EBOV Mutation Detail Information

Virus Mutation EBOV Mutation T206A


Basic Characteristics of Mutations
Mutation Site T206A
Mutation Site Sentence Fig. 3. EBOV VP35 S187A impairs VP35 phosphorylation in HepG2 cells. HepG2 cells were transfected with plasmids pCAGGS-VP35, pCAGGS-VP35 S187A, pCAGGS-VP35 S205A/T206A/S208A, pCAGGS-VP35 S317A and pCAGGS-VP35 S187A/S205A/T206A/S208A/S317A as indicated, and the cell lysates were subjected to anti-VP35 immunoprecipitation.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region VP35
Standardized Encoding Gene VP35
Genotype/Subtype -
Viral Reference -
Functional Impact and Mechanisms
Disease Cell line    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 31694758
Title Ebola virus replication is regulated by the phosphorylation of viral protein VP35
Author Zhu L,Gao T,Yang W,Liu Y,Liu X,Hu Y,Jin Y,Li P,Xu K,Zou G,Zhao L,Cao R,Zhong W,Xia X,Cao C
Journal Biochemical and biophysical research communications
Journal Info 2020 Jan 15;521(3):687-692
Abstract Ebola virus (EBOV) is a zoonotic pathogen, the infection often results in severe, potentially fatal, systematic disease in human and nonhuman primates. VP35, an essential viral RNA-dependent RNA polymerase cofactor, is indispensable for Ebola viral replication and host innate immune escape. In this study, VP35 was demonstrated to be phosphorylated at Serine/Threonine by immunoblotting, and the major phosphorylation sites was S187, S205, T206, S208 and S317 as revealed by LC-MS/MS. By an EBOV minigenomic system, EBOV minigenome replication was shown to be significantly inhibited by the phosphorylation-defective mutant, VP35 S187A, but was potentiated by the phosphorylation mimic mutant VP35 S187D. Together, our findings demonstrate that EBOV VP35 is phosphorylated on multiple residues in host cells, especially on S187, which may contribute to efficient viral genomic replication and viral proliferation.
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.