EBV Mutation Detail Information

Virus Mutation EBV Mutation I68L


Basic Characteristics of Mutations
Mutation Site I68L
Mutation Site Sentence Four polymorphisms L29V, V43L, D46N and I68L are unique to A2 and three, I137L, L178M and E328A, are unique to CAO, which also contains two additional direct repeats (Figure S2).
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region LMP-1
Standardized Encoding Gene LMP-1  
Genotype/Subtype -
Viral Reference -
Functional Impact and Mechanisms
Disease Lymphoproliferative Disorders    
Immune -
Target Gene NFKB1   
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location Swiss
Literature Information
PMID 22384168
Title Genetic diversity of EBV-encoded LMP1 in the Swiss HIV Cohort Study and implication for NF-Kappab activation
Author Zuercher E,Butticaz C,Wyniger J,Martinez R,Battegay M,Boffi El Amari E,Dang T,Egger JF,Fehr J,Mueller-Garamvogyi E,Parini A,Schaefer SC,Schoeni-Affolter F,Thurnheer C,Tinguely M,Telenti A,Rothenberger S
Journal PloS one
Journal Info 2012;7(2):e32168
Abstract Epstein-Barr virus (EBV) is associated with several types of cancers including Hodgkin's lymphoma (HL) and nasopharyngeal carcinoma (NPC). EBV-encoded latent membrane protein 1 (LMP1), a multifunctional oncoprotein, is a powerful activator of the transcription factor NF-kappaB, a property that is essential for EBV-transformed lymphoblastoid cell survival. Previous studies reported LMP1 sequence variations and induction of higher NF-kappaB activation levels compared to the prototype B95-8 LMP1 by some variants. Here we used biopsies of EBV-associated cancers and blood of individuals included in the Swiss HIV Cohort Study (SHCS) to analyze LMP1 genetic diversity and impact of sequence variations on LMP1-mediated NF-kappaB activation potential. We found that a number of variants mediate higher NF-kappaB activation levels when compared to B95-8 LMP1 and mapped three single polymorphisms responsible for this phenotype: F106Y, I124V and F144I. F106Y was present in all LMP1 isolated in this study and its effect was variant dependent, suggesting that it was modulated by other polymorphisms. The two polymorphisms I124V and F144I were present in distinct phylogenetic groups and were linked with other specific polymorphisms nearby, I152L and D150A/L151I, respectively. The two sets of polymorphisms, I124V/I152L and F144I/D150A/L151I, which were markers of increased NF-kappaB activation in vitro, were not associated with EBV-associated HL in the SHCS. Taken together these results highlighted the importance of single polymorphisms for the modulation of LMP1 signaling activity and demonstrated that several groups of LMP1 variants, through distinct mutational paths, mediated enhanced NF-kappaB activation levels compared to B95-8 LMP1.
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.