HIV Mutation Detail Information

Virus Mutation HIV Mutation S40A


Basic Characteristics of Mutations
Mutation Site S40A
Mutation Site Sentence Kudoh and coworkers reported that (i) an S40A substitution in p6Gag abolished incorporation of exogenously expressed Vpr into virus-like Gag particles (VLPs) and (ii) a PKC inhibitor, presumed to prevent phosphorylation of S40, impaired HIV-1 replication in primary macrophages.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region Gag
Standardized Encoding Gene Gag  
Genotype/Subtype HIV-1
Viral Reference -
Functional Impact and Mechanisms
Disease Cell line    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 25524645
Title Re-visiting the functional Relevance of the highly conserved Serine 40 Residue within HIV-1 p6(Gag)
Author Radestock B,Burk R,Muller B,Krausslich HG
Journal Retrovirology
Journal Info 2014 Dec 19;11:114
Abstract BACKGROUND: HIV-1 formation is driven by the viral structural polyprotein Gag, which assembles at the plasma membrane into a hexagonal lattice. The C-terminal p6(Gag) domain harbors short peptide motifs, called late domains, which recruit the cellular endosomal sorting complex required for transport and promote HIV-1 abscission from the plasma membrane. Similar to late domain containing proteins of other viruses, HIV-1 p6 is phosphorylated at multiple residues, including a highly conserved serine at position 40. Previously published studies showed that an S40F exchange in p6(Gag) severely affected virus infectivity, while we had reported that mutation of all phosphorylatable residues in p6(Gag) had only minor effects. FINDINGS: We introduced mutations into p6(Gag) without affecting the overlapping pol reading frame by using an HIV-1 derivative where gag and pol are genetically uncoupled. HIV-1 derivatives with a conservative S40N or a non-conservative S40F exchange were produced. The S40F substitution severely affected virus maturation and infectivity as reported before, while the S40N exchange caused no functional defects and the variant was fully infectious in T-cell lines and primary T-cells. CONCLUSIONS: An HIV-1 variant carrying a conservative S40N exchange in p6(Gag) is fully functional in tissue culture demonstrating that neither S40 nor its phosphorylation are required for HIV-1 release and maturation. The phenotype of the S40F mutation appears to be caused by the bulky hydrophobic residue introduced into a flexible region.
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.