Fig. 1.
Fig. 1. (A) HGV markers and serum ALT levels of a patient (patient no. 12) with relapse of HGV viremia during chemotherapy. The patient was 14 years old at development of ALL. The horizontal line and solid bar mean years from diagnosis and periods under immunosuppressive therapy or chemotherapy, respectively. The inverted triangle indicates the timing of BMT. In the clinical course of ALT, the normal range for ALT is indicated as a horizontal line. Phylogenetic analysis was performed with the strains obtained at the timing of figures in the circle. (B) Phylogenetic analysis of different HGV isolates from the patient with reactivation of HGV infection. Figures in the circles show the strains from patient no. 12. Homology of nucleotide sequence of 312-bp E2 cDNA between reappearing and former isolates from patient no. 12 were 98% to 99%, although the homology among the other sequences was 79.8% to 88.3%. In the phylogenetic tree, HGV R10291 and PNF2164 are in the same E2 regions of the original HGV strain, and GBV-C is also in the original. We sequenced two strains derived from another patient (patient no. 15), and the strain first appearing showed just the same nucleotide sequence as the other that was obtained 2 years later. D90600, 90601, 87262, 87263, and U63715 are the accession numbers of previously reported HGV or GBV-C sequences in GenBank. Numbers 1 through 10 are strains derived from Taiwanese patients reported by Kao et al.18 (C) HGV markers and serum ALT levels of another patient (patient no. 15) with reactivation of HGV viremia during chemotherapy. Clinical courses are represented by similar notations as in (A).

(A) HGV markers and serum ALT levels of a patient (patient no. 12) with relapse of HGV viremia during chemotherapy. The patient was 14 years old at development of ALL. The horizontal line and solid bar mean years from diagnosis and periods under immunosuppressive therapy or chemotherapy, respectively. The inverted triangle indicates the timing of BMT. In the clinical course of ALT, the normal range for ALT is indicated as a horizontal line. Phylogenetic analysis was performed with the strains obtained at the timing of figures in the circle. (B) Phylogenetic analysis of different HGV isolates from the patient with reactivation of HGV infection. Figures in the circles show the strains from patient no. 12. Homology of nucleotide sequence of 312-bp E2 cDNA between reappearing and former isolates from patient no. 12 were 98% to 99%, although the homology among the other sequences was 79.8% to 88.3%. In the phylogenetic tree, HGV R10291 and PNF2164 are in the same E2 regions of the original HGV strain, and GBV-C is also in the original. We sequenced two strains derived from another patient (patient no. 15), and the strain first appearing showed just the same nucleotide sequence as the other that was obtained 2 years later. D90600, 90601, 87262, 87263, and U63715 are the accession numbers of previously reported HGV or GBV-C sequences in GenBank. Numbers 1 through 10 are strains derived from Taiwanese patients reported by Kao et al.18 (C) HGV markers and serum ALT levels of another patient (patient no. 15) with reactivation of HGV viremia during chemotherapy. Clinical courses are represented by similar notations as in (A).

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