HCMV Mutation Detail Information

Virus Mutation HCMV Mutation D84Y


Basic Characteristics of Mutations
Mutation Site D84Y
Mutation Site Sentence Among these mutations however, four were found in envelope glycoprotein complexes I, II and III, and were therefore considered the most plausible candidates for a causal relation with the partial resistance against the entry inhibitor GT40, i.e., L47P in gO, I417V in gH, D84Y in gN and H177N in gB (Figure 4A).
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region gN
Standardized Encoding Gene UL73  
Genotype/Subtype -
Viral Reference KU317610.1
Functional Impact and Mechanisms
Disease Cell line    
Immune -
Target Gene PDGFRA   
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 34201364
Title Selection of Human Cytomegalovirus Mutants with Resistance against PDGFRalpha-Derived Entry Inhibitors
Author Laib Sampaio K,Lutz C,Engels R,Stohr D,Sinzger C
Journal Viruses
Journal Info 2021 Jun 8;13(6):1094
Abstract The human cytomegalovirus (HCMV) infects fibroblasts via an interaction of its envelope glycoprotein gO with the cellular platelet-derived growth factor receptor alpha (PDGFRalpha), and soluble derivatives of this receptor can inhibit viral entry. We aimed to select mutants with resistance against PDGFRalpha-Fc and the PDGFRalpha-derived peptides GT40 and IK40 to gain insight into the underlying mechanisms and determine the genetic barrier to resistance. An error-prone variant of strain AD169 was propagated in the presence of inhibitors, cell cultures were monitored weekly for signs of increased viral growth, and selected viruses were tested regarding their sensitivity to the inhibitor. Resistant virus was analyzed by DNA sequencing, candidate mutations were transferred into AD169 clone pHB5 by seamless mutagenesis, and reconstituted virus was again tested for loss of sensitivity by dose-response analyses. An S48Y mutation in gO was identified that conferred a three-fold loss of sensitivity against PDGFRalpha-Fc, a combination of mutations in gO, gH, gB and gN reduced sensitivity to GT40 by factor 4, and no loss of sensitivity occurred with IK40. The resistance-conferring mutations support the notion that PDGFRalpha-Fc and GT40 perturb the interaction of gO with its receptor, but the relatively weak effect indicates a high genetic barrier to resistance.
Sequence Data MZ327301
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.