the HBV quasispecies population (Kato et al, 2002b).…”
mentioning
confidence: 99%
“…Clinical monoinfection with HBV/G has been suggested following LiPA analysis of an acutely infected blood donor and the corresponding platelet recipients (Chudy et al, 2006), and by LiPA analysis of Mexican (Alvarado-Esquivel et al, 2006) and European (Pas et al, 2008) chronic carriers. HBV/G has also been shown to be capable of replication in the absence of a co-infecting genotype following in vitro transfection of Huh7 cells (Li et al, 2007) or uPA/SCID mouse infection (Sugiyama et al, 2007;Tanaka et al, 2008), albeit at close to undetectable levels.…”
mentioning
confidence: 99%