Replication advantage and host factor-independent phenotypes attributable to a common naturally occurring capsid mutation (I97L) in human hepatitis B virus.
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Regulation of Hepatitis B Virus Replication by the Phosphatidylinositol 3-Kinase-Akt Signal Transduction PathwayReduced secretion of virions and hepatitis B virus (HBV) surface antigen of a naturally occurring HBV variant correlates with the accumulation of the small S envelope protein in the endoplasmic reticulum and Golgi apparatusHepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon αImpact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibilityStructural and functional analysis of full-length hepatitis B virus genomes in patients: implications in pathogenesis.The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitroMicroRNA miR-204 and miR-1236 inhibit hepatitis B virus replication via two different mechanisms.HBV maintains electrostatic homeostasis by modulating negative charges from phosphoserine and encapsidated nucleic acidsCoexistence of two distinct secretion mutations (P5T and I97L) in hepatitis B virus core produces a wild-type pattern of secretion.Exposure of RNA templates and encapsidation of spliced viral RNA are influenced by the arginine-rich domain of human hepatitis B virus core antigen (HBcAg 165-173).Nucleolar localization of human hepatitis B virus capsid proteinHepatitis B virus capsid assembly is enhanced by naturally occurring mutation F97L.Stability and morphology comparisons of self-assembled virus-like particles from wild-type and mutant human hepatitis B virus capsid proteins.Hepatocyte-like cells transdifferentiated from a pancreatic origin can support replication of hepatitis B virus.A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assemblyIn vitro drug susceptibility analysis of hepatitis B virus clinical quasispecies populations.Hot-spot mutations in hepatitis B virus core gene: eliciting or evading immune clearance?Hepatitis B virus core protein variations differ in tumor and adjacent nontumor tissues from patients with hepatocellular carcinoma.
P2860
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P2860
Replication advantage and host factor-independent phenotypes attributable to a common naturally occurring capsid mutation (I97L) in human hepatitis B virus.
description
2002 nî lūn-bûn
@nan
2002年の論文
@ja
2002年学术文章
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2002年学术文章
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2002年学术文章
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2002年学术文章
@zh-my
2002年学术文章
@zh-sg
2002年學術文章
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2002年學術文章
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2002年學術文章
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name
Replication advantage and host ...... L) in human hepatitis B virus.
@en
Replication advantage and host ...... ally occurring capsid mutation
@nl
type
label
Replication advantage and host ...... L) in human hepatitis B virus.
@en
Replication advantage and host ...... ally occurring capsid mutation
@nl
prefLabel
Replication advantage and host ...... L) in human hepatitis B virus.
@en
Replication advantage and host ...... ally occurring capsid mutation
@nl
P2093
P2860
P1433
P1476
Replication advantage and host ...... L) in human hepatitis B virus.
@en
P2093
Chiaho Shih
Fat-Moon Suk
Jean-Dean Liu
Margaret Newman
Min-Hui Lin
Sheng-Hsuan Chen
P2860
P304
12069-12077
P356
10.1128/JVI.76.23.12069-12077.2002
P407
P577
2002-12-01T00:00:00Z