HBV Mutation Detail Information

Virus Mutation HBV Mutation A1676T


Basic Characteristics of Mutations
Mutation Site A1676T
Mutation Site Sentence The following X gene mutations occurred in two patients: G1390A, G1437A, A1574T, A1676T, A1703C, T1741C, C1449T/A, A1511G/T, G1634A/T and C1637G/T.
Mutation Level Nucleotide level
Mutation Type
Gene/Protein/Region X
Standardized Encoding Gene X  
Genotype/Subtype -
Viral Reference -
Functional Impact and Mechanisms
Disease Polyarteritis Nodosa    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 15256984
Title Polyarteritis nodosa associated with hepatitis B virus infection. The role of antiviral treatment and mutations in the hepatitis B virus genome
Author Janssen HL,van Zonneveld M,van Nunen AB,Niesters HG,Schalm SW,de Man RA
Journal European journal of gastroenterology & hepatology
Journal Info 2004 Aug;16(8):801-7
Abstract Polyarteritis nodosa (PAN) is a systemic inflammatory disease causing vasculitis of medium sized and small arteries. Circulating immune complexes containing viral proteins have been implicated in the pathogenesis of hepatitis B virus (HBV) related PAN and several immunosuppressive and antiviral regimens have been used with varying success. In our hospital seven HBV positive patients with a confirmed diagnosis of PAN could be identified between 1984 and 2001. Most patients had an acute HBV infection and all patients were treated with prednisone. A combination of prednisone and antiviral therapy with alpha-interferon (IFN) was used only in the last four patients. HBV DNA was isolated from serum samples obtained before treatment from the four IFN treated patients and amplified by using the polymerase chain reaction technique. None of the patients without, but two of four with antiviral therapy exhibited HBsAg seroconversion. In three out of four patients HBV DNA decreased rapidly after starting IFN therapy. Clinical remission of PAN was observed in three of the four treated patients, but in none of the three patients who were not receiving antiviral medication. Analysis of the HBV genome revealed no mutations that could be associated with PAN. In one patient a stop codon in the pre-core region and a double mutation A1762T-G1764A were found during antiviral therapy. We did not find HBV heterogeneity predisposing to the development of PAN. In our group of patients it appeared that clinical remission of PAN was primarily related to spontaneous or therapy induced loss of HBV DNA replication. The combined administration of a priming steroid course and IFN appears to be an improvement over prednisone monotherapy and should be considered for every patient with HBV related PAN. The efficacy of new generation nucleoside analogues should be further elucidated in future studies.
Sequence Data -
Mutation Information
Note
Basic Characteristics of Mutations
  • Mutation Site: The specific location in a gene or protein sequence where a change occurs.
  • Mutation Level: The level at which a mutation occurs, including the nucleotide or amino acid level.
  • Mutation Type: The nature of the mutation, such as missense mutation, nonsense mutation, synonymous mutation, etc.
  • Gene/Protein/Region: Refers to the specific region of the virus where the mutation occurs. Including viral genes, viral proteins, or a specific viral genome region. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main
  • Gene/Protein/Region studied in the article is marked.
  • Genotype/Subtype: Refers to the viral genotype or subtype where the mutation occurs. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main Genotype/Subtype studied in the article is marked.
  • Viral Reference: Refers to the standard virus strain used to compare and analyze viral sequences.
Functional Impact and Mechanisms
  • Disease: An abnormal physiological state with specific symptoms and signs caused by viral infection.
  • Immune: The article focuses on the study of mutations and immune.
  • Target Gene: Host genes that viral mutations may affect.
Clinical and Epidemiological Correlations
  • Clinical Information: The study is a clinical or epidemiological study and provides basic information about the population.
  • Treatment: The study mentioned a certain treatment method, such as drug resistance caused by mutations. If the study does not specifically indicate the relationship between mutations and their correspondence treatment, the main treatment studied in the article is marked.
  • Location: The source of the research data.
Literature Information
  • Sequence Data: The study provides the data accession number.