HIV Mutation Detail Information

Virus Mutation HIV Mutation A20L


Basic Characteristics of Mutations
Mutation Site A20L
Mutation Site Sentence In agreement with published data, mutations in an alanine interface in the transmembrane domain of Vpu (A15L/A19L in subtype B, A20L/A24L in subtype C) abrogated the ability of all three viruses to decrease tetherin surface levels (Figure 1D and Figure 1:figure supplement 2A) and to counteract tetherin-mediated restriction of virus release (Figure 1E and Figure 1:figure supplement 2B).
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region Vpu
Standardized Encoding Gene Vpu  
Genotype/Subtype HIV-1 C
Viral Reference "CH293, CH077, and STCO1"
Functional Impact and Mechanisms
Disease HIV Infections    
Immune -
Target Gene BST2   
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location Germany
Literature Information
PMID 30717826
Title HIV-1 Vpu is a potent transcriptional suppressor of NF-kappaB-elicited antiviral immune responses
Author Langer S,Hammer C,Hopfensperger K,Klein L,Hotter D,De Jesus PD,Herbert KM,Pache L,Smith N,van der Merwe JA,Chanda SK,Fellay J,Kirchhoff F,Sauter D
Journal eLife
Journal Info 2019 Feb 5;8:e41930
Abstract Many viral pathogens target innate sensing cascades and/or cellular transcription factors to suppress antiviral immune responses. Here, we show that the accessory viral protein U (Vpu) of HIV-1 exerts broad immunosuppressive effects by inhibiting activation of the transcription factor NF-kappaB. Global transcriptional profiling of infected CD4 +T cells revealed that vpu-deficient HIV-1 strains induce substantially stronger immune responses than the respective wild type viruses. Gene set enrichment analyses and cytokine arrays showed that Vpu suppresses the expression of NF-kappaB targets including interferons and restriction factors. Mutational analyses demonstrated that this immunosuppressive activity of Vpu is independent of its ability to counteract the restriction factor and innate sensor tetherin. However, Vpu-mediated inhibition of immune activation required an arginine residue in the cytoplasmic domain that is critical for blocking NF-kappaB signaling downstream of tetherin. In summary, our findings demonstrate that HIV-1 Vpu potently suppresses NF-kappaB-elicited antiviral immune responses at the transcriptional level.
Sequence Data GSE117655
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.