Virus Dataset Sample Info

> Dataset: 20119580 Search Result

Summary

Sample

ID	Sample ID	Age	Gender	Origin	Detail
1	C1	33	Male	South Korea	View
2	C2	40	Male	South Korea	View
3	C3	39	Male	South Korea	View
4	C4	34	Male	South Korea	View
5	C5	28	Male	South Korea	View
6	C6	30	Male	South Korea	View
7	C7	75	Male	South Korea	View
8	C8	51	Male	South Korea	View
9	C9	43	Male	South Korea	View
10	P1	57	Female	South Korea	View
11	P2	57	Male	South Korea	View
12	P3	50	Female	South Korea	View
13	P4	45	Male	South Korea	View
14	P5	70	Female	South Korea	View
15	P6	40	Male	South Korea	View
16	P7	46	Male	South Korea	View
17	P8	41	Male	South Korea	View
18	P9	45	Male	South Korea	View
19	P10	57	Male	South Korea	View
20	P11	49	Male	South Korea	View
21	P12	43	Male	South Korea	View
22	P13	47	Male	South Korea	View

Literature

Item	Summary
PMID	20119580
Title	Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations.
Abstract	The hepatitis B virus (HBV) polymerase gene has overlapping reading frames with surface genes, which allows to alter the amino acid codon of the surface genes. In adefovir (ADV) treated chronic hepatitis B patients carrying rtA181T/rtA181V mutations, overlap with surface gene mutations such as sW172stop/sL173F has been reported. However, the clinical consequences of such surface mutations have not been determined. The aim of this study was to determine the surface gene sequence in ADV-resistant patients carrying the A181T/V mutation and to describe the clinical significance. Of the 22 patients included in this study, 13 were ADV-resistant with rtA181T/V mutations (polymerase mutation group, Group P) and nine were antiviral treatment-naive (control group, Group C). The Pre-S1 gene mutation, V60A, was detected in 11 patients (Group P=8, Group C=3). A start codon mutation in the Pre-S2 gene was found in five patients (Group P=3, Group C=2). An S gene mutation, sA184V, was found in nine patients, all of whom were in group P. Although sW172stop and sL173F mutations were detected, reduced HBsAg titer was not observed. Further study of these mutations and their clinical implications are needed.